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International Journal of Biomedical Engineering ; (6): 527-533, 2018.
Article in Chinese | WPRIM | ID: wpr-732759

ABSTRACT

Objective To investigate the malignant biological behavior and mechanism of LncRNA TCF7 in lung cancer cells by regulating miR-29 and activating JAK/STAT2 signaling pathway.Methods qPCR was used to detect the expression of TCF7 and miR-29 in lung cancer tissues and different lung cancer cell lines.The relationship between TCF7 and clinicopathological data of lung cancer patients was analyzed.The dual luciferase reporter assay was used to detect the interaction between TCF7 and miR-29.MTT proliferation assay and Transwell invasion assay was used to detect the proliferation and invasion of lung cancer cells after inhibition of TCF7,respectively,and to analyze the relevant recovery after the overexpression of miR-29.The expression of JAK/STAT2 signaling pathway protein was detected by Western Blotting after TCF7 inhibition.The effect of TCF7 on tumor formation in vivo was detected by in vitro tumor formation assay in nude mice.Results Compared with other lung cancer cell lines,A549 cells had the highest expression of TCF7 and miR-29.The expression of TCF7 was associated with the pathological stage of lung cancer and lymph node metastasis,in which TCF7 was positively correlated with cancer stage and lymph node metastasis.The dual luciferase assay confirmed that TCF7 can specifically bind to the target of miR-29,and regulate the expression and activity of miR-29.The inhibition of the expression of TCF7 can promote the proliferation and invasion of lung cancer cells.After inhibiting the expression level of miR-29,the proliferation and invasion ability of lung cancer cells were partly restored.After inhibiting the expression of TCF7,JAK/STAT2 signaling pathway was activated accordingly.Compared with the non-small carcinoma group,the average tumor volume and mass of the transplanted tumor in the TCF7-siRNA group were reduced.Conclusions TCF7 can regulate the expression of miR-29 and affect the proliferation and invasion of lung cancer cells through JAK/STAT2 signaling pathway.

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