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Chrysin Modulates Cell Cycle Progression, Apoptosis, and Angiogenic Signaling in HPV16-Positive CaSki Cervical Cancer Cells | ||
| Journal of Epigenetics | ||
| مقالات آماده انتشار، پذیرفته شده، انتشار آنلاین از تاریخ 23 آبان 1405 | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22111/jep.2026.55611.1108 | ||
| نویسندگان | ||
| Mahdis Gholami Fashkhami؛ Hadi Habibollahi* ؛ Seyedeh Tooba Shafighi | ||
| Department of Biology, Ra.C., Islamic Azad University, Rasht, Iran. | ||
| چکیده | ||
| Background: Cervical cancer remains a major global health issue, mainly caused by persistent high-risk HPV infection, especially HPV16. Key molecular events include abnormal cell-cycle progression, evasion of apoptosis, and increased angiogenesis, which drive cancer progression and resistance. Naturally occurring flavonoids show promise as multi-target anticancer agents by affecting various oncogenic pathways. This study examined the cytotoxic, apoptotic, and transcriptional effects of chrysin (5,7-dihydroxyflavone) in HPV16-positive CaSki cervical cancer cells. Methods: Cell viability was evaluated using an MTT assay after 48 h of chrysin treatment, and the half-maximal inhibitory concentration (IC₅₀) was determined. Apoptosis induction was quantified by Annexin V/PI flow cytometry, and the mRNA expression levels of Cyclin D1, Survivin, and VEGF were analyzed by quantitative real-time PCR (qRT-PCR). Results: Chrysin significantly reduced CaSki cell viability in a dose-dependent manner, with an IC₅₀ of 112 µg/ml at 48 h. Flow cytometric analysis revealed a statistically significant increase in early and late apoptotic cell populations after chrysin exposure compared with untreated controls. At the molecular level, chrysin treatment significantly downregulated Cyclin D1 mRNA (~45% reduction; P < 0.05), indicating inhibition of the G1/S cell-cycle transition. In parallel, expression of the anti-apoptotic gene Survivin was markedly decreased (P < 0.001), consistent with enhanced apoptotic signaling. Furthermore, VEGF expression was significantly suppressed (P < 0.05), suggesting attenuation of angiogenesis-associated pathways. Conclusions: Collectively, these findings demonstrate that chrysin exerts a coordinated, multi-target anticancer effect in HPV16-positive cervical cancer cells by suppressing proliferation, promoting apoptosis, and inhibiting angiogenic signaling, supporting its potential as a complementary therapeutic candidate for cervical cancer management. | ||
| کلیدواژه‌ها | ||
| Chrysin؛ Cervical carcinoma؛ HPV16 oncogenesis؛ Cyclin D1/Survivin/VEGF axis؛ Multi target flavonoid therapy | ||
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