MIRO2 Regulates Prostate Cancer Cell Growth via GCN1-Dependent Stress Signaling

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Abstract

There is a continued need to identify novel therapeutic targets prostate cancer led to the identification of MIRO2 159L, which to prevent the mortality associated with prostate cancer. In this increased GCN1 binding. Importantly, MIRO2 was necessary for context, mitochondrial Rho GTPase 2 (MIRO2) mRNA was efficient GCN1-mediated GCN2 kinase signaling and induction upregulated in metastatic prostate cancer compared with local-of the transcription factor activating transcription factor 4 ized tumors, and higher MIRO2 levels were correlated with poor (ATF4) levels. Further, MIRO20s effect on regulating prostate patient survival. Using human cell lines that represent androgen-cancer cell growth was mediated by ATF4. Finally, levels of independent or -sensitive prostate cancer, we showed that activated GCN2 and ATF4 were correlated with MIRO2 expresMIRO2 depletion impaired cell growth, colony formation, and sion in prostate cancer xenografts. Both MIRO2 and activated tumor growth in mice. Network analysis of MIRO20s binding GCN2 levels were higher in hypoxic areas of prostate cancer partners identified metabolism and cellular responses to extra-xenografts. Overall, we propose that targeting the MIRO2-GCN1 cellular stimuli as top overrepresented pathways. The top hit on axis may be a valuable strategy to halt prostate cancer growth. our screen, General Control Nonderepressible 1 (GCN1), was overexpressed in prostate cancer, and interacted with MIRO2 in Implications: MIRO2/GCN1/GCN2 constitute a novel mitochonprostate cancer cell lines and in primary prostate cancer cells. drial signaling pathway that controls androgen-independent and Functional analysis of MIRO2 mutations present in patients with androgen-sensitive prostate cancer cell growth.

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APA

Furnish, M., Boulton, D. P., Genther, V., Grofova, D., Ellinwood, M. L., Romero, L., … Caino, M. C. (2022). MIRO2 Regulates Prostate Cancer Cell Growth via GCN1-Dependent Stress Signaling. Molecular Cancer Research, 20(4), 607–621. https://doi.org/10.1158/1541-7786.MCR-21-0374

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