Target Cancer Cells Research Articles

Computational insights into Sitahe (Leuconotis eugenifolia) bioactive compounds: A promising approach for radioprotection through p53 inhibition

The radioprotective potential of Sitahe (Leuconotis eugenifolia) phytochemicals in cancer radiotherapy remains largely unexplored. In this study, in silico docking simulations were conducted to systematically assess the ability of key phytochemicals from Sitahe to modulate p53 activity, a critical gene in DNA repair and cancer therapy. SwissADME analysis revealed favorable physicochemical properties for compounds such as baurenol, alpha amyrin, and beta amyrin, although high lipophilicity may pose challenges for bioavailability. Molecular docking studies identified strong binding affinities between these compounds and the p53 DNA binding domain, with baurenol demonstrating the highest binding affinity at −6.75 kcal/mol, which is better compared to rhazinilam (−4.55 kcal/mol), leuconolam (−4.36 kcal/mol), leuconoxine (−4.26 kcal/mol), and dehydroleuconoxine (−4.76 kcal/mol). Hydrogen bonding with key residues such as Thr123 further enhanced the stability of these complexes. The low inhibition constants (Ki) suggest significant inhibitory potential, particularly for baurenol (11.31 μM). To evaluate the stability and reliability of these interactions, molecular dynamics (MD) simulations were performed over a duration of 500 ns. The results demonstrated that the selected compounds maintained stable molecular dynamics profiles, showing consistent interactions with the target protein throughout the simulation period. Among the compounds tested, baurenol exhibited the best performance with a MM/PBSA binding energy of −68.568 kJ/mol, which is better than rhazinilam (−63.538 kJ/mol). These findings suggest that baurenol, along with other Sitahe phytochemicals, could serve as dual-function agents, offering protection to healthy tissues from radiation-induced damage while targeting cancer cells through p53 modulation. Although these in silico and MD results are promising, further validation through in vitro and in vivo studies is essential to confirm their therapeutic potential and optimize their pharmacokinetic properties. This study positions Sitahe phytochemicals, particularly baurenol, as promising candidates for the development of novel radioprotective agents in cancer treatment.

Monte Carlo simulation of polymer phantoms in proton therapy for eye tumor treatment

Traditional methods for treating eye tumors, such as surgery and radiation therapy, can cause damage to surrounding healthy tissues and unwanted side effects. In recent years, proton therapy has emerged as a significant alternative for the treatment of eye tumors. Proton therapy targets cancer cells using proton particles while minimizing damage to the surrounding healthy tissues. Unlike other radiation therapy techniques, proton therapy uses the Bragg peak, which allows protons to concentrate on a specific depth within the tissue. Proton therapy can deliver a high dose of radiation to the tumor area while protecting nearby healthy tissues. Additionally, proton therapy has a more favorable side effect profile than other treatment methods. This study focuses on simulations conducted on eyes and eye phantoms to examine the effects of proton therapy on eye tissues. The simulations analyzed physical effects such as ionization, recoils, and lateral straggle of proton beams using Bragg curves, recoil analyses, and atomic-level interactions. Results indicate that as the energy levels of proton beams increase, the range and energy transfer in eye tissues also increase. These findings emphasize the potential effectiveness of proton therapy for treating eye tumors. Polymer eye phantoms can serve as reliable tools in proton therapy simulations to optimize treatment planning. This study highlights the importance of proton therapy simulations and demonstrates the successful use of various polymer materials. Future studies may also examine the effects of heavy particles in addition to different polymer materials to comprehensively evaluate the impact of proton beams in biomedical applications.

