Human Cell Cancer Research Articles

Sustained release of curcumin from fibrin matrix induces cancer cell death and immunomodulation

Despite the role of curcumin in controlling inflammation, angiogenesis, and cancer in human cells, its therapeutic use is limited. The reasons are quick metabolic breakdown, low aqueous solubility, and bioavailability. This study describes the advantages of clinical-grade curcumin-incorporated fibrin matrix either in lyophilized off-the-shelf wafer or injectable hydrogel forms, as a biodegradable local delivery system. To produce the curcumin-fibrin wafer, used clinical-grade fibrin sealant in a modified composition. To fabricate wafer, we premixed the curcumin with either fibrinogen or thrombin, before clotting into a hydrogel. Sustained release of active curcumin from fibrin wafer, suspended in culture medium at 37 °C lasted for seven days. Upon premixing albumin with thrombin and subsequently adding curcumin into the mixture improved the loading concentration and stability. Dose- and time-dependent apoptotic function of curcumin on cancer cell lines upon release from fibrin wafer, were demonstrated in vitro. In vivo immuno-modulation and a nontoxic response to curcumin released from fibrin into the peritoneal cavity of mice were established. The cytotoxic effect of released curcumin was demonstrated; showing both a preventive and therapeutic role against tumor growth. In vivo studies used Dalton's Lymphoma Ascites (DLA) mice model. Both implanted fibrin wafer and injected hydrogel can breakdown by a physiological process and get cleared by the fibrinolytic mechanism. The lyophilized fibrin wafer could function as a hemostat, adhere to surgical cancer tissues, and arrest bleeding. The potential of curcumin in preventing solid tumor metastasis may be explored upon the sustained delivery of the molecule from the fibrin wafer.

Cytotoxic Activity of New Thiol Derivatives

This research included synthesized ten new compounds (1–10) based on alkyl halides, and estimated their anti-cancer effectiveness. All prepared products are proven by Proton nuclear magnetic resonance (1H NMR) and infrared spectroscopy (IR). The anti-cancer effect of compounds 6, 9, and 10 were assessed on MCF-7 breast cancer in human cells, then WRL68 cancer cells. Compound 9 revealed to be most strong with IC50 119.2 μg/mL against MCF-7, while other compounds showed moderate anti-cancer activity. The discoveries of ponder can upgrade the understood of natural exercises of these thiols compounds.

Biogenic copper nanoparticles and their applications: A review

The objective of the present work is the introduction of a quick and simple literature survey about the green bio-synthesized of copper nanoparticles. The survey revealed that the eco-friendly preparation methods using different plant species, properties and potential applications as alternative promising for silver and gold nanoparticles. The review enumerates the classification of nanomaterials in general, green biosynthesis of nanoparticles using plant extracts and its advantages over using bacteria and fungi. The manuscript gives more details about the specific properties for copper nanoparticles as optical properties of copper nanoparticles especially surface plasmon resonance in the visible range, photoluminescence, and bandgap energy. The current review spotlights and focuses on antimicrobial and anticancer activities for copper nanoparticles against several and various types of gram-negative, gram-positive bacteria, fungi, and human cell cancers. Moreover, a new promising activity as adsorptive efficiency of copper nanoparticles for wastewater treatment was revealed.

Rad52 function prevents chromosome loss and truncation in Candida albicans

RAD52 is required for almost all recombination events in Saccharomyces cerevisiae. We took advantage of the heterozygosity of HIS4 in the Candida albicans SC5314 lineage to study the role of Rad52 in the genomic stability of this important fungal pathogen. The rate of loss of heterozygosity (LOH) at HIS4 in rad52-ΔΔ strains was ∼10(-3) , at least 100-fold higher than in Rad52(+) strains. LOH of whole chromosome 4 or truncation of the homologue that carries the functional HIS4 allele was detected in all 80 rad52-ΔΔ His auxotrophs (GLH -GL lab His(-)) obtained from six independent experiments. Isolates that had undergone whole chromosome LOH, presumably due to loss of chromosome, carried two copies of the remaining homologue. Isolates with truncations carried centric fragments of broken chromosomes healed by de novo telomere addition. GLH strains exhibited variable degrees of LOH across the genome, including two strains that became homozygous for all the heterozygous markers tested. In addition, GLH strains exhibited increased chromosomal instability (CIN), which was abolished by reintroduction of RAD52. CIN of GLH isolates is reminiscent of genomic alterations leading to cancer in human cells, and support the mutator hypothesis in which a mutator mutation or CIN phenotype facilitate more mutations/aneuploidies.

Genomic instability due to germline p53 mutations drives preneoplastic Progression toward cancer in human cells

Cells heterozygous for mutations in p53 demonstrate extreme genomic instability and develop mutations detectable at the chromosome level as well as the molecular level. This genomic instability causes initially nontumorigenic ras-expressing immortal LFS cells to progress to a tumorigenic state presumably due to additional mutational events. It is not surprising that LFS families with these p53 mutations develop the additional mutations necessary for cancer to occur at such high frequencies. This observation is consistent with increased cancer rates in these families being due to abrogation of a rate limiting step rather than a rate expected for one less step in a multistep carcinogenic process. Although p53 has been shown to be able to function as a transcription factor, mutations in p53 appear to affect genomic stability in LFS fibroblasts with double minutes and telomeric associations being prominent early events. One possibility is that p53 controls the expression of genes required for fidelity of replication or telomerase activity. Alternatively p53 may itself be a replication factor like the transcription factor CTF. In the future, we plan to investigate whether p53 plays a direct role in replication.