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Irshad, Sana, Khan, Hazar, Khawer, Asma, Khan, Muhammad, Razzak, Anum, Azhar, Mudassar, Roome, Talat, Faizi, Shaheen, Farooq, Ahsana, Kashif, Muhammad. (1405). Patuletin Caused Growth Inhibition of NCI-H460 Cancer Cells via Induction of Apoptosis. سامانه مدیریت نشریات علمی, (), -. doi: 10.30476/mejc.2026.107774.2301
Sana Irshad; Hazar Khan; Asma Khawer; Muhammad Aitmaud Uddolah Khan; Anum Razzak; Mudassar Azhar; Talat Roome; Shaheen Faizi; Ahsana Dar Farooq; Muhammad Kashif. "Patuletin Caused Growth Inhibition of NCI-H460 Cancer Cells via Induction of Apoptosis". سامانه مدیریت نشریات علمی, , , 1405, -. doi: 10.30476/mejc.2026.107774.2301
Irshad, Sana, Khan, Hazar, Khawer, Asma, Khan, Muhammad, Razzak, Anum, Azhar, Mudassar, Roome, Talat, Faizi, Shaheen, Farooq, Ahsana, Kashif, Muhammad. (1405). 'Patuletin Caused Growth Inhibition of NCI-H460 Cancer Cells via Induction of Apoptosis', سامانه مدیریت نشریات علمی, (), pp. -. doi: 10.30476/mejc.2026.107774.2301
Irshad, Sana, Khan, Hazar, Khawer, Asma, Khan, Muhammad, Razzak, Anum, Azhar, Mudassar, Roome, Talat, Faizi, Shaheen, Farooq, Ahsana, Kashif, Muhammad. Patuletin Caused Growth Inhibition of NCI-H460 Cancer Cells via Induction of Apoptosis. سامانه مدیریت نشریات علمی, 1405; (): -. doi: 10.30476/mejc.2026.107774.2301

Patuletin Caused Growth Inhibition of NCI-H460 Cancer Cells via Induction of Apoptosis

Middle East Journal of Cancer
مقالات آماده انتشار، پذیرفته شده، انتشار آنلاین از تاریخ 09 مهر 1405    اصل مقاله (459.71 K)
نوع مقاله: Original Article(s)
شناسه دیجیتال (DOI): 10.30476/mejc.2026.107774.2301
نویسندگان
Sana Irshad1؛ Hazar Khan2؛ Asma Khawer1؛ Muhammad Aitmaud Uddolah Khan3؛ Anum Razzak1؛ Mudassar Azhar4؛ Talat Roome1؛ Shaheen Faizi5؛ Ahsana Dar Farooq6؛ Muhammad Kashif* 1
1Department of Pharmacology, Dow University of Health Sciences, Karachi, Pakistan
2Department of Pharmacology, Makran Medical College, Turbat, Pakistan
3Department of Pharmacology, Liaquat National Medical College, Karachi, Pakistan
4Department of Basic Medical Sciences, Salim Habib University, Karachi, Pakistan
5International Center for Chemical and Biological Sciences, University of Karachi, Karachi, Pakistan
6Hamdard Al-Majeed College of Eastern Medicine, Hamdard University, Karachi, Pakistan
چکیده
Background: Non-small cell lung cancer is among the major causes of mortality, globally. Previous studies demonstrated therapeutic potential of Tagetes patula flower methanolic extract against this cancer. The present study aimed at evaluating the anti-cancer potential of patuletin, a flavonoid believed to underlie medicinal effects of Tagetes flower. 
Method: This experimental study was performed on NCI-H460 cell lines. The cell viability was assessed using Sulforhodamine B assay followed by flow-cytometry-based cell cycle analysis (propidium iodide), assessment of apoptosis [mitochondrial membrane potential and Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) fluorescence], and deoxyribonucleic acid [DNA (plasmid and genomic)] fragmentation. The expression of BAK, BCL-XL and p53 genes were assessed using quantitative polymerase chain reaction. The doxorubicin served as standard drug. Statistical analysis (One-way ANOVA followed by Least Significant Difference) was performed using SPSS software (v19.0, Chicago, IL, USA).  The level of significance was set at *(P < 0.05), **(P < 0.01), and ***(P < 0.005).
Results:  Patuletin arrested the growth of NCI-H460 cells with a 50% growth inhibition (GI50) of 61 µg/mL. The cell cycle analysis revealed a significant increase in Go/G1 and S phases, while G2/M phase demonstrated a decline. The apoptotic index exhibited significant elevation, while DNA remained intact. The expression of all tested genes was altered, but BAK exhibited remarkable upregulation.
Conclusion: Patuletin caused growth inhibition of NCI-H460 via the induction of BAK-mediated apoptosis. Therefore, it presents itself as a promising candidate for anti-non-small cell lung cancer drug discovery program.
کلیدواژه‌ها
Carcinoma؛ Non-small-cell lung؛ Apoptosis؛ Antineoplastic agents
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