Mitochondrial dynamics links PINCH-1 signaling to proline metabolic reprogramming and tumor growth
Authors:Ling Guo1 and Chuanyue Wu2
1 Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Academy for Advanced Interdisciplinary Studies and Department of Biology, Southern University of Science and Technology, China.
2 Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.
Keywords:
tumor growth, fibrosis, mitochondrial dynamics, proline metabolism, cell-extracellular matrix adhesion, PINCH-1.
Corresponding Author(s):
Conflict of interest statement:
The authors declare no conflict of interest.
Please cite this article as:
Ling Guo and Chuanyue Wu (2020). Mitochondrial dynamics links PINCH-1 signaling to proline metabolic reprogramming and tumor growth. Cell Stress 5(2): 23-25. doi: 10.15698/cst2021.02.241
© 2020 Guo and Wu. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
Proline metabolism is critical for cellular response to microenvironmental stress in living organisms across different kingdoms, ranging from bacteria, plants to animals. In bacteria and plants, proline is known to accrue in response to osmotic and other stresses. In higher organisms such as human, proline metabolism plays important roles in physiology as well as pathological processes including cancer. The importance of proline metabolism in physiology and diseases lies in the fact that the products of proline metabolism are intimately involved in essential cellular processes including protein synthesis, energy production and redox signaling. A surge of protein synthesis in fast proliferating cancer cells, for example, results in markedly increased demand for proline. Proline synthesis is frequently unable to meet the demand in fast proliferating cancer cells. The inadequacy of proline or “proline vulnerability” in cancer may provide an opportunity for therapeutic control of cancer progression. To this end, it is important to understand the signaling mechanism through which proline synthesis is regulated. In a recent study (Guo et al., Nat Commun 11(1):4913, doi: 10.1038/s41467-020-18753-6), we have identified PINCH-1, a component of cell-extracellular matrix (ECM) adhesions, as an important regulator of proline synthesis and cancer progression.