Abstract
Objectives
The objectives of the study are to investigate the anti-cancer properties of quercetin, a widely distributed phytochemical, and assess its potential as a chemopreventive and therapeutic agent for cervical cell carcinoma.
Methods
The study employed cell viability assays for cytotoxicity, flow cytometry for cell cycle arrest, comet assays for DNA damage, nuclear morphology to assess apoptosis, and Western blotting to measure caspase 3 expression, a key apoptosis-related marker.
Results
Notably, a significantly lower half-maximal inhibitory concentration (25.5 μM) at 48 h compared to 24 h highlights the time-dependent nature of quercetin’s cytotoxic effects. Quercetin significantly (P < 0.001) inhibited human cervix epithelioid carcinoma (HeLa) cell viability compared to the control group, indicating its cytotoxic potential. Morphological changes observed in quercetin-treated cells further supported its cytotoxic effects. Quercetin-induced substantial increase in the percentage of cells in the sub-G0/G1 phase relative to controls (P < 0.001) reveals cell cycle arrest and the initiation of apoptosis. In addition, quercetin caused notable DNA damage, as evidenced by the significant increase (P < 0.001) in the comet tail length, highlighting the genotoxic effects of quercetin. Moreover, quercetin treatment significantly (P < 0.001) upregulated the expression of caspase-3, suggesting the activation of the intrinsic apoptotic pathway.
Conclusion
The findings of the current study suggest that quercetin can effectively inhibit HeLa cell viability, induce cell cycle arrest, promote DNA damage, and activate caspase-mediated apoptosis. This underscores quercetin’s therapeutic potential against cervical cancer and highlights caspase-mediated apoptosis as a promising strategy. Prolonged exposure may further enhance its efficacy, offering valuable insights into its potential for long-term cancer treatment.
| Original language | American English |
|---|---|
| Article number | 19(3) |
| Pages (from-to) | 43-51 |
| Number of pages | 9 |
| Journal | International Journal of Health Science |
| Volume | 19 |
| Issue number | 3 |
| DOIs | |
| State | Published - 16 May 2025 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
-
SDG 3 Good Health and Well-being
Keywords
- Apoptosis
- Caspase-3
- Cell cycle arrest
- Cytotoxicity
- Human cervix epithelioid carcinoma cells
- Quercetin
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In: International Journal of Health Science, Vol. 19, No. 3, 19(3), 16.05.2025, p. 43-51.
Research output: Contribution to journal › Article › peer-review
TY - JOUR
T1 - Apoptosis, DNA damage, and cell cycle arrest:
T2 - The anticancer mechanisms of quercetin in human cervix epithelioid carcinoma cells
AU - Fatima, Sabiha
AU - Borappa, Muthukala
AU - Kanakarajan, Sivakumari
AU - Selvaraj, Rajesh
AU - Siddiqi, Nikhat J.
AU - Wasi, Samina
AU - Siyal, Abdulaziz
AU - Patel, Nidhi
AU - Sharma, Preeti
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PY - 2025/5/16
Y1 - 2025/5/16
N2 - Abstract Objectives The objectives of the study are to investigate the anti-cancer properties of quercetin, a widely distributed phytochemical, and assess its potential as a chemopreventive and therapeutic agent for cervical cell carcinoma. Methods The study employed cell viability assays for cytotoxicity, flow cytometry for cell cycle arrest, comet assays for DNA damage, nuclear morphology to assess apoptosis, and Western blotting to measure caspase 3 expression, a key apoptosis-related marker. Results Notably, a significantly lower half-maximal inhibitory concentration (25.5 μM) at 48 h compared to 24 h highlights the time-dependent nature of quercetin’s cytotoxic effects. Quercetin significantly (P < 0.001) inhibited human cervix epithelioid carcinoma (HeLa) cell viability compared to the control group, indicating its cytotoxic potential. Morphological changes observed in quercetin-treated cells further supported its cytotoxic effects. Quercetin-induced substantial increase in the percentage of cells in the sub-G0/G1 phase relative to controls (P < 0.001) reveals cell cycle arrest and the initiation of apoptosis. In addition, quercetin caused notable DNA damage, as evidenced by the significant increase (P < 0.001) in the comet tail length, highlighting the genotoxic effects of quercetin. Moreover, quercetin treatment significantly (P < 0.001) upregulated the expression of caspase-3, suggesting the activation of the intrinsic apoptotic pathway. Conclusion The findings of the current study suggest that quercetin can effectively inhibit HeLa cell viability, induce cell cycle arrest, promote DNA damage, and activate caspase-mediated apoptosis. This underscores quercetin’s therapeutic potential against cervical cancer and highlights caspase-mediated apoptosis as a promising strategy. Prolonged exposure may further enhance its efficacy, offering valuable insights into its potential for long-term cancer treatment.
AB - Abstract Objectives The objectives of the study are to investigate the anti-cancer properties of quercetin, a widely distributed phytochemical, and assess its potential as a chemopreventive and therapeutic agent for cervical cell carcinoma. Methods The study employed cell viability assays for cytotoxicity, flow cytometry for cell cycle arrest, comet assays for DNA damage, nuclear morphology to assess apoptosis, and Western blotting to measure caspase 3 expression, a key apoptosis-related marker. Results Notably, a significantly lower half-maximal inhibitory concentration (25.5 μM) at 48 h compared to 24 h highlights the time-dependent nature of quercetin’s cytotoxic effects. Quercetin significantly (P < 0.001) inhibited human cervix epithelioid carcinoma (HeLa) cell viability compared to the control group, indicating its cytotoxic potential. Morphological changes observed in quercetin-treated cells further supported its cytotoxic effects. Quercetin-induced substantial increase in the percentage of cells in the sub-G0/G1 phase relative to controls (P < 0.001) reveals cell cycle arrest and the initiation of apoptosis. In addition, quercetin caused notable DNA damage, as evidenced by the significant increase (P < 0.001) in the comet tail length, highlighting the genotoxic effects of quercetin. Moreover, quercetin treatment significantly (P < 0.001) upregulated the expression of caspase-3, suggesting the activation of the intrinsic apoptotic pathway. Conclusion The findings of the current study suggest that quercetin can effectively inhibit HeLa cell viability, induce cell cycle arrest, promote DNA damage, and activate caspase-mediated apoptosis. This underscores quercetin’s therapeutic potential against cervical cancer and highlights caspase-mediated apoptosis as a promising strategy. Prolonged exposure may further enhance its efficacy, offering valuable insights into its potential for long-term cancer treatment.
KW - Apoptosis
KW - Caspase-3
KW - Cell cycle arrest
KW - Cytotoxicity
KW - Human cervix epithelioid carcinoma cells
KW - Quercetin
U2 - 10.25259/OA05_8747
DO - 10.25259/OA05_8747
M3 - Article
SN - 1791-4299
VL - 19
SP - 43
EP - 51
JO - International Journal of Health Science
JF - International Journal of Health Science
IS - 3
M1 - 19(3)
ER -