Prostate Cancer Cells Research Articles

Comparison of In Vitro Hair Growth Promotion and Anti-Hair Loss Potential of Thai Rice By-Product from Oryza sativa L. cv. Buebang 3 CMU and Sanpatong.

The bioactive compounds in herbal extracts may provide effective hair loss treatments with fewer side effects compared to synthetic medicines. This study evaluated the effects of Buebang 3 CMU and Sanpatong rice bran extracts, macerated with dichloromethane or 95% ethanol, on hair growth promotion and hair loss prevention. Overall, Buebang 3 CMU extracts contained significantly higher levels of bioactive compounds, including γ-oryzanol, tocopherols, and various polyphenols such as phytic acid, ferulic acid, and chlorogenic acid, compared to Sanpatong extracts. Additionally, ethanolic extracts demonstrated greater bioactive content and antioxidant activities than those extracted with dichloromethane. These compounds enhanced the proliferation of human hair follicle dermal papilla cells (HFDPCs) by 124.28 ± 1.08% (p < 0.05) and modulated anti-inflammatory pathways by reducing nitrite production to 3.20 ± 0.36 µM (p < 0.05). Key hair growth signaling pathways, including Wnt/β-catenin (CTNNB1), Sonic Hedgehog (SHH, SMO, GLI1), and vascular endothelial growth factor (VEGF), were activated by approximately 1.5-fold to 2.5-fold compared to minoxidil. Also, in both human prostate cancer (DU-145) and HFDPC cells, the ethanolic Buebang 3 CMU extract (Et-BB3-CMU) suppressed SRD5A1, SRD5A2, and SRD5A3 expression-key pathways in hair loss-by 2-fold and 1.5-fold more than minoxidil and finasteride, respectively. These findings suggest that Et-BB3-CMU holds promise for promoting hair growth and preventing hair loss.

P001 The MTH1 inhibitor TH287 sensitizes castration-resistant prostate cancer cells to ionizing radiation therapy

P001 The MTH1 inhibitor TH287 sensitizes castration-resistant prostate cancer cells to ionizing radiation therapy

P099 Effect of the PARP inhibitor talazoparib in combination with radiation and enzalutamide in prostate cancer cell models

P099 Effect of the PARP inhibitor talazoparib in combination with radiation and enzalutamide in prostate cancer cell models

P138 The effect of BRAF inhibitor Encorafenib on cell migration and invasion ability in the BRAF-mutant metastatic castration-resistant prostate cancer cells

P138 The effect of BRAF inhibitor Encorafenib on cell migration and invasion ability in the BRAF-mutant metastatic castration-resistant prostate cancer cells

Talaketides A−G, linear polyketides with prostate cancer cytotoxic activity from the mangrove sediment-derived fungus Talaromyces sp. SCSIO 41027

Seven novel linear polyketides, talaketides A−G (1−7), were isolated from the rice media cultures of the mangrove sediment-derived fungus Talaromyces sp. SCSIO 41027. Among these, talaketides A−E (1−5) represented unprecedented unsaturated linear polyketides with an epoxy ring structure. The structures, including absolute configurations of these compounds, were elucidated through detailed analyses of nuclear magnetic resonance (NMR) and high-resolution mass spectrometry (HR-MS) data, as well as electronic custom distributors (ECD) calculations. In the cytotoxicity screening against prostate cancer cell lines, talaketide E (5) demonstrated a dose-dependent inhibitory effect on prostate cancer PC-3 cell lines, with an IC50 value of 14.44 μmol·L−1 . Moreover, compound 5 significantly inhibited the cloning formation of PC-3 cell lines and arrested the cell cycle in S-phase, ultimately inducing apoptosis. These findings indicate that compound 5 may serve as a promising lead compound for the development of a potential treatment for prostate cancer.

Immunogenic properties of nickel-doped maghemite nanoparticles and the implication for cancer immunotherapy

Nanoparticles are commonly used in diagnostics and therapy. They are also increasingly being implemented in cancer immunotherapy because of their ability to deliver drugs and modulate the immune system. However, the effect of nanoparticles on immune cells involved in the anti-tumor immune response is not well understood. The study reported here showed that nickel-doped maghemite nanoparticles (FN NP) are differentially cytotoxic to cultured mouse and human cancer cell lines, causing their death without negatively impacting the subsequent anticancer immune response. It also found that FN NP induced cell death in the mouse colorectal cancer cell line CT26 and human prostate cancer cell line PC-3, but not in the human prostate cancer cell line LNCaP. The induced cancer cell death did not affect the phenotype and responsivity of the isolated mouse peritoneal macrophages, or ex vivo-generated mouse bone marrow-derived, or human monocyte-derived dendritic cells. Additionally, the induced cancer cell death did not prevent the ex vivo-generated mouse or human dendritic cells from stimulating lymphocytes and enriching cell cultures with cancer cell-reactive T-cells. In conclusion, this study shows that FN NP could be a valuable platform for targeting cancer cells without causing immunosuppressive effects on the subsequent anticancer immune response.

