RETRACTED: Upregulated expression of ROCK1 promotes cell proliferation by functioning as a target of miR‐335‐5p in non‐small cell lung cancer
Lung cancer is regarded as one of the dominant causes in cancer patients among men and women all over the world. Rho‐associated coiled‐coil forming protein kinase l (ROCK1) is characterized as pivotal downstream effectors of the small GTPase RhoA and reported to participate in tumor metastasis. miR‐...
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Veröffentlicht in: | Journal of cellular physiology 2022-04, Vol.237 (4), p.E1-E12 |
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Sprache: | eng |
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Zusammenfassung: | Lung cancer is regarded as one of the dominant causes in cancer patients among men and women all over the world. Rho‐associated coiled‐coil forming protein kinase l (ROCK1) is characterized as pivotal downstream effectors of the small GTPase RhoA and reported to participate in tumor metastasis. miR‐335‐5p acts as tumor suppressor microRNA and is identified to be downregulated in tumor tissues. miR‐335‐5p/ROCK1 axis has been demonstrated to promote cell proliferation and metastasis in gastric cancer, hepatocellular carcinoma and so on. However, the role it plays in promoting cell proliferation in non‐small cell lung cancer (NSCLC) is poorly understood. Here, we demonstrated that the upregulated expression of ROCK1 was highly correlated with downregulated expression of miR‐335‐5p in NSCLC tissues and cell lines. Mechanistically, Knockdown of ROCK1 inhibited cell proliferation in vitro, accompanied by cell cycle change confirmed by flow analysis. Furthermore, miR‐335‐5p can downregulate the ROCK1 expression by directly binding to the 3′‐untranslated region in posttranscriptional level. In vivo animal model showed similar results. Our findings highlighted the crucial role that miR‐335‐5p acted as a tumor suppressor to modulate cell proliferation and cell cycle progression via downregulating ROCK1 expression. And this miR‐335‐5p/ROCK1 axis contributed to NSCLC pathogenesis and might be promising targets for NSCLC therapy. |
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ISSN: | 0021-9541 1097-4652 |
DOI: | 10.1002/jcp.28886 |