Decrease of miR-622 expression promoted the proliferation, migration and invasion of cholangiocarcinoma cells by targeting regulation of c-Myc.

To explore the mechanism of miR-622 in regulating the proliferation, migration and invasion of cholangiocarcinoma (CCA) cells. Quantitative real-time PCR was conducted to measure the expression of miR-622 and c-Myc in CCA tissues and cell lines. Protein level of c-Myc was measured by Western blot. The effect of miR-622 on cell proliferation, migration and invasion was analyzed by MTT assay and Transwell chamber migration assay. Luciferase reporter assay was performed to measure the effect of miR-622 on c-Myc. miR-622 expression was downregulated in both CCA tissues and cell lines, while c-Myc expression was uregulated. Overexpression of miR-622 in CCA cells was statistically correlated with a decrease of cell proliferation, migration and invasion, while inhibition of miR-622 made an inverse result. We also proved c-Myc was identified as a target gene of miR-622 in CCA. Moreover, we found overexpression of c-Myc can strengthen the effects of miR-622 on the proliferation, migration and invasion of CCA cells. Decrease of miR-622 promotes the proliferation, migration and invasion of CCA cells by directly targeting c-Myc.

Wu YF ，Li ZR ，Cheng ZQ ，Yin XM ，Wu JS ... -  《-》

MicroRNA-144 suppresses cholangiocarcinoma cell proliferation and invasion through targeting platelet activating factor acetylhydrolase isoform 1b.

Yang R ，Chen Y ，Tang C ，Li H ，Wang B ，Yan Q ，Hu J ，Zou S ... -  《BMC CANCER》

miR-378 serves as a prognostic biomarker in cholangiocarcinoma and promotes tumor proliferation, migration, and invasion.

Zhou Z ，Ma J 《-》

Hepatocyte nuclear factor 6 inhibits the growth and metastasis of cholangiocarcinoma cells by regulating miR-122.

Zhu H ，Mi Y ，Jiang X ，Zhou X ，Li R ，Wei Z ，Jiang H ，Lu J ，Sun X ... -  《-》

LINC01410 promotes cell proliferation and migration of cholangiocarcinoma through modulating miR-124-3p/SMAD5 axis.

Cholangiocarcinoma (CCA) is generally associated with high incidence and poor prognosis. Nowadays, increasing experimental data demonstrate that long non-coding RNA (lncRNA) plays an indispensable role in tumor occurrence. Nevertheless, the specific mechanism of lncRNA is not clear in CCA. The relative expressions of lncRNAs, miRNAs, and mRNAs were detected by real-time quantitative PCR (RT-qPCR). CCK8 and colony formation assays were applied to examine cell proliferation ability in CCA. Transwell assay was conducted to measure the migration and invasion capabilities of CCA cells. Nuclear and cytoplasmic separation assay was implemented to figure out the location of LINC01410. Luciferase reporter assay, RIP and RNA pull-down assays were applied to certify the molecular bindings. Western blot was applied to detect the protein level. The high expression of LINC01410 was proved in CCA tissues and CCA cell lines. Also, CCA patients with high LINC01410 level presented poor prognosis. LINC01410 deficiency impeded cell proliferation, migration and invasion in HuCCT1 and RBE cell lines. What's more, LINC01410 interacted with miR-124-3p. Meanwhile, SMAD5 targeted and inhibited by miR-124-3p. SMAD5 expression was enhanced by LINC01410. LINC01410 facilitates cell proliferation, migration and invasion through miR-124-3p/SMAD5 axis.

Jiang T ，Wang C ，Zhu Y ，Han H ... -  《-》