Engineering PSMA-targeted nanoparticles co-encapsulating mitoxantrone and indocyanine green for precise combinatory therapy in prostate cancer

Prostate cancer is the 2nd most common cancer in men worldwide. Chemotherapeutic treatment of prostate cancer with mitoxantrone (MTX) has limited efficacy due to severe side effects in which cardiotoxicity and myelosuppression are the two major causes of its dose-limiting toxicity. This study aimed to obtain a poly (lactic-co-glycolic acid) (PLGA) nanoparticle that can precisely deliver MTX to the prostate cancer cells overexpressing the Prostate-specific membrane antigen (PSMA) receptor-sparing healthy tissues and co-loading Indocyanine green (ICG) as a fluorescent photothermal/photodynamic agent for precise combinatory therapy in prostate cancer. The biocompatible polymer PLGA was covalently modified with the peptide of sequence (WQPDTAHHWATL) to actively target the PSMA receptor. Factors like the peptide-to-polymer ratio or the peptide's orientation during the polymer's chemical modification were investigated to enhance the active targeting of the nanoparticles (NPs). NPs were characterised using dynamic light scattering, scanning electron microscopy, and UV–vis spectroscopy to determine their morphological and colloidal properties and optimal MTX and ICG encapsulation efficiency. Quantitative FACS analysis of LNCaP and PC-3 cells incubated with Nile Red-labelled non-targeted PLGA or PLGA-PSMA targeted NPs was assessed to identify the best formulation that bound selectively to PSMA. The orientation of the peptide conjugated to the polymer, which has the C-terminal end of the peptide sequence accessible for interaction with the cell receptor, maximises the targeting capacity of the system. Photothermal experiments using 808 nm near-infrared laser irradiation were conducted, and cytotoxicity was assessed using the resazurin viability assay. Remarkably, our results confirmed the safety and efficacy of a targeted and activatable therapy using polymeric NPs functionalised with the peptide and co-loaded with MTX and ICG. This pioneer nanosystem opens new perspectives for exploring advanced targeted delivery in prostate cancer. It offers a straightforward methodology for functionalising drug delivery systems with bioactive peptides that can be applied to different types of cancer.

Wnt5a promotes VM formation by modulating the stemness and EMT progression of prostate cancer cell.

The incidence of prostate cancer (PCa) is increasing annually, making it the leading cause of tumor-related mortality in males. The available treatment options for metastatic PCa are limited. Vasculogenic mimicry (VM), an emerging phenomenon involving aggressive tumor cells, has a significant impact on patient survival. Misregulation of Wnt5a expression is commonly observed during cancer progression. However, there is a lack of comprehensive studies investigating the effects of Wnt5a on tumor VM formation. In this study, we demonstrate that alterations in wnt5a expression, either through gain or loss, have a significant influence on the formation of VM in tumor cells mediated by cell stemness and EMT progression. Further research has demonstrated that Wnt5a regulates the formation of VM through the PI3K/JNK signaling pathway. These experimental findings offer a novel avenue for the clinical management of prostate cancer.

Management of Dry Mouth Toxicity Following 177Lu-PSMA-617 Radioligand Therapy

Treatment options for patients with metastatic castration-resistant prostate cancer include use of radioligand therapy with 177Lu-PSMA-617. While 177Lu-PSMA-617 can be used to selectively target prostate cancer cells, salivary glands express PSMA on the apical lumen of the acinar epithelium. Xerostomia resulting from the use of radioligand therapy is common. Herein, we report on a case of a Common Terminology Criteria for Adverse Events version 5 grade 2 dry mouth event after administration of 177Lu-PSMA-617. The patient was managed with oral hygiene and xerostomia mitigation strategies using oral rinses.

