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CDCA7 promotes TGF-β-induced epithelial-mesenchymal transition via transcriptionally regulating Smad4/Smad7 in ESCC

ABSTRACT: Purpose：Cell division cycle associated 7 (CDCA7) is a copy number amplification gene that contributes to the metastasis and invasion of tumors, including esophageal squamous cell carcinoma (ESCC). This present study aimed at clarifying whether high expression of CDCA7 promotes the metastasis and invasion of ESCC cell lines and exploring the underlying mechanisms implicated in EMT of ESCC. Mehtod：We established KYSE150 cell lines in which target gene has been knocked down by shRNA and KYSE180 cell lines in which target gene has been ovexpressed by plasmid.We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells.Each cell has three repetions. Result：KEGG pathway enrichment analysis on the data of RNA-seq showed that Wnt signaling pathway and TGF-β signaling pathway which are related to EMT process were screened out. Conclusion：CDCA7 was heavily involved in EMT by regulating the expression of Smad4 and Smad7 in TGF-β signaling pathway.

ORGANISM(S): Homo sapiens

PROVIDER: GSE201735 | GEO | 2023/01/11

REPOSITORIES: GEO

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Project description:SET (Su) and MYND (myeloid-Nervy-DEAF-1) domain-containing protein (SMYD) is a methyltransferase family, including five members of which SMYD1, SMYD2, SMYD3 and SMYD4, has been found to play critical roles in human carcinogenesis. It has been demonstrated that the altered expression of SMYD3 is associated with the progression of several solid tumors, including bladder cancer, glioma, gastric cancer, prostate cancer and colorectal cancer. Several trials have explored the effects of SMYD3 overexpression on proliferation, viability, cancer cells migration and invasion. The series of elegant experiments suggested that SMYD3 could serve as a potential biomarker for clinically aggressive disease and an attractive therapeutic target. In our previous study (PMID: 26980013), we found SMYD3 expression is frequently upregulated in human esophageal squamous cell carcinoma (ESCC) clinical tissues, correlating with overall survival of ESCC patients. RNAi-mediated knockdown of SMYD3 suppressed ESCC cell proliferation, migration and invasion in vitro, and inhibited local tumor invasion in vivo. To identify genes and biological pathways associated with SMYD3 functions and mechanism, SMYD3 was knockdowned bypGLV3/H1/GFP/+Puro Vector in ESCC cell line KYSE150 with an empty plasmid as a control, these two cells were applied for mRNA expression profile analyses to find the differentially expressed genes using GeneChipÂ® PrimeViewâ¢ Human Gene Expression Array. shRNA sequences targeting SMYD3 was ligated into the pGLV3/H1/GFP/+Puro Vector and transfected into ESCC cell line KYSE150 with an empty plasmid as a control. The mRNA expression profiles of SMYD3 knockdown was analyzed by GeneChipÂ®Â PrimeViewâ¢Â HumanÂ Gene Expression Array (Affymetrix,Â USA). The knockdown of SMYD3 was confirmed by QRT-PCR and Western blot. Total RNAs from SMYD3 knockdown cells and control cells were extracted for GeneChipÂ® PrimeViewâ¢ Human Gene Expression Array.

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CDCA7 promotes TGF-β-induced epithelial-mesenchymal transition via transcriptionally regulating Smad4/Smad7 in ESCC

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