Induction of microRNA‑let‑7a inhibits lung adenocarcinoma cell growth by regulating cyclin�D1
Adult
Male
0301 basic medicine
Lung Neoplasms
Apoptosis
Articles
Cell Cycle Checkpoints
Adenocarcinoma
Middle Aged
Prognosis
3. Good health
Gene Expression Regulation, Neoplastic
MicroRNAs
03 medical and health sciences
Cell Movement
Case-Control Studies
Biomarkers, Tumor
Humans
Cyclin D1
Female
Neoplasm Invasiveness
Aged
Cell Proliferation
Follow-Up Studies
DOI:
10.3892/or.2018.6593
Publication Date:
2018-07-24T07:51:37Z
AUTHORS (11)
ABSTRACT
Lung cancer is the most common cause of cancer‑associated mortality. MicroRNAs (miRNAs), as oncogenes or tumor suppressor genes, serve crucial roles not only in tumorigenesis, but also in tumor invasion and metastasis. Although miRNA‑let‑7a (let‑7a) has been reported to suppress cell growth in multiple cancer types, the biological mechanisms of let‑7a in lung adenocarcinoma are yet to be fully elucidated. In the present study, the molecular roles of let‑7a in lung adenocarcinoma were investigated by detecting its expression in lung adenocarcinoma tissues and exploring its roles in the regulation of lung cancer cell proliferation. Let‑7a expression was identified to be downregulated in lung adenocarcinoma tissues compared with normal tissues. Overexpression of let‑7a effectively suppressed cancer cell proliferation, migration and invasion in H1299 and A549 cells. Let‑7a also induced cell apoptosis and cell cycle arrest. Furthermore, let‑7a significantly inhibited cell growth by directly regulating cyclin D1 signals. This novel regulatory mechanism of let‑7a in lung adenocarcinoma provides possible avenues for future targeted therapies of lung cancer.
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CITATIONS (11)
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