Abstract Background Kidney renal clear cell carcinoma (KIRC) is the most common pathological subtype of kidney tumor. Reportedly, LINC00174 is a key regulator in cancer progression. This study aims to… Click to show full abstract
Abstract Background Kidney renal clear cell carcinoma (KIRC) is the most common pathological subtype of kidney tumor. Reportedly, LINC00174 is a key regulator in cancer progression. This study aims to clarify the role and molecular mechanism of LINC00174 in the progression of KIRC. Methods LINC00174 expression in KIRC and its prognostic value were analyzed by bioinformatics. LINC00174, miR-612 and FOXM1 mRNA expression levels in KIRC clinical samples and cell lines were detected by qRT-PCR. After LINC00174 was overexpressed or knocked down, CCK-8, BrdU and Transwell assays were adopted to evaluate the proliferation and metastatic potential of KIRC cells. Bioinformatics and dual luciferase reporter assays were employed to validate the targeting relationship between miR-612 and LINC00174 or FOXM1 mRNA, respectively. Western blot assay was performed to detect FOXM1 protein expression in KIRC cells. Results LINC00174 expression and FOXM1 expression were up-regulated in 42 cases of KIRC tissues (p < 0.001), while miR-612 expression was down-regulated (p < .001). LINC00174 overexpression or miR-612 inhibitor promoted the viability and proliferation of KIRC cells (p < .01). Migration and invasion of KIRC cells were promoted when the cells were transfected with LINC00174 overexpression or miR-612 inhibitor (p < .05). LINC00174 can competitively bind with miR-612 to repress the expression of miR-612, in turn up-regulate the expression of FOXM1 mRNA. Conclusion LINC00174 facilitates the proliferation and metastatic potential of KIRC cells via regulating the miR-612/FOXM1 axis.
               
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