Targeting the 8-oxodG Base Excision Repair Pathway for Cancer Therapy

Genomic integrity is critical for cellular homeostasis, preventing the accumulation of mutations that can drive diseases such as cancer. Among the mechanisms safeguarding genomic stability, the Base Excision Repair (BER) pathway plays a pivotal role in counteracting oxidative DNA damage caused by reactive oxygen species. Central to this pathway are enzymes like 8-oxoguanine glycosylase 1 (OGG1), which recognize and excise 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) lesions, thereby initiating a series of repair processes that restore DNA integrity. BER inhibitors have recently been identified as a promising approach in cancer therapy, increasing the sensitivity of cancer cells to radiotherapy and chemotherapy. By exploiting tumor-specific DNA repair dependencies and synthetic lethal interactions, these inhibitors could be used to selectively target cancer cells while sparing normal cells. This review provides a robust reference for scientific researchers, offering an updated perspective on small-molecule inhibitors targeting the 8-oxodG-BER pathway and highlighting their potential role in expanding cancer treatment strategies.

Squalene-Conjugated Drugs Exploit Endogenous Low-Density Lipoproteins for Enhanced Targeting for Cancer Therapy

Cancer is a major global health threat and a leading cause of mortality worldwide. Nucleotide analog chemodrugs are commonly used in the treatment of various solid tumors, but their clinical efficacy is often limited by rapid blood metabolization, poor intracellular diffusion and significant side effects due to non-selectivity targeting. To address these challenges, this study investigates the potential of conjugating squalenea natural triterpene and cholesterol biosynthesis precursorto two model chemodrugs to enhance the drug's incorporation into endogenous low-density lipoproteins (LDLs) for targeted cancer delivery. By leveraging the natural affinity of lipoproteins for cancer cells with overexpressed lipoprotein receptors, this approach can potentially improve the drugs specificity to cancer cells and accumulation at tumor sites. Using molecular dynamics (MD) simulations, we found that squalene-conjugated drugs have favorable partitioning into LDL interior with a deep negative free energy well. It confirms that squalene-drug conjugates possess the significantly higher affinity to LDL and the potential to exploit LDL for targeting cancer cells. The improved drug behaviors are expected to improve drug circulation and tumor accumulation. The findings provide valuable insights into the potential of squalene-conjugated chemodrugs as a novel strategy for improving the therapeutic efficacy of nucleoside analogs in cancer treatment

DNA vaccines as promising immuno-therapeutics against cancer: a new insight

Cancer is one of the leading causes of mortality around the world and most of our conventional treatments are not efficient enough to combat this deadly disease. Harnessing the power of the immune system to target cancer cells is one of the most appealing methods for cancer therapy. Nucleotide-based cancer vaccines, especially deoxyribonucleic acid (DNA) cancer vaccines are viable novel cancer treatments that have recently garnered significant attention. DNA cancer vaccines are made of plasmid molecules that encode tumor-associated or tumor-specific antigens (TAAs or TSAs), and possibly some other immunomodulatory adjuvants such as pro-inflammatory interleukins. Following the internalization of plasmids into cells, their genes are expressed and the tumor antigens are loaded on major histocompatibility molecules to be presented to T-cells. After the T-cells have been activated, they will look for tumor antigens and destroy the tumor cells upon encountering them. As with any other treatment, there are pros and cons associated with using these vaccines. They are relatively safe, usually well-tolerated, stable, easily mass-produced, cost-effective, and easily stored and transported. They can induce a systemic immune response effective on both the primary tumor and metastases. The main disadvantage of DNA vaccines is their poor immunogenicity. Several approaches including structural modification, combination therapy with conventional and novel cancer treatments (such as chemotherapy, radiotherapy, and immune checkpoint blockade (ICB)), and the incorporation of adjuvants into the plasmid structure have been studied to enhance the vaccine’s immunogenicity and improve the clinical outcome of cancer patients. In this review, we will discuss some of the most promising optimization strategies and examine some of the important trials regarding these vaccines.

A Smart mRNA-Initiated Theranostic Multi-shRNA Nanofactory for Precise and Efficient Cancer Gene Therapy.

