[No authors listed]
Lung cancer is the leading cause of cancerârelated death worldwide. The underlying molecular mechanisms that trigger this disease remain largely unknown. The IâBAR family is involved in regulating cell membrane formation and some members, such as BAIAP2L1, IRSp53 and MIM have been shown to participate in tumorigenic progression. However, the role of BAI1âassociated protein 2âlike 2 (BAIAP2L2) in cancer development is unclear. In the present study, we determined that BAIAP2L2 was upregulated in lung adenocarcinoma tissues and various lung cancer cell lines. In vitro, BAIAP2L2 silencing resulted in decreased viability and colony formation capacity of both A549 and H1299 cells. By contrast, BAIAP2L2 overexpression promoted the proliferation and growth of 95D cells. These results indicated that BAIAP2L2 was essential for lung cancer cell proliferation and growth. We also found that BAIAP2L2 knockdown increased the apoptosis of A549 and H1299 cells. At the molecular level, BAIAP2L2 knockdown led to dysregulation of numerous genes, among which the Estrogenâmediated Sâphase Entry pathway was significantly suppressed. Collectively, our findings revealed BAIAP2L2 as a novel biomarker and potential therapeutic target for lung cancer.
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