Differential expression and bioinformatics analysis of epsin3 in colorectal cancer

doi:10.16098/j.issn.0529-1356.2022.04.014

Acta Anatomica Sinica ›› 2022, Vol. 53 ›› Issue (4): 507-514.doi: 10.16098/j.issn.0529-1356.2022.04.014

• Cancer Biology • Previous Articles Next Articles

Differential expression and bioinformatics analysis of epsin3 in colorectal cancer

XIANG Li-chun¹ JIANG Zhong-xiang² JIANG Xiao-ye¹ CHEN Xue-nuo¹ JIANG Zheng^1*

Objective To investigate the expression and significance of the adaptor protein epsin 3(EPN3) in colorectal cancer in order to provide reference for further study of EPN3. Methods GEPIA and GEDS were used to analyze the expression of EPN3 in colorectal cancer tissues and cells. SMART and cBioPortal databases were used to analyze the relationship between EPN3 gene methylation and copy number variation and its expression level. Metascape was used to complete analysis of gene ontology functional annotation and related pathways of EPN3 related genes and BioPlex was applied to construct a protein network in HCT116 cell. Thirteen pairs of colorectal cancer adjacent tissues and cancer tissue specimens were collected, and EPN3 mRNA expression were detected by Realtime PCR. The effect of abilities of cell proliferation, clone formation and migration via silencing EPN3 in HCT116 and HT29 were observed. Results GEPIA, GEDS, SMART and cBioPortal analyses showed that EPN3 was highly expressed in colorectal tumor tissues (P<0.01), and was related to methylation and copy number variation. The enrichment result of EPN3 related genes showed that it was mainly related to cell adhesion. And a protein interaction network constructed by CCDC130, TNFAIP1, PHGDH, EPN2, etc. was related to protein ubiquitination. Real-time PCR result showed that EPN3 was highly expressed in tumor tissues (P<0.05). Silencing EPN3 inhibited the proliferation, clony formation and migration abilities of HCT116 and HT29 cells. Conclusion EPN3 is highly expressed in colorectal cancer tissues and is related to cell adhesion and protein ubiquitination. Down-regulated EPN3 can inhibit abilities of proliferation, clony formation and migration of HCT116 and HT29 cells, which could provide a reference for further research on EPN3.

Received:2020-12-10 Revised:2021-03-02 Online:2022-08-06 Published:2022-09-11
Contact: JIANG Zheng E-mail:zhengjiang1753@163.com

Abstract

Abstract: Objective To investigate the expression and significance of the adaptor protein EPN3 (Epsin 3) in colorectal cancer in order to provide reference for further study of EPN3. Methods We used tools of GEPIA and GEDS to analyze the expression of EPN3 in colorectal cancer tissues and cells. SMART and cBioPortal databases were used to analyze the relationship between EPN3 gene methylation and copy number variation and its expression level. Metascape was used to complete analysis of gene ontology (GO) functional annotation and related pathways of EPN3 related genes and BioPlex was applied to constructed a protein network in HCT116 cell. We collected 13 pairs of colorectal cancer adjacent tissue and cancer tissue specimens, and detected EPN3 mRNA expression by using RT-qPCR. We observed the effect of abilities of cell proliferation, clone formation and migration via silencing EPN3 in HCT116 and HT29. Results GEPIA, GEDS, SMART and cBioPortal analyses showed that EPN3 was highly expressed in colorectal tumor tissues (p<0.01), and was related to methylation and copy number variation. The enrichment results of EPN3 related genes showed that it was mainly related to cell adhesion. And a protein interaction network constructed by CCDC130, TNFAIP1, PHGDH, EPN2, etc. was related to protein ubiquitination. RT-qPCR result showed that EPN3 was highly expressed in tumor tissues (p<0.05). Silencing EPN3 inhibited the proliferation, clone formation and migration abilities of HCT116 and HT29 cells. Conclusion EPN3 is highly expressed in colorectal cancer tissues and is related to cell adhesion and protein ubiquitination. Down-regulated EPN3 can inhibit abilities of proliferation, clone formation and migration of HCT116 and HT29 cells, and this could provide a reference for further research on EPN3.

Key words: Colorectal cancer, Epsin3, Bioinformatics, Colony formation, Scratch test, Real-time PCR, Human

CLC Number:

R735. 3

XIANG Li-chun JIANG Zhong-xiang JIANG Xiao-ye CHEN Xue-nuo JIANG Zheng. Differential expression and bioinformatics analysis of epsin3 in colorectal cancer[J]. Acta Anatomica Sinica, 2022, 53(4): 507-514.

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Differential expression and bioinformatics analysis of epsin3 in colorectal cancer

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