Despite the significant potential of short hairpin RNA (shRNA)-mediated gene therapy for various diseases, the clinical success of cancer treatment remains poor, partly because of low selectivity and low efficiency. In this study, an mRNA-initiated autonomous multi-shRNA nanofactory (RNF@CM) is designed for in vivo amplification imaging and precise cancer treatment. The RNF@CM consists of a gold nanoparticle core, an interlayer of two types of three-stranded DNA/RNA hybrid probes, one of which is bound to aptamer-inhibited DNA polymerases, and an outer layer of the cancer cell membrane. After the specific delivery of RNF@CM into target cancer cells, an intracellular tumour-related mRNA target can initiate the RNF@CM with a circular strand-displacement polymerisation reaction, resulting in the release of significantly amplified fluorescence and continuous production of three types of shRNAs. The RNF@CM effectively distinguished cancer cells from normal cells, exclusively produced multiple shRNAs in response to a specific mRNA target in cancer cells, accurately diagnosed tumours in vivo, and significantly inhibited tumour growth with negligible toxicity, expanding the toolbox for on-demand gene delivery and precision theranostics.

A Conjugate of an EGFR-Binding Peptide and Doxorubicin Shows Selective Toxicity to Triple-Negative Breast Cancer Cells.

Selective targeting of cancer cells via overexpressed cell-surface receptors is a promising strategy to enhance chemotherapy efficacy and minimize off-target side effects. In this study, we designed peptide 31 (YHWYGYTPERVI) to target the overexpressed epidermal growth factor receptor (EGFR) in triple-negative breast cancer (TNBC) cells. Peptide 31 is internalized by TNBC cells through EGFR-mediated endocytosis and shares sequence and structural similarities with human EGF (hEGF), a natural EGFR ligand. Unlike hEGF, peptide 31 does not induce cell migration in TNBC cells. A novel conjugate of peptide 31 with doxorubicin (Dox) retains selectivity for TNBC cells and exhibits significant toxicity comparable to that of unconjugated Dox. Importantly, this conjugate shows no toxicity toward normal breast epithelial cells up to a high concentration (25 μM). Thus, peptide 31 serves as a versatile targeting ligand for developing novel conjugates with high selectivity for EGFR-positive cancers.

Y2O3NPs induce selective cytotoxicity, genomic instability, oxidative stress and ROS mediated mitochondrial apoptosis in human epidermoid skin A-431 Cancer cells

Yttrium oxide nanoparticles (Y2O3NPs) have emerged as a promising avenue for cancer therapy, primarily due to their distinctive properties that facilitate selective targeting of cancer cells. Despite their potential, the therapeutic effects of Y2O3NPs on human epidermoid skin cancer remain largely unexplored. This study was thus conducted to investigate the impact of Y2O3NPs on both human skin normal and cancer cells, with an emphasis on assessing their cytotoxicity, genotoxicity, and the mechanisms underlying these effects. Cell viability and apoptosis induction were assessed using the Sulforhodamine B and chromatin diffusion assay, respectively. Reactive oxygen species (ROS) level, mitochondrial membrane potential integrity, oxidative stress markers and expression level of apoptotic and mitochondrial genes were also estimated. Our findings highlight the selective and significant cytotoxicity of Y2O3NPs against human epidermoid A-431 cancer cells. Notably, exposure to five Y2O3NPs concentrations (0.1, 1, 10, 100 and 1000 µg/ml) resulted in a high concentration-dependent reduction in cell viability and a corresponding increase in cell death observed 72 h post-treatment specifically in A-431 cancer cells, while normal skin fibroblast (HSF) cells exhibited minimal toxicity. When A-431 cancer cells were treated with the half-maximal inhibitory concentration (IC50) of Y2O3NPs for 72 h, a significant increase in ROS generation was noted. This led to oxidative stress, along with severe damage to genomic DNA and mitochondrial membrane potential, triggering substantial apoptosis. Furthermore, a concurrent significant upregulation of apoptotic p53 and mitochondrial ND3 genes was observed, coupled with a notable decrease in the anti-apoptotic Bcl2 gene expression.Overall, Y2O3NPs demonstrate considerable promise as a therapeutic agent for skin epidermoid cancer due to their ability to selectively target and induce cytotoxic effects in A-431 cancer cells, all while causing minimal harm to normal HSF cells. This selective cytotoxicity appears to be associated with Y2O3NPs’ ability to induce excessive ROS production and subsequent oxidative stress, leading to significant genomic DNA fragmentation, loss of mitochondrial permeability, and alterations in apoptotic and mitochondrial genes’ expression, ultimately promoting apoptosis in A-431 cancer cells. These findings establish a foundation for further research into the utilization of Y2O3NPs in targeted cancer therapies and underscore the necessity for ongoing investigation into their safety and efficacy in clinical applications.

