Abstract
Although chemotherapy can improve the overall survival and prognosis of cancer patients, chemoresistance remains an obstacle due to the diversity, heterogeneity, and adaptability to environmental alters in clinic. To determine more possibilities for cancer therapy, recent studies have begun to explore changes in the metabolism, especially glycolysis. The Warburg effect is a hallmark of cancer that refers to the preference of cancer cells to metabolize glucose anaerobically rather than aerobically, even under normoxia, which contributes to chemoresistance. However, the association between glycolysis and chemoresistance and molecular mechanisms of glycolysis-induced chemoresistance remains unclear. This review describes the mechanism of glycolysis-induced chemoresistance from the aspects of glycolysis process, signaling pathways, tumor microenvironment, and their interactions. The understanding of how glycolysis induces chemoresistance may provide new molecular targets and concepts for cancer therapy.
Highlights
As a disease with a low cure rate, cancer is accompanied by abnormalities in proliferation, metastasis, and invasion and by metabolic disorders [1, 2]
Chemoresistance is caused by multifactor interaction, and its mechanism can be summarized as mutation in drug targets and metabolism, apoptosis inhibition, activation of intracellular survival signaling pathways, enhanced deoxyribonucleic acid (DNA) repair, immune escape of cancer stem cells (CSCs), epigenetic alteration, and aberrant metabolism [16,17,18]
LDHA is significantly related to octamer-binding transcription factor 4, which plays a key role in the self-renewal of embryonic stem cells in gastric cancer [132]
Summary
Department of Breast Surgery, The First Hospital of Jilin University, Changchun, China Reviewed by: Khalid Omer Alfarouk, Alfarouk Biomedical Research LLC, United States Ramandeep Rattan, Henry Ford Health System, United States Specialty section: This article was submitted to Cancer Metabolism, a section of the journal
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