期刊
IUBMB LIFE
卷 71, 期 1, 页码 81-92出版社
WILEY
DOI: 10.1002/iub.1944
关键词
MCL1; glioma; PI3K/Akt signaling pathway; senescence; apoptosis; gene silencing
资金
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- 2016 333 Project Award of Jiangsu Province
- 2013 Qinglan Project of the Young and Middle-aged Academic Leader of Jiangsu College and University
- National Natural Science Foundation of China [81571055, 81400902, 81271225, 31201039, 81171012, 30950031]
- Major Fundamental Research Program of the Natural Science Foundation of the Jiangsu Higher Education Institutions of China [13KJA180001]
- Cultivate National Science Fund for Distinguished Young Scholars of Jiangsu Normal University
Glioma is known to be the most prevalent primary brain tumor. In recent years, there has been evidence indicating myeloid cell leukemia-1 (MCL1) plays a role in brain glioblastoma. Therefore, the present study was conducted with aims of exploring the ability of MCL1 silencing to influence glioma cell senescence and apoptosis through the mediation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. Glioma and tumor-adjacent tissues were collected in order to detect the presence of higher levels of MCL1 protein expression. Next, the mRNA and protein expression of MCL1, PI3K, Akt, B cell lymphoma 2 (Bcl2), Bcl2-associated X (Bax), B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1), and phosphatase and tensin homolog (PTEN) were determined. Cell counting kit-8 assay was applied to detect cell proliferation, beta-galactosidase staining for cell senescence, and flow cytometry for cell cycle entry and apoptosis. Initially, the results revealed higher positive expression rate of MCL1 protein, increased mRNA and protein expression of MCL1, PI3K, Akt, Bmi-1, and Bcl-2 and decreased that of Bax and PTEN in human glioma tissues. The silencing of MCL1 resulted in a decrease in mRNA and protein expression of PI3K, Akt, Bmi-1, and Bcl-2 and an increase in Bax and PTEN expressions in glioma cells. Moreover, silencing of MCL1 also inhibited cell proliferation and cell cycle entry in glioma cells, and promoted glioma cell senescence and apoptosis. In conclusion, the aforementioned results collectively suggested that the silencing of MCL1 promotes senescence and apoptosis in glioma cells through inhibiting the PI3K/Akt signaling pathway. Thus, decreasing the expression of MCL1 might have therapeutic functions in glioma. (c) 2018 IUBMB Life, 71(1):81-92, 2019
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