KDM4A Silencing Reverses Cisplatin Resistance in Ovarian Cancer Cells by Reducing Mitophagy via SNCA Transcriptional Inactivation.

Ovarian cancer is one of the deadliest gynecologic cancers, with chemotherapy resistance as the greatest clinical challenge. Autophagy occurrence is associated with cisplatin (DDP)-resistant ovarian cancer cells. Herein, the role and mechanism of alpha-synuclein (SNCA), the autophagy-related gene, in DDP resistance of ovarian cancer cells are explored. Differentially expressed genes in DDP resistance of ovarian cancer cells were analyzed by GEO2R tools. DDP-resistant ovarian cancer cells (A2780/DDP) were transfected and treated with 2.5 μg/mL DDP for 72 h, followed by the determination of cell viability, proliferation, apoptosis, and expressions of SNCA, lysine demethylase 4A (KDM4A), histone H3 lysine 9 trimethylation (H3K9me3), and mitophagy-related proteins. The H3K9me3 demethylation of SNCA by KDM4A was confirmed by chromatin immunoprecipitation. SNCA and KDM4A were highly expressed in DDP-resistant ovarian cancer cells and their parental cells. KDM4A knockdown diminished expressions of KDM4A and SNCA and elevated H3K9me3 expression and H3K9me3 enrichment on SNCA promoter in A2780/DDP cells. SNCA or KDM4A knockdown inhibited cell viability, proliferation, and levels of LC3-II/LC3-I and Parkin while inducing cell apoptosis and upregulating Cyt-C expression of A2780/DDP cells with/without DDP treatment; however, SNCA overexpression not only did conversely but also reversed the effects of KDM4A knockdown on DDP-treated A2780/DDP cells and vice versa. Silencing of KDM4A-mediated transcription inactivation of SNCA reduces mitophagy, thus inhibiting the resistance of ovarian cancer cells to cisplatin. KDM4A may be a promising drug target for DDP-resistant ovarian cancer cells.

Carbon-based nanozymes for cancer therapy and diagnosis: A review.

Carbon-based nanozymes (CNs) have emerged as a significant innovation in targeted cancer therapy, demonstrating great potential for advancing cancer diagnosis and treatment. With exceptional catalytic properties, remarkable biocompatibility, and the ability to precisely target cancer cells, CNs provide a promising avenue for the development of novel oncological therapies. By functionalizing their surfaces with targeting ligands, such as antibodies or peptides, CNs can specifically recognize and bind to cancer cells. This targeted approach ensures that therapeutic agents are delivered directly to the tumor site, minimizing off-target effects, and reducing systemic toxicity. Additionally, the enzyme-like activities of CNs, when combined with conventional therapies such as chemotherapeutics, photothermal therapy, and photodynamic therapy, or other modalities can enhance therapeutic outcomes. Integrating CNs into clinical practice could significantly improve therapeutic efficacy, reduce probable side effects, enhance patient outcomes, and drive a shift towards more personalized cancer care. Besides, CNs can also be employed in biosensors and diagnostic nanomaterials, enabling rapid, selective, and highly accurate detection of specific biomarkers. Their versatile functionalities open new avenues for refining imaging techniques, ultimately contributing to early diagnosis and better clinical decision-making. This review consolidates recent studies exploring CNs in cancer targeting, highlighting both their diagnostic and therapeutic potential in oncology.

