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Oncol Rep. 2019 Feb;41(2):1113-1121. doi: 10.3892/or.2018.6853. Epub 2018 Nov 6.

Long non‑coding RNA MALAT1 correlates with cell viability and mobility by targeting miR‑22‑3p in renal cell carcinoma via the PI3K/Akt pathway.

Li Z1, Ma Z2, Xu X3.

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Department of Urology, The Second Hospital Affiliated to Tianjin Medical University, Tianjin 300211, P.R. China.
Department of Urology, The Third Hospital of Shijiazhuang, Shijiazhuang, Hebei 050000, P.R. China.
Department of Urology, Tai'an City Central Hospital, Tai'an, Shandong 271000, P.R. China.


Renal cell carcinoma (RCC) is one of the most common types of cancer of the urinary tract in the world. Long non‑coding RNA MALAT1 (lncR‑MALAT1) is upregulated in RCC and is associated with the proliferation and migration of RCC. The present study aimed to investigate the regulating role of lncR‑MALAT1 in RCC as well as the possible underlying mechanisms. The relative expression of MALAT1 and miR‑22‑3p in RCC tumor tissues and cell lines was detected by qRT‑PCR. CCK‑8 and wound healing assay were used to evaluate cell proliferation and migration ability. Western blot analysis was used to detect the expression of Ki‑67, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase‑3 (MMP‑3), migration and invasion inhibitory protein (MIIP), p‑PI3K and p‑Akt. The relationship between MALAT1 and miR‑22‑3p was examined by bioinformatic prediction analysis and luciferase reporter assay. Immunofluorescence was used to detect the activation of Akt. MALAT1 was highly expressed and the expression of miR‑22‑3p was suppressed in RCC tissues and cell lines. ShRNA‑mediated knockdown of MALAT1 significantly inhibited the viability and mobility of RCC cells in vitro and in vivo. Further experiments revealed that miR‑22‑3p was a target of MALAT1 and that miR‑22‑3p inhibitor abolished the effect of MALAT1 shRNA on cell proliferation, migration and inactivation of PI3K/AKT pathway. In conclusion, lncR‑MALAT1 affected the proliferation and migration of RCC cells by targeting miR‑22‑3p through the inactivation of the PI3K/Akt signaling pathway.

[Indexed for MEDLINE]

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