AI Article Synopsis
- EMT is linked to aggressive tumors, but the role of metabolic stress in this process is unclear. Researchers found that CRMP2A is induced in cancer cells under metabolic stress and helps suppress EMT and cancer stem cell-like traits.
- When CRMP2A is lost, particularly in favorable environments like areas near blood vessels, cancer cells undergo changes that promote EMT, increased migration, and resistance to treatment.
- A study on prostate cancer patients showed that lower levels of CRMP2A in metastatic tumors correlate with higher aggressiveness, suggesting CRMP2A acts as a brake on tumor progression.
Article Abstract
An epithelial-to-mesenchymal transition (EMT) phenotype with cancer stem cell-like properties is a critical feature of aggressive/metastatic tumors, but the mechanism(s) that promote it and its relation to metabolic stress remain unknown. Here we show that Collapsin Response Mediator Protein 2A (CRMP2A) is unexpectedly and reversibly induced in cancer cells in response to multiple metabolic stresses, including low glucose and hypoxia, and inhibits EMT/stemness. Loss of CRMP2A, when metabolic stress decreases (e.g., around blood vessels in vivo) or by gene deletion, induces extensive microtubule remodeling, increased glutamine utilization toward pyrimidine synthesis, and an EMT/stemness phenotype with increased migration, chemoresistance, tumor initiation capacity/growth, and metastatic potential. In a cohort of 27 prostate cancer patients with biopsies from primary tumors and distant metastases, CRMP2A expression decreases in the metastatic versus primary tumors. CRMP2A is an endogenous molecular brake on cancer EMT/stemness and its loss increases the aggressiveness and metastatic potential of tumors.
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| http://dx.doi.org/10.1016/j.celrep.2022.110511 | DOI Listing |
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