Threonine and tyrosine kinase (TTK) mRNA and protein expression in breast cancer; prognostic significance in the neoadjuvant setting.

Threonine and tyrosine kinase (TTK) is up-regulated in triple-negative breast cancer (TNBC), yet its expression in patients undergoing neoadjuvant chemotherapy (NACT) remains unexplored. This investigation aims to assess TTK protein expression in treatment-naïve pre-treatment cores and paired pre- and post-NACT breast cancer (BC) cohorts, as well as its correlation with microcephaly 1 (MCPH1) protein expression. Transcriptomic data were sourced from the Gene Expression Omnibus microarray database for mRNA expression analysis. TTK protein expression was evaluated using immunohistochemistry staining, employing receiver operating characteristic curve analysis to determine an optimal TTK expression cut-off point. The association between TTK expression, clinicopathological parameters and survival outcomes was examined. Additionally, MCPH1 protein expression was assessed in a pilot study. Analysis revealed a significantly elevated TTK mRNA expression in BC tissue compared to normal breast tissue, with high TTK mRNA levels predicting reduced overall survival. Notably, TTK protein expression increased significantly post-NACT in a paired cohort. Conversely, decreased TTK protein expression pre-NACT was correlated with improved overall survival. High TTK and low MCPH1 protein expression was significantly correlated, highlighting TTK's potential as a biomarker for BC and a therapeutic target for MCPH1-deficient cancer cells.

Design and Evaluation of 5-Oxo-1,2,4-triazole-3-carboxamide Compounds as Promising Anticancer Agents: Synthesis, Characterization, In vitro Cytotoxicity and Molecular Docking Studies.

Cancer presents a significant global health challenge, necessitating effective treatment strategies. While chemotherapy is widely employed, its non-specific nature can induce adverse effects on normal cells, prompting the exploration of targeted therapies. The 1,2,4-triazole scaffold has emerged as a promising element in anticancer drug development due to its structural diversity and potential to target cancer cells. This study aims to synthesize and evaluate novel derivatives derived from the 1,2,4-triazole scaffold for their potential as anticancer agents. Molecular docking techniques are employed to investigate the interactions between the designed derivatives and specific cancer-related targets, providing insights into potential underlying mechanisms. The synthesis involves a three-step process to produce 5-oxo-1,2,4-triazole-3-carboxamide derivatives. Various analytical techniques, including NMR and HRMS, validate the successful synthesis. Molecular docking studies utilize X-ray crystal structures of EGFR and CDK-4 obtained from the Protein Data Bank, employing the Schrödinger suite for ligand preparation and Glide's extra-precision docking modes for scoring. The synthesis yields compounds with moderate to good yields, supported by detailed characterization. Molecular docking scores for the derivatives against EGFR and CDK-4 revealed diverse affinities influenced by distinct substituents. Compounds with hydroxyl, and halogen, substitutions exhibited notable binding affinities, while alkyl and amino substitutions showed varying effects. The 1,2,4-triazole derivatives demonstrated potential for targeted cancer therapy. The study highlights the successful synthesis of 5-oxo-1,2,4-triazole-3-carboxamides and their diverse interactions with cancer-related targets. The findings emphasized the potential of these derivatives as candidates for further development as anticancer agents, offering insights into structure-activity relationships. The 1,2,4-triazole scaffold stands out as a promising platform for advancing cancer treatment with enhanced precision and efficacy.

S6K1 is a Targetable Vulnerability in Tumors Exhibiting Plasticity and Therapy Resistance.