Integrated single-cell transcriptomic analyses identify a novel lineage plasticity-related cancer cell type involved in prostate cancer progression

Cancer cell plasticity is the ability of neoplastic cells to alter their identity and acquire new biological properties under microenvironmental pressures. In prostate cancer (PCa), lineage plasticity often results in therapy resistance and trans-differentiation to neuroendocrine (NE) lineage. However, identifying the cancer cells harboring lineage plasticity-related status remains challenging. Based on 13 multi-center human PCa bulk transcriptomic cohorts (samples=3314) and 9 bulk transcriptomic datasets derived from PCa experimental models, we established an integrated lineage plasticity-related gene signature, termed LPSig. Leveraging this gene signature, AUCell enrichment analysis was applied to identify the cell population with high lineage plasticity from a comprehensive single-cell RNA-sequencing (scRNA-seq) meta-atlas assembled by us, which consisted of 10 public human PCa scRNA-seq datasets (samples=93, cells=222,529). Moreover, additional scRNA-seq dataset of human PCa, multiplex immunohistochemistry staining for human PCa tissues, invitro and invivo functional experiments, as well as qPCR and Western blot analyses were employed to validate our findings. We found that LPSig could finely capture the dynamics of tumor lineage plasticity throughout the progression of PCa, accurately estimating the status of lineage plasticity. Based on LPSig, we identified a previously undefined minority population of lineage plasticity-related PCa cells (LPCs) from the human PCa scRNA-seq meta-atlas assembled by this study. Furthermore, in-depth dissection revealed pivotal roles of LPCs in trans-differentiation, tumor recurrence, and poor patient survival during PCa progression. Furthermore, we identified HMMR as a representative cell surface marker for LPCs, which was validated using additional scRNA-seq datasets and multiplexed immunohistochemistry. Moreover, HMMR was transcriptionally inhibited by androgen receptor (AR), and was required for the aggressive adenocarcinoma features and NE phenotype. Our study uncovers a novel population of lineage plasticity-related cells with low AR activity, stemness-like traits, and elevated HMMR expression, that may facilitate poor prognosis in PCa. This work was supported by National Key R&D Program of China (2022YFA0807000), National Natural Science Foundation of China (82160584), Advanced Prostate Cancer Diagnosis and Treatment Technology Innovation Team of Kunming Medical University (CXTD202216), and Reserve Talents of Young and Middle-aged Academic Leaders in Yunnan Province (202105AC160013).

Discovery of the first selective and potent PROTAC degrader for the pseudokinase TRIB2

Pseudokinase TRIB2, a member of the CAMK Ser/Thr protein kinase family, regulates various cellular processes through phosphorylation-independent mechanisms. Dysregulation of TRIB2 has been implicated in promoting tumor growth, metastasis, and therapy resistance, making it a promising target for cancer treatment. In this study, we designed and synthesized a series of TRIB2 PROTAC degraders by conjugating a TRIB2 binder 1 with VHL or CRBN ligands via linkers of varying lengths and compositions. Among these compounds, 5k demonstrated potent TRIB2 degradation with a DC50 value of 16.84 nM (95 % CI: 13.66–20.64 nM) in prostate cancer PC3 cells. Mechanistic studies revealed that 5k directly interacted with TRIB2, selectively inducing its degradation through a CRBN-dependent ubiquitin-proteasomal pathway. Moreover, 5k outperformed the TRIB2 binder alone in inhibiting cell proliferation and inducing apoptosis, confirming that TRIB2 protein degradation could be a promising therapeutic strategy for TRIB2-associated cancers. Additionally, compound 5k also serves as an effective tool for probing TRIB2 biology.

The Role of Serine Protease 8 in Mediating Gefitinib Resistance in Non-small Cell Lung Cancer.

