TAGLN2 promotes the proliferation, migration, invasion and EMT of renal clear cell carcinoma through PI3K/Akt signaling pathway

Author:

He Yang1,Zhang Bin1,Han Dali1,Du Yuelin1,Zhang Xingxing1,Wang Hongbo1,Yue Zhongjin2,Shang Panfeng2

Affiliation:

1. Lanzhou University

2. Lanzhou University Second Hospital

Abstract

Abstract The effect of TAGLN2 in clear cell renal cell carcinoma (ccRCC) is till unknown. This paper explored its potential role and mechanism in ccRCC. The expression of TAGLN2 in Pan-cancers was analyzed through the Genotype-Tissue Expression (GTEx) database and The Cancer Genome Atlas (TCGA) database. TCGA-KIRC database were used to analyze the subsequent prognostic survival, pathway enrichment and immune infiltration. Relevant experimental methods could explain the effect of TAGLN2 expression on tumor cell proliferation, migration, invasion and apoptosis. Apoptosis, proliferation, EMT and PI3K/AKT signaling pathway related proteins expression can be realized through Western Blot. In TCGA + GTEx database, mRNA-TAGLN2 expression was obviously increased in pan-cancer tissues, and the same result was found in ccRCC patients, based on KIRC analysis results. In addition, TAGLN2 was related to poor clinical stage, pathological grade and survival prognosis. In vitro, TAGLN2 can be highly expressed in ccRCC tissues and cells. TAGLN2 silencing could inhibit the proliferation, migration and invasion and EMT in ccRCC cancer cells. Furthermore, TAGLN2 related differential genes enriched in PI3K/AKT signaling pathway were negatively regulated after TAGLN2 silencing. Moreover, TAGLN2 may promote tumor immune escape and increase the risk of distant metastasis in immune infiltration-related analysis. TAGLN2 can be used as a single indicator to explain the survival probability of ccRCC patients. In vitro, TAGLN2 silencing inhibited malignant biological properties of ccRCC by blocking PI3K/AKT signaling pathway. In addition, TAGLN2 contributes to the development of tumor immune escape and may become the potential therapeutic target of ccRCC.

Publisher

Research Square Platform LLC

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