چاپ صفحه |  صفحه نخست سامانه |  چکیده مقاله |  نویسندگان |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| Background: Lung cancer is the leading cause of cancer‐related death with less than 5‐year survival rate for both men and women worldwide. KRAS (Kirsten rat sarcoma), nuclear factor‐κB (NF‐κB), and mitogen‐activated protein kinase (MAPK) signaling pathways have a critical role in the proliferation and progression of various cancers, including lung cancer. The p38 MAPK plays a different role in various tissue hence show a tissue‐dependent behavior. It acts as an oncogene in some tissues while plays as a tumor suppressor in some other tissues. Also, KRAS and NF‐κB act as an oncogene in various cancer. This study was dedicated to analyzing the combined effect of NF‐κB inhibitor, specific KRAS, and p38α small interfering RNA (siRNA) in A549 cell line. Materials and Methods: The cytotoxic effects of p38α siRNA, KRAS siRNA, and NF‐κB inhibitor were determined using the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5 diphenyl tetrazolium bromide (MTT) assay. Relative p38α, KRAS, and NF‐κB messenger RNA (mRNA) levels were measured by quantitative reverse‐transcription polymerase chain reaction. Induction of apoptosis by treatments was measured by fluorescenceactivated cell sorting (FACS) analysis. Results: The expression of mRNA related to p38α and KRAS genes was reduced to 23.4% and 26.7%, respectively, after treatment with specific siRNAs. Also, MTT assay showed that the cell viability after treatment with p38α siRNA, KRAS siRNA, NF‐κB inhibitor and their combination was reduced. FACS results indicated that p38α siRNA, KRAS siRNA, and NF‐κB inhibitor, and their combination, reduced the population of live cells in comparison with the population of untreated control cells (99.5%). The results are expressed as mean ±SD (n=3); *P<0.05; **P < 0.01; ***P< 0.001; ****P <0.0001 vs control group. Conclusion: The results of this study indicated that p38α, KRAS, and NF‐κB signaling pathways might play an important role in the development and growth of lung cancer and might be a potential therapeutic target for treatment of lung cancer. |
| نویسنده | نفر چندم مقاله |
|---|---|
| صفر فرج نیا | سوم |
| حبیب ذره دار | اول |
| شادی پاشاپور محمدیار | دوم |
| خلیل انصارین | چهارم |
| بهزاد برادران | پنجم |
| فاطمه صفری | هفتم |
| وحیده احمدزاده | ششم |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| zarredar-pashapour16301197.pdf | 1398/01/31 | 609245 | دانلود |
