Chunyu Ma
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Chunyu Ma has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
Chengjie Ji
Department of Clinical Medicine, The People’s Hospital of jianyang, Chengdu, China
1 shared publicationDie Hu
Department of Clinical Medicine, The People’s Hospital of jianyang, Chengdu, China
1 shared publicationDongqing Chu
Graduated School of Jinzhou Medical University Jinzhou China
1 shared publicationJialin Li
First Affiliated Hospital of Jinzhou Medical University Jinzhou China
1 shared publication- Jianhua Huang
First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China
1 shared publication Kan Chen
First Affiliated Hospital of Jinzhou Medical University Jinzhou China
1 shared publication
Latest Publications
- Open Access
- 9 July 2026
- Published by Springer Nature in Virology Journal
- Vol. 23 (1)
Identification of key genes associated with T cell exhaustion in HIV infection based on transcriptomic data
Human immunodeficiency virus (HIV) is a lentivirus belonging to the retrovirus subclass. HIV specifically targets and infects human CD4 + T lym
- 9 July 2026
- Published by Springer Nature in Virology Journal
- Vol. 23 (1)
Open AccessIdentification of key genes associated with T cell exhaustion in HIV infection based on transcriptomic data
Human immunodeficiency virus (HIV) is a lentivirus belonging to the retrovirus subclass. HIV specifically targets and infects human CD4 + T lym
- 19 September 2021
- Published by Wiley in Phytotherapy Research
- Vol. 35 (11) , 6389-6400
Asiatic acid inhibits angiogenesis and vascular permeability through the VEGF/VEGFR2 signaling pathway to inhibit the growth and metastasis of breast cancer in mice
Anti‐angiogenic medicines have been evaluated as anticancer therapies, however, their use remains limited in clinical practice due to associated adverse effects. Asiatic acid (AA) is known to have broad‐spectrum anticancer properties, however, its effects on angiogenesis in breast cancer remain to be fully established. In this study, we analyzed the inhibitory effects of AA on angiogenesis using human umbilical vein endothelial cells (HUVECs) cultured in vitro and on the growth and metastasis of a subcutaneous breast cancer 4T1 tumor model and a lung metastasis model in vivo. AA significantly inhibited HUVECs proliferation, migration, and tube formation in vitro. In vivo, AA significantly reduced the microvascular density and blood vascular permeability in breast cancer tumors and inhibited growth and lung metastasis. AA inhibited the expression of vascular endothelial growth factor (VEGF) in HUVECs and subsequently downregulated the phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2) and its downstream target proteins including ERK1/2, Src, and FAK. These results indicate that AA significantly inhibits angiogenesis and blood vessel permeability through the VEGF/VEGFR2 signal axis to inhibit the growth and metastasis of breast cancer. Our data strongly demonstrate the potential applications of AA in the treatment of breast cancer.
- 19 September 2021
- Published by Wiley in Phytotherapy Research
- Vol. 35 (11) , 6389-6400
Asiatic acid inhibits angiogenesis and vascular permeability through the VEGF/VEGFR2 signaling pathway to inhibit the growth and metastasis of breast cancer in mice
Anti‐angiogenic medicines have been evaluated as anticancer therapies, however, their use remains limited in clinical practice due to associated adverse effects. Asiatic acid (AA) is known to have broad‐spectrum anticancer properties, however, its effects on angiogenesis in breast cancer remain to be fully established. In this study, we analyzed the inhibitory effects of AA on angiogenesis using human umbilical vein endothelial cells (HUVECs) cultured in vitro and on the growth and metastasis of a subcutaneous breast cancer 4T1 tumor model and a lung metastasis model in vivo. AA significantly inhibited HUVECs proliferation, migration, and tube formation in vitro. In vivo, AA significantly reduced the microvascular density and blood vascular permeability in breast cancer tumors and inhibited growth and lung metastasis. AA inhibited the expression of vascular endothelial growth factor (VEGF) in HUVECs and subsequently downregulated the phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2) and its downstream target proteins including ERK1/2, Src, and FAK. These results indicate that AA significantly inhibits angiogenesis and blood vessel permeability through the VEGF/VEGFR2 signal axis to inhibit the growth and metastasis of breast cancer. Our data strongly demonstrate the potential applications of AA in the treatment of breast cancer.