The novel target of esophageal squamous cell carcinoma: lncRNA GASL1 regulates cell migration, invasion and cell cycle stagnation by inactivating the Wnt3a/β-catenin signaling

Nov 28, 2020Pathology, research and practice

lncRNA GASL1 may slow esophageal cancer cell growth and spread by blocking the Wnt3a/β-catenin signaling pathway

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Abstract

LncRNA GASL1 was down-regulated in esophageal cancer cell lines and is associated with inhibited tumor growth.

GASL1 may suppress cell progression and regulate cell cycle arrest in esophageal cancer cells.
In vivo experiments indicated that GASL1 inhibited tumor growth in mice.
Decreased protein levels of DKK1, Wnt3a, β-catenin, and c-MYC were observed with GASL1 expression.
Interfering DKK1 may activate the Wnt3a/β-catenin signaling pathway, reversing the effects of GASL1 on cell behavior.
GASL1 is suggested to regulate cell migration, invasion, and cell cycle stagnation through inactivation of the Wnt/β-catenin signaling pathway.

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Long non-coding RNA (lncRNA) Growth-Arrest Associated LncRNA 1 (GASL1) is a lncRNA with a suppressive role in glioma, prostate carcinoma and gastric carcinoma, whereas its involvement in esophageal cancer is unknown. In the present study, we used RT-qPCR to detect the expression of GASL1 in esophageal cancer cell carcinoma (ESCC) cell lines, and constructed the overexpression and interference plasmids of GASL1 and the interference plasmid of DKK1. CCK8 was used to detect the cell proliferation level, clone formation experiment was used to detect the cell clonal formation ability, flow cytometry was used to detect the cell cycle level, and wound healing and Transwell experiments were respectively used to detect the cell invasion and migration. The interference and overexpression plasmids of GASL1 were injected into mice subcutaneously for tumor-bearing experiment. The body weight, tumor growth curve, and tumor weight of mice were recorded, and western blot was used to detect the expression of proliferation-, invasion-, and migration-related proteins and the expression of Wnt3a/β-catenin signal-related proteins in tumor tissues. LncRNA GASL1 was down-regulated in ESCC cell lines, and GASL1 inhibited ESCC cell progression and regulated cell cycle arrest in ESCC cells. In vivo, GASL1 inhibited tumor growth. GASL1 decreased the protein levels of DDK1, Wnt3a, β-catenin, and c-MYC in ESCC cell lines. Interfering DKK1 activates Wnt3a/β--catenin signal to reverse the inhibitory effects of GASL1 on proliferation, cell cycle acceleration, invasion, and migration. In conclusion, lncRNA GASL1 regulates cell migration, invasion and cell cycle stagnation by inactivating the wnt/β-catenin signaling.

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The novel target of esophageal squamous cell carcinoma: lncRNA GASL1 regulates cell migration, invasion and cell cycle stagnation by inactivating the Wnt3a/β-catenin signaling

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