Exogenous Let-7a-5p Induces A549 Lung Cancer Cell Death Through BCL2L1-Mediated PI3Kγ Signaling Pathway.

作者: Shuyin Duan , Songcheng Yu , Teng Yuan , Sanqiao Yao , Lin Zhang

DOI: 10.3389/FONC.2019.00808

关键词:

摘要: Elevated expression of let-7a-5p contributes to suppression lung cancer, in which let-7a-5p, as exosome cargo, can be transported from macrophages cancer cells, yet the role remains unclear. Utilizing bioinformatics methods and cellular experiments, this study was designed conducted identify regulatory network cancer. Bioinformatics analysis Kaplan-Meier survival revealed that could directly target BCL2L1, aberrant affects patients, confirmed A549 cells using luciferase reporter assay. Moreover, inhibited BCL2L1 suppressed cell proliferation, migration, invasion. Functionally, overexpression promoted both autophagy death through PI3Kγ signaling pathway, whereas apoptosis pyroptosis were unaffected. Furthermore, significantly altered biomarkers such MYC, EGFR, Vimentin. To sum up, these data demonstrate exogenous induces BCL2L1-mediated may a useful for treatment.

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