Dataset Information

SMYD2 suppresses APC2 expression to activate the Wnt/?-catenin pathway and promotes epithelial-mesenchymal transition in colorectal cancer.

ABSTRACT: Cancer metastasis is a significant challenge in colorectal cancer (CRC) therapy. SET and MYND domain-containing protein 2 (SMYD2) is highly expressed in multiple cancers but is rarely studied in CRC. This study aims to identify whether abnormal expression of SMYD2 is associated with cancer metastasis in CRC. In this study, we demonstrated that SMYD2 not only promoted cell proliferation but also increased the metastatic ability of CRC. The expression of adenomatous polyposis coli 2 (APC2), an inhibitor of the Wnt/?-catenin pathway, was suppressed by SMYD2 overexpression. Overexpression of SMYD2 activated the Wnt/?-catenin pathway and then induced the epithelial-mesenchymal transition (EMT) program in CRC. Mechanistically, low APC2 expression in CRC cells was due to SMYD2-mediated DNA methylation modification. This modification might require synergism with DNMT1. In summary, our study provides new insights into SMYD2-related transcriptional regulation patterns and indicates that SMYD2 could be a potential therapeutic target for CRC patients.

SUBMITTER: Meng F

PROVIDER: S-EPMC7136915 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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SMYD2 suppresses APC2 expression to activate the Wnt/β-catenin pathway and promotes epithelial-mesenchymal transition in colorectal cancer.

Meng Fanchao F Liu Xin X Lin Changwei C Xu Lei L Liu Jinjin J Zhang Pengbo P Zhang Xiuzhong X Song Jun J Yan Yichao Y Ren Zeqiang Z Zhang Yi Y

American journal of cancer research 20200301 3

Cancer metastasis is a significant challenge in colorectal cancer (CRC) therapy. SET and MYND domain-containing protein 2 (SMYD2) is highly expressed in multiple cancers but is rarely studied in CRC. This study aims to identify whether abnormal expression of SMYD2 is associated with cancer metastasis in CRC. In this study, we demonstrated that SMYD2 not only promoted cell proliferation but also increased the metastatic ability of CRC. The expression of adenomatous polyposis coli 2 (APC2), an inh ...[more]

PMID: 32266106

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Project description:BackgroundCigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD) and lung cancer. Epithelial-mesenchymal transition (EMT) is an essential pathophysiological process in COPD and plays an important role in airway remodeling, fibrosis, and malignant transformation of COPD. Previous studies have indicated FERMT3 is downregulated and plays a tumor-suppressive role in lung cancer. However, the role of FERMT3 in COPD, including EMT, has not yet been investigated.MethodsThe present study aimed to explore the potential role of FERMT3 in COPD and its underlying molecular mechanisms. Three GEO datasets were utilized to analyse FERMT3 gene expression profiles in COPD. We then established EMT animal models and cell models through cigarette smoke (CS) or cigarette smoke extract (CSE) exposure to detect the expression of FERMT3 and EMT markers. RT-PCR, western blot, immunohistochemical, cell migration, and cell cycle were employed to investigate the potential regulatory effect of FERMT3 in CSE-induced EMT.ResultsBased on Gene Expression Omnibus (GEO) data set analysis, FERMT3 expression in bronchoalveolar lavage fluid was lower in COPD smokers than in non-smokers or smokers. Moreover, FERMT3 expression was significantly down-regulated in lung tissues of COPD GOLD 4 patients compared with the control group. Cigarette smoke exposure reduced the FERMT3 expression and induces EMT both in vivo and in vitro. The results showed that overexpression of FERMT3 could inhibit EMT induced by CSE in A549 cells. Furthermore, the CSE-induced cell migration and cell cycle progression were reversed by FERMT3 overexpression. Mechanistically, our study showed that overexpression of FERMT3 inhibited CSE-induced EMT through the Wnt/β-catenin signaling.ConclusionsIn summary, these data suggest FERMT3 regulates cigarette smoke-induced epithelial-mesenchymal transition through Wnt/β-catenin signaling. These findings indicated that FERMT3 was correlated with the development of COPD and may serve as a potential target for both COPD and lung cancer.

Dataset Information

SMYD2 suppresses APC2 expression to activate the Wnt/?-catenin pathway and promotes epithelial-mesenchymal transition in colorectal cancer.

Publications

SMYD2 suppresses APC2 expression to activate the Wnt/β-catenin pathway and promotes epithelial-mesenchymal transition in colorectal cancer.

Similar Datasets

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