Original articleIntracellular pH controls growth factor-induced ribosomal protein S6 phosphorylation and protein synthesis in the G0→G1 transition of fibroblasts☆
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pH gradient reversal fuels cancer progression
2020, International Journal of Biochemistry and Cell BiologyCitation Excerpt :In response to growth factors, quiescent fibroblast needs a sodium/proton antiporter (NHE)- dependent cytosolic alkalinization to enter the S phase of the cell cycle (Pouyssegur et al., 1985). Both protein synthesis activation and DNA synthesis re-initiation are pH-regulated events that are dependent on a permissive cytosolic pH of 7.2 and an optimal cytosolic pH of 7.5 (Pouyssegur et al., 1985; Chambard and Pouyssegur, 1986). Mechanistically, ion transporting activity of NHEs positively regulates the G2/M entry and transition by alkalinizing cytosol which further activates cyclin-dependent kinase Cdc2.
Sodium homeostasis in the tumour microenvironment
2019, Biochimica et Biophysica Acta - Reviews on CancerCitation Excerpt :Increased NHE1 activity leads to intracellular alkalinisation [87] and this may be a critical early event in oncogene-induced malignant transformation [88]. Maintenance of a high pHi by NHE1 activity is permissive for upregulation of both glycolytic activity and protein synthesis required for rapid cell growth and division [1,89,90]. On the other hand, extracellular acidification promotes invasion and suppresses the immune response [91,92].
Acid Suspends the Circadian Clock in Hypoxia through Inhibition of mTOR
2018, CellCitation Excerpt :Our conclusion that mTORC1 is rapidly and durably inhibited by acid is corroborated by other work. Remarkably, prior to the discovery of mTOR, it was observed that intracellular acidification (due to acidic media exposure or genetic or pharmacologic inhibition of H+ export) could potently suppress phosphorylation of ribosomal protein S6 and translation (Chambard and Pouyssegur, 1986). More recently, a group has rediscovered acid’s effect and reported it to act via TSC2 or independently even in the same cells depending on context (Balgi et al., 2011; Fonseca et al., 2012).
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This work was supported by grants from the Centre National de la Recherche Scientifique (LP 7300, ATP 136 and ASP 394), the Institut National de la Santé et de la Recherche Médicale (CRE 84-2015), the Fondation pour la Recherche Médicale and the Association pour la Recherche contre le Cancer.
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J. C. C. was supported by the Fondation pour la Recherche Médicale and EMBO fellowship (ASTF 4307).