Background: Most tumors initially respond to treatment, yet refractory clones subsequently develop owing to resistance mechanisms associated with cancer cell plasticity and heterogeneity. Methods: We used a chemical biology approach to identify protein targets in cancer cells exhibiting diverse driver mutations and representing models of tumor lineage plasticity and therapy resistance. An unbiased screen of a drug library was performed against cancer cells followed by synthesis of chemical analogs of the most effective drug. The cancer subtype target range of the leading drug was determined by PRISM analysis of over 900 cancer cell lines at the Broad Institute, MA. RNA-sequencing and enrichment analysis of differentially expressed genes, as well as computational molecular modeling and pull-down with biotinylated small molecules were used to identify and validate RPS6KB1 (p70S6K or S6K1) as an essential target. Genetic restoration was used to test the functional role of S6K1 in cell culture and xenograft models. Results: We identified a novel derivative of the antihistamine drug ebastine, designated Super-ebastine (Super-EBS), that inhibited the viability of cancer cells representing diverse KRAS and EGFR driver mutations and models of plasticity and treatment resistance. Interestingly, PRISM analysis indicated that over 95% of the diverse cancer cell lines tested were sensitive to Super-EBS and the predicted target was the serine/threonine kinase S6K1. S6K1 is upregulated in various cancers relative to counterpart normal/benign tissues and phosphorylated-S6K1 predicts poor prognosis for cancer patients. We noted that inhibition of S6K1 phosphorylation was necessary for tumor cell growth inhibition, and restoration of phospho-S6K1 rendered tumor cells resistant to Super-EBS. Inhibition of S6K1 phosphorylation by Super-EBS induced caspase-2 dependent apoptosis via inhibition of the Cdc42/Rac-1/p-PAK1 pathway that led to actin depolymerization and caspase-2 activation. The essential role of S6K1 in the action of Super-EBS was recapitulated in xenografts, and knockout of S6K1 abrogated tumor growth in mice. Conclusion: S6K1 is a therapeutic vulnerability in tumors exhibiting intrinsic and/or acquired resistance to treatment.

Anticancer Effectivity of Nanocrystals Derived from Mangosteen (Garcinia mangostana) Peel Extract on Leukemia HL-60 Cells

Leukemia, characterized by abnormal leukocyte proliferation, ranks ninth in Indonesia as the most common cancer. While treatments such as chemotherapy and radiation effectively target cancer cells, they also risk damaging healthy blood cells. This has spurred interest in exploring low-toxicity herbal compounds as potential therapies, with mangosteen peel emerging as a widely researched option. Nanotechnology, which has the potential to enhance the bioavailability of herbal compounds, is also a focus of extensive research. This study objective was to assess the impact of Mangosteen Peel Nanocrystal (MPN) on HL-60 leukemia cells by analyzing various parameters, including cytotoxicity, reactive oxygen species (ROS) levels, senescence, and gene expression changes. MPN was prepared with high-speed milling and characterized using particle size analyzers, microscopy, and stability assessments. HL-60 cells were cultured and subjected to MPN treatment. Cytotoxicity was evaluated using WST-8 assays, ROS levels were assessed using flow cytometry, and senescence analyses using Senescence-Associated b-Galactosidase Staining. AKT and FLT-1 gene expression were determined via qRT-PCR. MPN has been successfully characterized as a nanoparticle based on size, stability, and morphology. MPN has an impact on leukemia cells by increasing cytotoxicity, decreasing ROS levels, inducing senescence, and modulating AKT and FLT-1 gene expressions. The findings suggest potential implications for MPN in targeting leukemia cells. The study sheds light on the promising effects of MPN in leukemia cell models, indicating its potential applications in targeting cancer cells, inducing senescence, decreasing ROS levels, and modulating gene expressions related to cell survival and proliferation.

Immunotherapy in colorectal cancer: Statuses and strategies.

