NLRX1 regulates TNF-α-induced mitochondria-lysosomal crosstalk to maintain the invasive and metastatic potential of breast cancer cells

Biochimica Et Biophysica Acta. Molecular Basis of Disease
Kritarth SinghRajesh Singh

Abstract

An increased level of proinflammatory cytokines, including TNF-α in tumor microenvironment regulates the bioenergetic capacity, immune evasion and survival of cancer cells. Emerging evidences suggest that mitochondrial immune signaling proteins modulates mitochondrial bioenergetic capacity, in addition to the regulation of innate immune response. The optimal oxidative phosphorylation (OxPhos) capacity is required for the maintenance of functional lysosomes and autophagy flux. NLRX1, a mitochondrial NOD family receptor protein, regulates mitochondrial function during apoptosis and tissue injury. However, its role in regulation of mitochondrial and lysosomal function to modulate autophagy flux during inflammatory conditions is not understood. In the current study, we investigated the role of NLRX1 in modulating TNF-α induced autophagy flux and mitochondrial turnover and its implication in regulating the invasive and metastatic capability of breast cancer cells. Expression analyses of clinical breast cancer samples and meta-analysis of multiple public databases revealed that NLRX1 expression is significantly increased in basal-like and metastatic breast carcinoma as compared to non-basal-like and primary breast cancer. Depletion o...Continue Reading

Citations

Nov 5, 2019·Frontiers in Immunology·Margaret A Nagai-SingerIrving C Allen
Dec 15, 2020·Immunology·Robert J Pickering, Lee M Booty
Dec 22, 2020·Frontiers in Cellular and Infection Microbiology·Tiia Snäkä, Nicolas Fasel
Feb 3, 2021·International Journal of Molecular Sciences·Tünde FeketeKitti Pázmándi
Nov 6, 2020·Acta Pharmaceutica : a Quarterly Journal of Croatian Pharmaceutical Society and Slovenian Pharmaceutical Society, Dealing with All Branches of Pharmacy and Allied Sciences·Qingfang ZengWei Zhou
Sep 9, 2021·Cell Communication and Signaling : CCS·Yalan DuanYongzhong Hou

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