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LRG‑1 enhances the migration of thyroid carcinoma cells through promotion of the epithelial‑mesenchymal transition by activating MAPK/p38 signaling.

ABSTRACT: Leucine‑rich‑alpha‑2‑glycoprotein 1 (LRG‑1) has been reported to be associated with multiple malignancies. However, its participation in thyroid carcinoma progression remains unclear. In the present study, the biological function and underlying molecular mechanisms of LRG‑1 in thyroid carcinoma were investigated. It was found that LRG‑1 was overexpressed in thyroid carcinoma tissues, and high LRG‑1 expression predicted poor patient survival and late tumor stage. As shown in the mouse xenograft study, knockdown of LRG‑1 significantly attenuated thyroid cancer growth in vivo. Based on wound healing, Transwell, proliferation and apoptosis assays, it was found that the knockdown of LRG‑1, using shLRG‑1, inhibited cell migration and invasion, but did not affect proliferation and apoptosis in thyroid cancer cells. Furthermore, LRG‑1 also induced epithelial‑mesenchymal transition (EMT) in thyroid carcinoma cells. Western blot analysis revealed that this tumor‑promoting bioactivity of LRG‑1 was attributed to its selective activation of MAPK/p38 signaling. All of these findings indicate that LRG‑1 plays a deleterious role in the progression of thyroid carcinoma. LRG‑1 may serve as a promising biomarker for predicting prognosis in thyroid carcinoma patients, and LRG‑1‑based therapy may be developed into a novel strategy for the treatment of thyroid carcinoma.

SUBMITTER: Ban Z

PROVIDER: S-EPMC6488982 | biostudies-literature |

REPOSITORIES: biostudies-literature

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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.

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LRG‑1 enhances the migration of thyroid carcinoma cells through promotion of the epithelial‑mesenchymal transition by activating MAPK/p38 signaling.

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