Yayuan Zheng
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Yayuan Zheng has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Bin Yu
Jilin University
1 shared publication - Haihong Zhang
National Engineering Laboratory for AIDS Vaccine, School of Life Science, Jilin University, Changchun 130012, China
1 shared publication - Hui Wu
National Engineering Laboratory for AIDS Vaccine, School of Life Science, Jilin University, Changchun 130012, China
1 shared publication - Jiaxin Wu
National Engineering Laboratory for AIDS Vaccine, School of Life Science, Jilin University, Changchun 130012, China
1 shared publication - Mingrui Dai
National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, Jilin province, People's Republic of China
1 shared publication - Wei Kong
National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, China
1 shared publication
Latest Publications
- Open Access
- 12 December 2018
- Published by Springer Nature in Clinical Epigenetics
- Vol. 10 (1) , 154
Epigenetic suppression of E-cadherin expression by Snail2 during the metastasis of colorectal cancer
The transcription factor Snail2 is a repressor of E-cadherin expression during carcinogenesis; however, the specific mechanisms involved in this process in human colorectal cancer (CRC) remain largely unknown. We checked the expression of Snail2 in several clinical CRC specimens. Then, we established Snail2-overexpressing and knockdown cell lines to determine the function of Snail2 during EMT and metastasis processes in CRC. In addition, we used luciferase reporter assay to explore how Snail2 inhibits the expression of E-cadherin and induces EMT. We found that the expression of Snail2 was higher in clinical specimens of colorectal cancer (CRC) compared to non-cancerous tissues. Overexpression of Snail2 induced migration and metastatic properties in CRC cells in vitro and in vivo. Furthermore, overexpression of Snail2 promoted the occurrence of the epithelial–mesenchymal transition (EMT), downregulating the expression of E-cadherin and upregulating that of vimentin. Specifically, Snail2 could interact with HDAC6 and then recruited HDAC6 and PRC2 to the promoter of E-cadherin and thus inhibited the expression of E-cadherin, promoting EMT and inducing invasion and metastasis of CRC. Our study reveals that Snail2 might epigenetically suppress the expression of E-cadherin during CRC metastasis.
- 12 December 2018
- Published by Springer Nature in Clinical Epigenetics
- Vol. 10 (1) , 154
Open AccessEpigenetic suppression of E-cadherin expression by Snail2 during the metastasis of colorectal cancer
The transcription factor Snail2 is a repressor of E-cadherin expression during carcinogenesis; however, the specific mechanisms involved in this process in human colorectal cancer (CRC) remain largely unknown. We checked the expression of Snail2 in several clinical CRC specimens. Then, we established Snail2-overexpressing and knockdown cell lines to determine the function of Snail2 during EMT and metastasis processes in CRC. In addition, we used luciferase reporter assay to explore how Snail2 inhibits the expression of E-cadherin and induces EMT. We found that the expression of Snail2 was higher in clinical specimens of colorectal cancer (CRC) compared to non-cancerous tissues. Overexpression of Snail2 induced migration and metastatic properties in CRC cells in vitro and in vivo. Furthermore, overexpression of Snail2 promoted the occurrence of the epithelial–mesenchymal transition (EMT), downregulating the expression of E-cadherin and upregulating that of vimentin. Specifically, Snail2 could interact with HDAC6 and then recruited HDAC6 and PRC2 to the promoter of E-cadherin and thus inhibited the expression of E-cadherin, promoting EMT and inducing invasion and metastasis of CRC. Our study reveals that Snail2 might epigenetically suppress the expression of E-cadherin during CRC metastasis.