This investigation aims to explore the expression levels of serine protease 8 (PRSS8) in gefitinib-resistant Non-Small Cell Lung Cancer (NSCLC) cell lines (PC9/GR) and elucidate its mechanism of action. We measured PRSS8 expression in gefitinib-resistant (PC9/GR) and sensitive (PC9) NSCLC cell lines using Western blot analysis. PRSS8-specific small interfering RNA (PRSS8-siRNA), a recombinant plasmid, and a corresponding blank control were transfected into PC9/GR cells. Subsequently, Western blot analyses were conducted to assess the expression levels of PRSS8, phosphorylated AKT (p-AKT), AKT, phosphorylated mTOR (p-mTOR), mTOR, and various apoptosis-related proteins within each group. Additionally, a cell proliferation assay utilizing Cell Counting Kit-8 (CCK8) was performed on each group treated with gefitinib. PRSS8 expression was markedly higher in PC9/GR cells compared to PC9 cells (p &#60; 0.05). The group treated with PRSS8-siRNA exhibited significantly reduced protein expression levels of PRSS8, p-AKT, p-mTOR, β-catenin, and BCL-2 compared to the control siRNA (Con-siRNA) group, whereas expressions of Caspase9 and Bax were significantly increased. In the untransfected PC9/GR cells, protein expressions of PRSS8, p-AKT, pmTOR, and BCL-2 were significantly elevated when compared with the plasmid-transfected group, which also showed a significant reduction in Bax expression. The proliferative activity of the PRSS8-siRNA group postgefitinib treatment was significantly diminished at 24, 48, and 72 hours in comparison to the Con-siRNA group. The findings indicate that PRSS8 contributes to the acquisition of resistance to gefitinib in NSCLC, potentially through regulation of the AKT/mTOR signaling pathway.

Design, Synthesis and Biological Activity Evaluation of β-Carboline Derivatives Containing Nitrogen Heterocycles.

A series of β-carboline derivatives containing nitrogen heterocycles were designed and synthesized. All compounds were screened for their antitumor activity against four human tumor cell lines (A549, K562, PC-3, T47D). Notably, compound N-(4-(morpholinomethyl)phenyl)-2-((5-(1-(3,4,5-trimethoxyphenyl)-9H-pyrido[3,4-b]indol-3-yl)-1,3,4-oxadiazol-2-yl)thio)acetamide (8q) exhibited significant inhibitory activity against PC-3 cells with an IC50 value of 9.86 µM. Importantly, compound 8q effectively suppressed both the proliferation and migration of PC-3 cells. Mechanistic studies revealed that compound 8q induced cell apoptosis and caused the accumulation of reactive oxygen species (ROS), leading to cell cycle arrest in the G0/G1 phase in PC-3 cells.

Fatty acid composition and anti-cancer activity of essential oil from Tenebrio molitor larvae in combination with zoledronic acid on prostate cancer

The essential oil extracted from Tenebrio molitor larvae (EOTM) is a natural product containing trace elements with potential therapeutic properties. This study aimed to assess the anticancer effects of EOTM and its synergistic interactions with zoledronic acid, a bisphosphonate drug, on prostate cancer cell lines. The chemical composition of EOTM was analyzed using GC-MS revealing a high concentration of fatty acids. The cytotoxicity of EOTM, both as a standalone treatment and in combination with zoledronic acid, was evaluated on prostate cancer cell lines (LNCaP, PC3) and normal hSKM using MTT assays. Results demonstrated that EOTM exhibited selective toxicity, inhibiting the growth of cancer cells in a dose-dependent manner while sparing normal cells. Morphological assessments and gene expression analyses of BCL2 and BAX were conducted through microscopy, Western blotting, and real-time RT-qPCR. These analyses indicated that EOTM induced apoptosis in cancer cells, as evidenced by cellular shrinkage, membrane blebbing, and nuclear fragmentation. Western blot results showed that EOTM downregulated the anti-apoptotic protein BCL2 and upregulated the proapoptotic protein BAX, suggesting activation of apoptosis pathways. Additionally, the combination of EOTM with zoledronic acid amplified these effects. Hoechst 33258 staining further confirmed the purity of cells following treatment. In conclusion, EOTM exhibits strong anticancer properties by inducing apoptosis in prostate cancer cells and demonstrates synergistic potential when combined with zoledronic acid. These findings warrant further investigation of EOTM as a natural and effective cancer treatment option.

Synthesis, Structure, and In Vitro Biological Evaluation of Semi-Synthetic Derivatives of Betulin

Betulin and α-lipoic acid are naturally occurring substances with different biological properties. Combining two phytochemical units into a conjugate is a frequently used method to obtain new compounds with better pharmacokinetic parameters. This research concerned the preparation of lipoate derivatives of betulin using the Steglich method. Experimental lipophilicity values were determined for target compounds 6–10 by reversed-phase thin-layer chromatography. In silico methods were used to calculate the physicochemical parameters and lipophilicity of new derivatives and to determine the probable directions of biological activity. α-Lipoic acid, betulin, and lipoate derivatives 6–10 were tested for antiproliferative activity against MV4-11, A549, MCF-7, PC-3, HCT116, MiaPaca-2, and Hs294T cancer cells. 3-(5-(1,2-Dithiolan-3-yl)pentanoyl))betulin 10 showed moderate anticancer activity against MV4-11, PC-3, and HCT116, with IC50 values in the range of 39.8–76.7 µM. The introduction of a dithiolate substituent at the C3 position in 28-acetylbetulin gave compound 9 the highest activity (IC50 = 37.9 µM), in the ratio of biphenotypic B myelomonocytic leukemia cells (MV4-11). All lipoate derivatives were inactive towards normal cells.

