BPBao-Gang Peng

Bao-Gang Peng

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Bao-Gang Peng has a total of 6 co-authors. Here are the top co-authors by number of shared publications:

  • Hong-Li Xi

    Department of Clinical Laboratory, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, China

    1 shared publication
  • Jian Wu

    Department of Hepatic Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China

    1 shared publication
  • Ling-Yun Liu

    Department of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Guilin 5410000, China

    1 shared publication
  • Shu-Tong Wang

    Department of Hepatic Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China

    1 shared publication
  • Wen-Jin Huang

    Department of Radiotherapy Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, China

    1 shared publication
  • Wenzhe Fan

    Department of Interventional Oncology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China

    1 shared publication

Latest Publications

  • Tumor-suppressive miR-3650 inhibits tumor metastasis by directly targeting NFASC in hepatocellular carcinoma

    by Jian Wu, Wen-Jin Huang, Hong-Li Xi, Ling-Yun Liu, Shu-Tong Wang, Wen-Zhe Fan, Bao-Gang Peng

    In recent years, a growing body of evidence has provided support for the important role of microRNAs (miRNAs) in the progression of human cancers. A recent study showed that a novel miRNA miR-3650 expression was significantly decreased in hepatocellular carcinoma (HCC). However, the precise role of miR-3650 in HCC have remained poorly understood. In this study, we found that miR-3650 expression was frequently decreased in HCC tissues. Low expression of miR-3650 is positively associated with tumor metastasis and poor survival of HCC patients. Forced expression of miR-3650 significantly inhibited the migration and epithelial-mesenchymal transition (EMT) of HCC cells. Through bioinformatic analysis and luciferase assays, we confirmed that neurofascin (NFASC) is a directly target mRNA of miR-3650. Rescue experiment demonstrated that NAFSC overexpression could partially counteracted the inhibitory effect of miR-3650 in HCC metastasis and EMT. In conclusion, our findings are the first time to demonstrate that reduced expression of miR-3650 in HCC was correlated with tumor metastasis and poor survival. MiR-3650 repressed HCC migration and EMT by directly targeting NFASC. Our findings suggested that miR-3650 may serve as a potential prognostic marker and promising application in HCC therapy.