Colorectal cancer (CRC) is widely recognized as the third most prevalent malignancy globally and the second leading cause of cancer-related mortality. Traditional treatment modalities for CRC, including surgery, chemotherapy, and radiotherapy, can be utilized either individually or in combination. However, these treatments frequently result in significant side effects due to their non-specificity and cytotoxicity affecting all cells. Moreover, a considerable number of patients face relapses following these treatments. Consequently, it is imperative to explore more efficacious treatment interventions for CRC patients. Immunotherapy, an emerging frontier in oncology, represents a novel therapeutic approach that leverages the body's immune system to target cancer cells. The principal advantage of immunotherapy is its capacity to selectively target cancer cells while minimizing damage to healthy cells. Its recent adoption as a neoadjuvant therapy presents significant potential to transform the treatment landscape for both primary resectable and metastatic CRC. This review endeavors to offer a comprehensive overview of current strategies in CRC immunotherapy, critically analyze existing literature, underscore anticipated outcomes from ongoing clinical trials, and deliberate on the challenges and impediments encountered within the field of immunotherapy.

Novel Mini-Protein Plays a Role in Targeting Cancer Cells

Novel Mini-Protein Plays a Role in Targeting Cancer Cells

Multifunctional Ru(III)/Fe3O4/DNA nanoplatform for photothermal-enhanced photodynamic and chemodynamic cancer therapy

Among the many cancer treatment methods, there have been many reports on the use of nanoplatforms with single treatment methods such as photothermal, photodynamic or chemodynamic for cancer treatment. In this study, Ru(III) with photodynamic effect and Fe3O4 nanoparticles with photothermal and chemodynamic effects are connected through long DNA chains with efficient active targeting rolling circle amplification to construct Ru(III)/Fe3O4/DNA nano-platform realizes the combination of photothermal, photodynamic and chemodynamic treatment, which significantly improves the therapeutic effect of the nano-platform. Its multiple active targeting capabilities reduce the damage to normal cells. Ru(III) has excellent photodynamic effect and can catalyze the respiration product NADH (Nicotinamide adenine dinucleotide)to produce highly oxidizing H2O2. Fe3O4 NPs has weak absorption at 808 nm indicates that it can perform mild photothermal treatment, and the Fe2+ in it can react with H2O2 to produce ·OH and participate in chemodynamic treatment. Each repeating unit on the rolling circle amplified DNA long chain is connected to the AS1411 aptamer that can actively target cancer cells. Unlike the passive targeting of other nanomedicines, active and efficient targeting is achieved, and a small amount of drugs can achieve high efficacy. The therapeutic effect also reduces the damage to normal cells. The comprehensive killing effect of Ru(III)/Fe3O4/DNA can reach 85.1 %. Its high targeting of cancer cells can also be used for imaging detection of cancer cells. This new nanoplatform provides an idea for the synergy of multiple cancer treatments.

Perfluorocarbon-polyepinephrine core-shell nanoparticles as a near-infrared light activatable theranostic platform for bimodal imaging-guided photothermal/chemodynamic synergistic cancer therapy.

Background: Activatable multifunctional nanoparticles present considerable advantages in cancer treatment by integrating both diagnostic and therapeutic functionalities into a single platform. These nanoparticles can be precisely engineered to selectively target cancer cells, thereby reducing the risk of damage to healthy tissues. Once localized at the target site, they can be activated by external stimuli such as light, pH changes, or specific enzymes, enabling precise control over the release of therapeutic agents or the initiation of therapeutic effects. Furthermore, these nanoparticles can be designed to incorporate multiple therapeutic modalities, including chemotherapy, photothermal therapy (PTT), and chemodynamic therapy (CDT). This comprehensive approach facilitates real-time monitoring of treatment efficacy and allows for dynamic adjustments to therapy, resulting in more personalized and effective cancer treatments. Methods: This study reports the synthesis of perfluorocarbon (PFC)-encapsulated fluorescent polyepinephrine (PEPP) nanoshells chelated with Fe2+ (PFC@PEPP-Fe) and explores their potential for bimodal imaging and synergistic combination therapy in cancer treatment. The cellular uptake, cytotoxicity, and in vitro therapeutic efficacy of PFC@PEPP-Fe were assessed using 4T1 breast cancer cells. In vivo bimodal imaging using fluorescence (FL) and ultrasound (US) was conducted after injection into 4T1 tumor-bearing balb/c nude mice. The synergistic anticancer effects of PFC@PEPP-Fe, combining CDT and PTT, were evaluated following 808 nm laser irradiation (1 W/cm²) for 5 min, with treatment outcomes monitored over a 14 days period. Results: Both in vitro and in vivo studies demonstrated that PFC@PEPP-Fe enables effective bimodal imaging and exhibits substantial anticancer efficacy through the synergistic effects of PTT and CDT. Near-infrared (NIR) laser irradiation increased the temperature, enhancing the release of O2 and the production of H2O2, which in turn amplified the CDT effect. The combination of PFC@PEPP-Fe administration and NIR laser significantly reduced tumor volume, slowed tumor growth, and improved survival in 4T1 tumor-bearing mice, confirming the strong anticancer activity due to the PTT/CDT synergy. Conclusions: As a multifunctional theranostic nanoparticle, PFC@PEPP-Fe not only enables cancer cell-specific US/FL bimodal imaging through the generation of microbubbles from its PFC core and fluorescent PEPP shells but also facilitates synergistic chemodynamic and photothermal therapeutic actions under NIR laser irradiation, which induces the self-supply of H2O2 and O2 within cancer cells.