TRIM65 regulates prostate cancer cell growth and stemness through the WNT/β-catenin axis

TRIM65 regulates prostate cancer cell growth and stemness through the WNT/β-catenin axis

Assessing the antiproliferative properties of various teas against the DU-145 prostate cancer cell line: A combined in vitro and in silico investigation

BackgroundPhytotherapy emerges as a promising solution to the challenges posed by cancer treatment. Black, green, and purple teas, renowned for their antioxidant properties, exhibit efficacy against various cancers, including prostate cancer. Study DesignThis was an experimental study conducted from the Kenya Medical Research Institute (KEMRI). Aim of the Studythe present study aimed to evaluate the Cytotoxic effect of black, green and purple teas against prostate cancer cell line DU-145 and in silico prediction of Tea catechins interaction with prostate cancer proteins such as 3D-crystal structures of Androgen-receptor(5T8E) and Human p38 MAPK(1KV2). MethodsThe study started by quantifying tea catechins (Epigallocatechin gallate (EGCG), Epigallocatechin EGC, Epicatechin gallate (ECG) and Epicatechin (EC) with high-liquid chromatography (HPLC), cytotoxicity analysis of black, green and purple tea crude extracts against DU-145 cell line at 24hr and 48 hrs by Resazurin assay and molecular docking was performed with Autodock Vina 1.1.2 software. ResultsEGCG appeared the most predominant catechin with 552.2 ± 10.61 (mg g-1 DW) while EC was the lowest detected with 118.08 ± 9.45 (mg g-1 DW). Purple tea extract exhibited high antiproliferative activity with IC50 of 98.69±1.99 µg/ml at 24hr and 91.21±6.91 µg/ml at 48hr, green tea followed with 121 ± 5.97µg/ml at 24hr and 107.1 ± 2.03 µg/ml at 48hr IC50; black tea was the least effective tea at both 24hr and 48hr with IC50 of 290.8 ± 2.46µg/ml and 237.8 ± 5.59µg/ml respectively. Prediction of catechin target genes and Prostate cancer (Pca)-related genes discovered 121 catechin target genes and 34,926 Pca-related genes. EGC exhibited high binding interaction to 5T8E with the lowest affinity of -9.1Kcal/mol followed by EGCG at -8.4 (Kcal/mol then EC with -8.2 (Kcal/mol) and EGC at -8.1 (Kcal/mol). Catechins interaction with 1KV2 was in the following order EGCG (-9.4 Kcal/mol) ˃ECG (-8.2 Kcal/mol) ˃EC (-8.2 Kcal/mol) ˃EGC (-8.1 Kcal/mol). ConclusionIn vitro experiment detected a very significant antiproliferative activity of black, green and purple tea crude extracts against the DU-145 cell line; furthermore, in silico analysis revealed a strong binding interaction with proteins associated with prostate cancer, indicating that black, green, and purple teas, along with catechins, hold promise as potential herbal remedies for combating prostate cancer.

The effect of pDNA-Buforin II on the expression changes of lncRNAs PCA3, PCAT1, PRNCR1, GAS5 in prostate cancer

