PMID- 38184121 OWN - NLM STAT- MEDLINE DCOM- 20240508 LR - 20240508 IS - 1638-6183 (Electronic) IS - 0300-9084 (Linking) VI - 220 DP - 2024 May TI - The determinants of metabolic discrepancies in aerobic glycolysis: Providing potential targets for breast cancer treatment. PG - 107-121 LID - S0300-9084(24)00003-8 [pii] LID - 10.1016/j.biochi.2024.01.003 [doi] AB - Altered aerobic glycolysis is the robust mechanism to support cancer cell survival and proliferation beyond the maintenance of cellular energy metabolism. Several investigators portrayed the important role of deregulated glycolysis in different cancers, including breast cancer. Breast cancer is the most ubiquitous form of cancer and the primary cause of cancer death in women worldwide. Breast cancer with increased glycolytic flux is hampered to eradicate with current therapies and can result in tumor recurrence. In spite of the low order efficiency of ATP production, cancer cells are highly addicted to glycolysis. The glycolytic dependency of cancer cells provides potential therapeutic strategies to preferentially kill cancer cells by inhibiting glycolysis using antiglycolytic agents. The present review emphasizes the most recent research on the implication of glycolytic enzymes, including glucose transporters (GLUTs), hexokinase (HK), phosphofructokinase (PFK), pyruvate kinase (PK), lactate dehydrogenase-A (LDHA), associated signalling pathways and transcription factors, as well as the antiglycolytic agents that target key glycolytic enzymes in breast cancer. The potential activity of glycolytic inhibitors impinges cancer prevalence and cellular resistance to conventional drugs even under worse physiological conditions such as hypoxia. As a single agent or in combination with other chemotherapeutic drugs, it provides the feasibility of new therapeutic modalities against a wide spectrum of human cancers. CI - Copyright (c) 2024 Elsevier B.V. and Societe Francaise de Biochimie et Biologie Moleculaire (SFBBM). All rights reserved. FAU - Littleflower, Ajeesh Babu AU - Littleflower AB AD - Division of Cancer Research, Regional Cancer Centre (Research Centre, University of Kerala), Thiruvananthapuram, Kerala, 695011, India. FAU - Parambil, Sulfath Thottungal AU - Parambil ST AD - Division of Cancer Research, Regional Cancer Centre (Research Centre, University of Kerala), Thiruvananthapuram, Kerala, 695011, India. FAU - Antony, Gisha Rose AU - Antony GR AD - Division of Cancer Research, Regional Cancer Centre (Research Centre, University of Kerala), Thiruvananthapuram, Kerala, 695011, India. FAU - Subhadradevi, Lakshmi AU - Subhadradevi L AD - Division of Cancer Research, Regional Cancer Centre (Research Centre, University of Kerala), Thiruvananthapuram, Kerala, 695011, India. Electronic address: rcc.lakshmi@gmail.com. LA - eng PT - Journal Article PT - Review DEP - 20240104 PL - France TA - Biochimie JT - Biochimie JID - 1264604 RN - 0 (Antineoplastic Agents) RN - EC 2.7.1.1 (Hexokinase) RN - 0 (Glucose Transport Proteins, Facilitative) SB - IM MH - Humans MH - *Breast Neoplasms/metabolism/drug therapy/pathology MH - Female MH - *Glycolysis/drug effects MH - Warburg Effect, Oncologic/drug effects MH - Antineoplastic Agents/therapeutic use/pharmacology MH - Hexokinase/metabolism/antagonists & inhibitors MH - Glucose Transport Proteins, Facilitative/metabolism OTO - NOTNLM OT - Aerobic glycolysis OT - Anti-glycolytic agents OT - Breast cancer OT - Glucose metabolism OT - Glycolytic enzymes OT - Targeted therapy COIS- Declaration of competing interest The authors have no conflict of interest with the contents of this article. EDAT- 2024/01/07 06:44 MHDA- 2024/05/09 00:48 CRDT- 2024/01/06 19:14 PHST- 2023/08/10 00:00 [received] PHST- 2023/12/22 00:00 [revised] PHST- 2024/01/03 00:00 [accepted] PHST- 2024/05/09 00:48 [medline] PHST- 2024/01/07 06:44 [pubmed] PHST- 2024/01/06 19:14 [entrez] AID - S0300-9084(24)00003-8 [pii] AID - 10.1016/j.biochi.2024.01.003 [doi] PST - ppublish SO - Biochimie. 2024 May;220:107-121. doi: 10.1016/j.biochi.2024.01.003. Epub 2024 Jan 4.