Jun Ren
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Jun Ren has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Daorong Wang
Northern Jiangsu People’s Hospital Affiliated to Yangzhou University, Yangzhou, China
1 shared publication - Dong Tang
Yangzhou University
1 shared publication - Muhammad Ali
Department of General Surgery, General Surgery Institute of Yangzhou, Northern Jiangsu People’s Hospital, Clinical Medical College, Yangzhou University, Yangzhou 225009, China
1 shared publication - Qi Zhang
Department of Gastrointestinal Surgery, Northern Jiangsu People’s Hospital, Clinical Teaching Hospital of Medical School, Nanjing University, Yangzhou, China
1 shared publication - Qiannan Sun
Department of General Surgery, General Surgery Institute of Yangzhou, Northern Jiangsu People’s Hospital, Clinical Medical College, Yangzhou University, Yangzhou 225009, China
1 shared publication - Wei Wang
Department of General Surgery, General Surgery Institute of Yangzhou, Northern Jiangsu People’s Hospital, Clinical Medical College, Yangzhou University, Yangzhou 225009, China
1 shared publication
Latest Publications
- Open Access
ATF4 Transcriptionally Activates SHH to Promote Proliferation, Invasion, and Migration of Gastric Cancer Cells
Activating transcription factor 4 (ATF4) is a DNA-binding protein widely generated in mammals, which has two biological characteristics that bind the cAMP response element (CRE). The mechanism of ATF4 as a transcription factor in gastric cancer affecting the Hedgehog pathway remains unclear. Here, we observed that ATF4 was markedly upregulated in gastric cancer (GC) using immunohistochemistry and Western blotting assays in 80 paraffin-embedded GC samples and 4 fresh samples and para-cancerous tissues. ATF4 knockdown using lentiviral vectors strongly inhibited the proliferation and invasion of GC cells. ATF4 upregulation using lentiviral vectors promoted the proliferation and invasion of GC cells. We predicted that the transcription factor ATF4 is bound to the SHH promoter via the JASPA database. Transcription factor ATF4 is bound to the promoter region of SHH to activate the Sonic Hedgehog pathway. Mechanistically, rescue assays showed that ATF4 regulated gastric cancer cells’ proliferation and invasive ability through SHH. Similarly, ATF4 enhanced the tumor formation of GC cells in a xenograft model.
Open AccessATF4 Transcriptionally Activates SHH to Promote Proliferation, Invasion, and Migration of Gastric Cancer Cells
Activating transcription factor 4 (ATF4) is a DNA-binding protein widely generated in mammals, which has two biological characteristics that bind the cAMP response element (CRE). The mechanism of ATF4 as a transcription factor in gastric cancer affecting the Hedgehog pathway remains unclear. Here, we observed that ATF4 was markedly upregulated in gastric cancer (GC) using immunohistochemistry and Western blotting assays in 80 paraffin-embedded GC samples and 4 fresh samples and para-cancerous tissues. ATF4 knockdown using lentiviral vectors strongly inhibited the proliferation and invasion of GC cells. ATF4 upregulation using lentiviral vectors promoted the proliferation and invasion of GC cells. We predicted that the transcription factor ATF4 is bound to the SHH promoter via the JASPA database. Transcription factor ATF4 is bound to the promoter region of SHH to activate the Sonic Hedgehog pathway. Mechanistically, rescue assays showed that ATF4 regulated gastric cancer cells’ proliferation and invasive ability through SHH. Similarly, ATF4 enhanced the tumor formation of GC cells in a xenograft model.