BackgroundThis work aims to analyze the alterations in the levels of PCA3, PCAT1, PRNCR1, and GAS5 long non-coding RNAs (lncRNAs) after the activation of pDNA-buforin II in PC3 cancer cells. Materials and methodsThe synthetic nucleic acid sequence of buforin II was included in the pcDNA3.1(+) Mammalian Expression Plasmid. The accuracy of cloning was assessed by using PCR and enzyme digestion techniques. The vectors were transfected into cells utilizing LipofectamineTM2000. The PC3 cancer cells were evaluated using flow cytometry and wound healing analysis. The expression levels of lncRNAs and apoptotic genes were assessed utilizing real-time PCR, with a significance threshold of P < 0.05. ResultsThe recombinant plasmid containing the pDNA-buforin II vector was successfully generated, and the gene sequence demonstrated complete uniformity (100 % similarity) with the buforin II gene. The transfection efficiency of PC3 cells was 79 %. The results are quantified utilizing the growth inhibition 50 % (GI50) parameter, representing the concentration of pDNA-buforin II required to halt 50 % of cell growth. The percentages of early apoptosis, late apoptosis, necrosis, and viable PC3 cells in the pDNA-buforin II group were 23.30 %, 12.70 %, 3.9 %, and 60.10 %, respectively. The RT-PCR study demonstrated that the presence of pDNA-buforin II in PC3 cells decreased the transcription of PCA3, PCAT1, and PRNCR1 lncRNAs compared to the control group treated with PBS. Furthermore, it enhanced the transcription of GAS5 lncRNA. The findings demonstrated a significant upregulation of transcription factors in programmed cell death after treatment with pDNA-buforin II (∗∗P < 0.01). ConclusionsAccording to the results of this study, it can be inferred that pDNA-buforin II can modify the transcription of genes in PC3 cancer cells, specifically about lncRNAs involved in cell apoptotic pathways. The pDNA-buforin II molecule has promising anticancer capabilities and can trigger apoptosis in cells.

Enhancing Effects of Olaparib by Alpha- and Beta-Emitting Radionuclides, X-Rays, and Ultraviolet A Light in Combination with Ortho-IodoHoechst in a Prostate Cancer Cell Model

Background: New therapeutic strategies for metastatic castration-resistant prostate cancer (mCRPC) have been developed in the past to achieve the best response rates. Most recently, the use of combination therapies has been explored to optimize patient outcomes. Poly(ADP-ribose) polymerase inhibitors (PARPi) may help to treat mCRPC more effectively. Objectives: This study aimed to determine whether the combination of a PARPi with different radiation qualities results in different levels of radiosensitization of PC-3 cells. Methods: The radiosensitizing potential of Olaparib in combination with 177Lu, 223Ra, X-rays and photodynamic therapy (PDT) using the UVA light-activated photosensitizer ortho-iodoHoechst33258 (oIH) was evaluated by determining the clonogenic survival, DNA damage and cell cycle analysis. Results: Here, we show that this combination strategy differentially sensitized PC-3 cells to different radiation qualities. The combination of 177Lu with Olaparib increased the numbers of persistent double-strand breaks (DSBs) by a factor of 3.3 and cell death in PC-3 cells. Overall, the β-emitter 177Lu indicated a higher radiosensitization efficacy compared to 223Ra, with X-rays corresponding to dose modification factors (DMF) of 1.77, 1.17 and 1.16 respectively. Even in the case of the α-emitter 223Ra, the effects were much less pronounced than for 177Lu. PARPi also showed a slight potentiation of the cytotoxic effects both in co-treatment with X-rays and with PDT. Conclusions: The results of our study indicate a potential role for Olaparib in further optimizing the PSMA radioligand therapy (PRLT) outcomes. However, further evaluation of the combination of PARPi with PRLT is needed to gain more insights into improving the benefit to patients suffering from mCRPC.

Investigating the in vitro Anticancer Potential and Phytochemical Constituents of Cheilanthes hirta Swartz Plant Extracts

Cancer, a complex group of diseases characterized by uncontrolled cell growth, remains a leading cause of death worldwide, accounting for approximately 10 million deaths in 2020. Despite advancements in chemotherapy and targeted therapies, survival rates have not significantly improved, necessitating the exploration of novel anticancer agents. This study investigates the in vitro anticancer potential and phytochemical constituents of Cheilanthes hirta Swartz, a fern known for its medicinal properties. The plant was collected from KwaZulu Natal, South Africa and extracts were prepared using water, ethanol and methanol. The phytochemical and FTIR screening were carried out using standard procedure and anticancer activities of the extracts were assessed against prostate (PC-3 and DU-145), human T-lymphocytes (SKU-T) and gastric (AGS) cancer cell lines using the MTT assay. The phytochemical screening revealed the presence of tannins, terpenoids, saponins, flavonoids, cardiac glycosides, anthraquinones, phlobatannins, alkaloids and steroids. FTIR spectroscopy identified the functional groups such as hydroxyl, carboxylic acid, terminal alkynes, ketones, phenols and phosphate ions. The cytotoxicity results showed that the ethanol extract exhibited the most potent antiproliferative effects on prostate cancer cell lines, while the aqueous extract had the strongest effect on the gastric cancer cells. This study highlights the potential of C. hirta as a source of bioactive compounds for anticancer drug development, however, further investigation into its mechanisms of action and therapeutic efficacy is needed.