Wenwen Chen
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Wenwen Chen has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Dongqin Yang
Central laboratory, Huashan Hospital, Fudan University
1 shared publication - Fuchen Liu
The Third Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital Second Military Medical University Shanghai China
1 shared publication - Lijun Wu
Fudan University Library Shanghai China
1 shared publication - Linlin Huang
Central Laboratory, Huashan Hospital Fudan University Shanghai China
1 shared publication - Mengxiao Ge
Central Laboratory, Huashan Hospital Fudan University Shanghai China
1 shared publication - Qiongzhu Dong
Key Laboratory of Whole-Period Monitoring and Precise Intervention of Digestive Cancer, Shanghai Municipal Health Commission (SMHC), Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, China
1 shared publication
Latest Publications
- 9 February 2024
- Published by Wiley in The FASEB Journal
- Vol. 38 (4) , e23475
ASB3 promotes hepatocellular carcinoma progression by mediating DR5 ubiquitination in TRAIL resistance
Ankyrin‐repeat proteins with a suppressor of cytokine signaling box (ASB) proteins belong to the E3 ubiquitin ligase family. 18 ASB members have been identified whose biological functions are mostly unexplored. Here, we discovered that ASB3 was essential for hepatocellular carcinoma (HCC) development and high ASB3 expression predicted poor clinical outcomes. ASB3 silencing induced HCC cell growth arrest and apoptosis in vitro and in vivo. Liver‐specific deletion of Asb3 gene suppressed diethylnitrosamine (DEN)‐induced liver cancer development. Mechanistically, ASB3 interacted with death receptor 5 (DR5), which promoted ubiquitination and degradation of DR5. We further showed that ASB3 knockdown stabilized DR5 and increased the sensitivity of liver cancer cells to the treatment of tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) in a DR5‐dependent manner in cellular and in animal models. In summary, we demonstrated that ASB3 promoted ubiquitination and degradation of DR5 in HCC, suggesting the potential of targeting ASB3 to HCC treatment and overcome TRAIL resistance.
- 9 February 2024
- Published by Wiley in The FASEB Journal
- Vol. 38 (4) , e23475
ASB3 promotes hepatocellular carcinoma progression by mediating DR5 ubiquitination in TRAIL resistance
Ankyrin‐repeat proteins with a suppressor of cytokine signaling box (ASB) proteins belong to the E3 ubiquitin ligase family. 18 ASB members have been identified whose biological functions are mostly unexplored. Here, we discovered that ASB3 was essential for hepatocellular carcinoma (HCC) development and high ASB3 expression predicted poor clinical outcomes. ASB3 silencing induced HCC cell growth arrest and apoptosis in vitro and in vivo. Liver‐specific deletion of Asb3 gene suppressed diethylnitrosamine (DEN)‐induced liver cancer development. Mechanistically, ASB3 interacted with death receptor 5 (DR5), which promoted ubiquitination and degradation of DR5. We further showed that ASB3 knockdown stabilized DR5 and increased the sensitivity of liver cancer cells to the treatment of tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) in a DR5‐dependent manner in cellular and in animal models. In summary, we demonstrated that ASB3 promoted ubiquitination and degradation of DR5 in HCC, suggesting the potential of targeting ASB3 to HCC treatment and overcome TRAIL resistance.