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Knockdown of c-MYC Controls the Proliferation of Oral Squamous Cell Carcinoma Cells in vitro via Dynamic Regulation of Key Apoptotic Marker Genes
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Hussein Sabit1    , Huseyin Tombuloglu 2, Emre Cevik1 , Shaimaa Abdel-Ghany3 , Engy El-Zawahri3 , Amr El-Sawy3 , Sevim Isik4 , Ebtesam Alsuhaimi5 |
1- Department of Genetics, Institute for Research and Medical Consultations, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia.
2- Department of Genetics, Institute for Research and Medical Consultations, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia. , htoglu@iau.edu.sa
3- College of Biotechnology, Misr University for Science and Technology, Giza, Egypt.
4- Department of Molecular Biology and Genetics, Faculty of Engineering and Natural Sciences, Uskudar University, Istanbul, Turkey.
5- Department of Biology, College of Science, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia. |
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Abstract: (4458 Views) |
| 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. |
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| Keywords: Oral squamous cell carcinoma, siRNA, c-MYC, knockdown, p27, CYCS |
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Full-Text [PDF 666 kb]
(1157 Downloads)
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Type of Study: Original Article |
Subject:
Cancer
Received: 2020/09/24 | Accepted: 2021/05/9 | Published: 2021/01/21
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