Dataset Information

LncRNA LOC105372579 promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma via activating miR-4316/FOXP4 signaling.

ABSTRACT: Background: Recently, a growing number of long noncoding RNAs (lncRNAs) have been identified to be important for human cancer development. However, how lncRNA regulates hepatocellular carcinoma (HCC) progression still remains largely unclear. We aimed to investigate the function of LOC105372579 in HCC progression. Materials and methods: The expression levels of lncRNA LOC105372579 in HCC tissues and cell lines were analyzed by qRT-PCR. The effects of LOC105372579 silencing on proliferation, migration and invasion were determined by using cell counting kit-8, colony formation assay and Transwell assay. Moreover, the xenograft mouse model was used to detect how LOC105372579 regulates HCC growth in vivo. Results: LOC105372579 was highly expressed in HCC tissues and cell lines. Moreover, upregulated levels of LOC105372579 predicted poor prognosis. LOC105372579 silencing suppressed the proliferation of HCC cells in vitro. We also validated that LOC105372579 knockdown inhibited the migration, invasion, and epithelial-mesenchymal transition of HCC cells. Xenograft assay demonstrated that LOC105372579 promotes tumor growth in vivo. Mechanistically, we identified that LOC105372579 is a sponge for miR-4316 and that FOXP4 is a direct target of miR-4316. Conclusion: Thus, our findings supported that LOC105372579 contributes to HCC cell proliferation, migration, invasion, and EMT by activating miR-4316/FOXP4 signaling.

SUBMITTER: E C

PROVIDER: S-EPMC6489618 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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LncRNA LOC105372579 promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma via activating miR-4316/FOXP4 signaling.

E Changyong C Yang Jinghui J Li Hang H Li Chunsheng C

Cancer management and research 20190411

<b>Background:</b> Recently, a growing number of long noncoding RNAs (lncRNAs) have been identified to be important for human cancer development. However, how lncRNA regulates hepatocellular carcinoma (HCC) progression still remains largely unclear. We aimed to investigate the function of LOC105372579 in HCC progression. <b>Materials and methods:</b> The expression levels of lncRNA LOC105372579 in HCC tissues and cell lines were analyzed by qRT-PCR. The effects of LOC105372579 silencing on proli ...[more]

PMID: 31114338

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Project description:PurposeThe aim of this work was to investigate the clinicopathological significance of fibrinogen gamma chain (FGG) and its biological roles during hepatocellular carcinoma (HCC) development and progression.MethodsThe expression of FGG was examined by Western blot and reverse transcription quantitative PCR in two different sample sets, including 24 or 35 pairs of HCC tumor tissues and their corresponding adjacent non-tumorous tissues. Afterward, association analysis between the expression of FGG and clinicopathological characteristics was systematically analyzed in 79 HCC patients. Subsequently, the mobility and invasiveness of SK-HEP-1 cells with FGG overexpression or knockdown were evaluated by transwell assay and wound healing assay. Additionally, the expressions of epithelial to mesenchymal transition (EMT)-associated markers were also detected in FGG overexpressed or silenced SK-HEP-1 cells.ResultsThe expression of FGG was significantly increased in primary HCC tissues comparing with its corresponding adjacent non-tumorous tissues. Clinical pathological analysis demonstrated that upregulation of intracellular FGG was significantly associated with increased vascular invasion, more satellite nodules, and more advanced TNM stage, and HCC patients with stronger expression of FGG had a higher recurrence rate and correspondingly a shorter overall survival time. Meanwhile, the high expression of FGG was also proved to be an independent risk factor for disease-free survival after surgical resection. In vitro phenotype studies showed that overexpression of FGG could promote the migration and invasion in SK-HEP-1 cells; conversely, these phenotypes could be significantly inhibited by knocking down the expression of FGG. Mechanism studies indicated that FGG could promote the migration and invasion through EMT signaling pathway by regulating the expressions of Slug and ZEB1.ConclusionFGG played important roles in enhancing cancer cell motility and invasiveness through EMT signaling, and might serve as a potential prognostic biomarker for HCC patients.

Dataset Information

LncRNA LOC105372579 promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma via activating miR-4316/FOXP4 signaling.

Publications

LncRNA LOC105372579 promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma via activating miR-4316/FOXP4 signaling.

Similar Datasets

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