دوره 10، شماره 1 - ( 10-1399 )                   | برگشت به فهرست نسخه ها

XML English Abstract Print

Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Sabit H, Tombuloglu H, Cevik E, Abdel-Ghany S, El-Zawahri E, El-Sawy A, et al . Knockdown of c-MYC Controls the Proliferation of Oral Squamous Cell Carcinoma Cells in vitro via Dynamic Regulation of Key Apoptotic Marker Genes. Int J Mol Cell Med 2021; 10 (1) :45-55
URL: http://ijmcmed.org/article-1-1457-fa.html
Knockdown of c-MYC Controls the Proliferation of Oral Squamous Cell Carcinoma Cells in vitro via Dynamic Regulation of Key Apoptotic Marker Genes. مجله بین المللی سلولی و مولکولی. 1399; 10 (1) :45-55

URL: http://ijmcmed.org/article-1-1457-fa.html

Knockdown of c-MYC Controls the Proliferation of Oral Squamous Cell Carcinoma Cells in vitro via Dynamic Regulation of Key Apoptotic Marker Genes
:   (5633 مشاهده)
Oral squamous cell carcinoma (OSCC) is the most common malignant epithelial cancer occurring in the oral cavity, where it accounts for nearly 90% of all oral cavity neoplasms. The c-MYC transcription factor plays an important role in the control of programmed cell death, normal-to-malignant cellular transformation, and progression of the cell cycle. However, the role of c-MYC in controlling the proliferation of OSCC cells is not well known. In this study, c-MYC gene was silenced in OSCC cells (ORL-136T), and molecular and cellular responses were screened. To identify the pathway through which cell death occurred, cytotoxicity, colony formation, western blotting, caspase-3, and RT-qPCR analyzes were performed. Results indicated that knockdown of c-MYC has resulted in a significant decrease in the cell viability and c-MYC protein synthesis. Furthermore, caspase-3 was shown to be upregulated leading to apoptosis via the intrinsic pathway. In response to c-MYC knockdown, eight cell proliferation-associated genes showed variable expression profiles: c-MYC (-21.2), p21 (-2.5), CCNA1(1.8), BCL2 (-1.4), p53(-3.7), BAX(1.1), and CYCS (19.3). p27 expression was dramatically decreased in c-MYC-silenced cells in comparison with control, and this might indicate that the relative absence of c-MYC triggered intrinsic apoptosis in OSCC cells via p27 and CYCS.
متن کامل [PDF 666 kb]   (1536 دریافت)    
نوع مطالعه: Original Article | موضوع مقاله: Cancer
دریافت: 1399/7/3 | پذیرش: 1400/2/19 | انتشار: 1399/11/2
ارسال نظر درباره این مقاله : نام کاربری یا پست الکترونیک شما:
CAPTCHA
بازنشر اطلاعات
Creative Commons License این مقاله تحت شرایط Creative Commons Attribution-NonCommercial 4.0 International License قابل بازنشر است.

کلیه حقوق این وب سایت متعلق به International Journal of Molecular and Cellular Medicine IJMCM می باشد.

طراحی و برنامه نویسی : یکتاوب افزار شرق

© 2025 CC BY-NC 4.0 | International Journal of Molecular and Cellular Medicine IJMCM

Designed & Developed by : Yektaweb