mTOR up-regulation of BEX4 promotes lung adenocarcinoma cell proliferation by potentiating OCT4.

Previously, BEX family members have been reported to participate in cancer development. However, little is known about the role of BEX4 in lung adenocarcinoma (LAC). Here, we found that BEX4 was over-expressed in LAC tissues compared with adjacent tissues. LAC tissues from metastatic patients exhibited higher expression of BEX4 comparing to those from non-metastatic ones. In vitro, BEX4 ectopic expression accelerated the proliferation of both A549 and H1975 cells. By contrast, knockdown of BEX4 suppressed the proliferation of A549 and H1975 cells. BEX4 positively regulated the expression of OCT4, silencing of which reduced the proliferation of A549 and H1975 cells with over-expressed BEX4. Additionally, mTOR activation, which is frequently observed in LAC, potentiated BEX4 depending on mTORC1 but not mTORC2. BEX4 abundance dictated the sensitivity of A549 and H1975 cells to rapamycin treatment. Our findings reveal that BEX4 is an oncogene in LAC and may contribute to the hyper-active mTOR-induced LAC development.

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