Mingfeng Ying
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
Research Interests
Mingfeng Ying has a total of 3 co-authors. Here are the top co-authors by number of shared publications:
- Xun Hu
Zhejiang University, China
2 shared publications - Hao Wu
Cancer Institute (Key Laboratory for Cancer Intervention and Prevention, China National Ministry of Education, Zhejiang Provincial Key Laboratory of Molecular Biology in Medical Sciences), The Second Affiliated Hospital, Zhejiang University School of Medicine
1 shared publication - Yuqi Wang
Department of gastroenterology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
1 shared publication
Latest Publications
- 28 October 2022
- Published by Elsevier in Seminars in Cancer Biology
- Vol. 87, 32-47
Tracing the electron flow in redox metabolism: The appropriate distribution of electrons is essential to maintain redox balance in cancer cells
- 28 October 2022
- Published by Elsevier in Seminars in Cancer Biology
- Vol. 87, 32-47
Tracing the electron flow in redox metabolism: The appropriate distribution of electrons is essential to maintain redox balance in cancer cells
- Open Access
Lactate dehydrogenases amplify reactive oxygen species in cancer cells in response to oxidative stimuli
Previous studies have revealed that lactate dehydrogenase A (LDHA) exhibited an indirect antioxidative activity, which played a crucial role in preventing cancer cells from oxidative stress. Here we demonstrated that, apart from antioxidative activities, LDHA and LDHB displayed prooxidative activity in cancer cells. In aqueous phase, LDHA and B both exhibited ROS-generating activity and LDHB was more active than LDHA. In cancer cells, the dominant antioxidative activity of LDH can be switched to dominant prooxidative activity or vice versa, depending on the strength of oxidative stimuli, indicating that LDH were bifunctional. Moreover, we demonstrated that mitochondrial superoxide served as an initiator to trigger LDH-catalyzed amplification of ROS. The oxidative stimuli, such as modulators of electron transfer chain and anticancer agents that kill cancer cells via ROS induction, induced a ROS generation involving 2 phases, induction of mitochondrial superoxide and amplification of ROS by LDH.
Open AccessLactate dehydrogenases amplify reactive oxygen species in cancer cells in response to oxidative stimuli
Previous studies have revealed that lactate dehydrogenase A (LDHA) exhibited an indirect antioxidative activity, which played a crucial role in preventing cancer cells from oxidative stress. Here we demonstrated that, apart from antioxidative activities, LDHA and LDHB displayed prooxidative activity in cancer cells. In aqueous phase, LDHA and B both exhibited ROS-generating activity and LDHB was more active than LDHA. In cancer cells, the dominant antioxidative activity of LDH can be switched to dominant prooxidative activity or vice versa, depending on the strength of oxidative stimuli, indicating that LDH were bifunctional. Moreover, we demonstrated that mitochondrial superoxide served as an initiator to trigger LDH-catalyzed amplification of ROS. The oxidative stimuli, such as modulators of electron transfer chain and anticancer agents that kill cancer cells via ROS induction, induced a ROS generation involving 2 phases, induction of mitochondrial superoxide and amplification of ROS by LDH.