Impact of Oncological Treatments on Reproductive Capacity: Alternatives to Minimize Risks and the Role of DEX Immunotherapy

Fertility preservation in cancer patients is an increasingly relevant challenge due to the gonadotoxic effects of conventional treatments, such as chemotherapy and radiotherapy. This article reviews current options for fertility preservation and explores the potential of DEX immunotherapy as a less invasive alternative. Initially, an overview of cancer incidence in fertile age and the importance of addressing reproductive concerns in this population group is presented. Subsequently, the negative impacts of conventional treatments on reproductive capacity are analyzed and strategies to minimize these risks, such as reducing treatment intensity and using cryopreservation techniques, are discussed DEX immunotherapy stands out as a promising option, with a lower risk of gonadotoxicity compared to traditional treatments. This immunological approach allows to specifically target cancer cells, reducing damage to reproductive cells and offering better fertility preservation in young patients. Finally, the article addresses future research needs and practical guidelines for clinicians, highlighting the importance of a multidisciplinary approach that integrates fertility preservation options in cancer treatment. It is concluded that, although DEX immunotherapy is a viable alternative, it is essential to promote further research and develop specific clinical protocols to maximize its effectiveness and safety in terms of long-term reproductive health

Nanocarriers in glioblastoma treatment: a neuroimmunological perspective.

Glioblastoma multiforme (GBM) is the most fatal brain tumor with a poor prognosis with current treatments, mainly because of intrinsic resistance processes. GBM is also referred to as grade 4 astrocytoma, that makes up about 15.4 % of brain cancers globally as well as 60-75 % of astrocytoma. The most prevalent therapeutic choices for GBM comprise surgery in combination with radiotherapy and chemotherapy, providing patients with an average survival of 6-14months. Nanocarriers provide various benefits such as enhanced drug solubility, biocompatibility, targeted activity, as well as minimized side effects. In addition, GBM treatment comes with several challenges such as the presence of the blood-brain barrier (BBB), blood-brain tumor barrier (BBTB), overexpressed efflux pumps, infiltration, invasion, drug resistance, as well as immune escape due to tumor microenvironment (TME) and cancer stem cells (CSC). Recent research has focused on nanocarriers due to their ability to self-assemble, improve bioavailability, provide controlled release, and penetrate the BBB. These nano-based components could potentially enhance drug accumulation in brain tumor tissues and reduce systemic toxicity, making them a compelling solution for GBM therapy. This review captures the complexities associated with multi-functional nano drug delivery systems (NDDS) in crossing the blood-brain barrier (BBB) and targeting cancer cells. In addition, it presents a succinct overview of various types of targeted multi-functional nano drug delivery system (NDDS) which has exhibited promising value for improving drug delivery to the brain.