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연세대학교 의과대학 Yonsei Medical Journal Yonsei Medical Journal 제61권 제3호
발행연도
2020.1
수록면
210 - 217 (8page)

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Purpose: The goal of this study was to explore the effects of hsa-let-7g on cell proliferation and apoptosis, and elucidate its role inlung cancer development. Materials and Methods: The expression levels of has-let-7g and HOXB1 in tissues and cells were measured by qRT-PCR. An inhibitorof hsa-let-7g or one targeting a control messenger RNA were transfected into A549 and H1944 lung cancer cells, and the effects ofhsa-let-7g dysregulation on cell viability and apoptosis were analyzed using CCK-8 and apoptosis detection assays. HOXB1 was confirmedas the target gene of hsa-let-7g, based on luciferase reporter assay results. The relationship between hsa-let-7g and HOXB1was confirmed by co-transfection of inhibitors of hsa-let-7g and HOXB1 followed by Western blot, CCK-8, and apoptosis detectionassays. Results: We observed high expression of hsa-let-7g in lung cancer tissues compared to the corresponding normal tissues, andgenerally higher expression of hsa-let-7g in patients with advanced tumor classification. The results of CCK-8 and apoptosis detectionexperiments showed that the inhibition of hsa-let-7g significantly inhibited proliferation of A549 and H1944 cells, but also promotedapoptosis. HOXB1 is a specific target of hsa-let-7g, and downregulation of HOXB1 in lung cancer cells reversed the suppressiveeffects caused by knocking down hsa-let-7g. Conclusion: These data collectively suggest that the expression of hsa-let-7g inhibits lung cancer cells apoptosis and promotesproliferation by down-regulating HOXB1. The results from this study demonstrate the potential of hsa-let-7g/HOXB1 axis as atherapeutic target for the treatment of lung cancer.

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