{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:59:37Z","timestamp":1792789177094,"version":"4.5.0"},"reference-count":106,"publisher":"MDPI AG","issue":"5","license":[{"start":{"date-parts":[[2023,2,23]],"date-time":"2023-02-23T00:00:00Z","timestamp":1677110400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"ITMO Cancer of Aviesan"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancers"],"abstract":"<jats:p>Lactic acidosis, a hallmark of solid tumour microenvironment, originates from lactate hyperproduction and its co-secretion with protons by cancer cells displaying the Warburg effect. Long considered a side effect of cancer metabolism, lactic acidosis is now known to play a major role in tumour physiology, aggressiveness and treatment efficiency. Growing evidence shows that it promotes cancer cell resistance to glucose deprivation, a common feature of tumours. Here we review the current understanding of how extracellular lactate and acidosis, acting as a combination of enzymatic inhibitors, signal, and nutrient, switch cancer cell metabolism from the Warburg effect to an oxidative metabolic phenotype, which allows cancer cells to withstand glucose deprivation, and makes lactic acidosis a promising anticancer target. We also discuss how the evidence about lactic acidosis\u2019 effect could be integrated in the understanding of the whole-tumour metabolism and what perspectives it opens up for future research.<\/jats:p>","DOI":"10.3390\/cancers15051417","type":"journal-article","created":{"date-parts":[[2023,2,23]],"date-time":"2023-02-23T05:23:43Z","timestamp":1677129823000},"page":"1417","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["How Warburg-Associated Lactic Acidosis Rewires Cancer Cell Energy Metabolism to Resist Glucose Deprivation"],"prefix":"10.3390","volume":"15","author":[{"given":"Zo\u00e9","family":"Daverio","sequence":"first","affiliation":[{"name":"Laboratoire CarMeN, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale U1060, Universit\u00e9 Claude Bernard Lyon 1, 69100 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8544-5778","authenticated-orcid":false,"given":"Aneta","family":"Balcerczyk","sequence":"additional","affiliation":[{"name":"Department of Oncobiology and Epigenetics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1064-0293","authenticated-orcid":false,"given":"Gilles J. P.","family":"Rautureau","sequence":"additional","affiliation":[{"name":"Institut de Chimie et Biochimie Mol\u00e9culaires et Supramol\u00e9culaires, Universit\u00e9 Claude Bernard Lyon 1, 69622 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9430-4061","authenticated-orcid":false,"given":"Baptiste","family":"Panthu","sequence":"additional","affiliation":[{"name":"Laboratoire CarMeN, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale U1060, Universit\u00e9 Claude Bernard Lyon 1, 69100 Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,2,23]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1298","DOI":"10.1038\/s41416-020-0777-y","article-title":"Lactic acidosis induces resistance to the pan-Akt inhibitor uprosertib in colon cancer cells","volume":"122","author":"Barnes","year":"2020","journal-title":"Br. J. 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