The cancerous cells interact with their microenvironment through various chemical and physical signals that contribute to cancer cell growth and death. Similar to normal cells, the growth of cancer cells is closely related to their microenvironment or local surroundings, including stroma and the extracellular matrix in which the cancer cells exist. Cancer cells ignore healthy cellular growth and death signals, and thus these cells can proliferate in an uninhibited and unlimited manner. Other terms used for cancer include malignant tumour and neoplasm. To sum up, tumour cells switch their metabolic state between glycolysis and oxidative phosphorylation through metabolic interplay with CAFs, which exhibit the Warburg effect under hypoxia and reverse Warburg effect under normoxia.Īccording to the World Health Organization (WHO), cancer is the uncontrolled growth of cells which can invade healthy tissue and spread to distant sites in the body ( 1). The LDHs catalyse the interchange of lactate and pyruvate, whereas MCTs facilitate the influx and efflux of monocarboxylates, especially lactate and pyruvate. In this mini review, we discuss the role of lactate dehydrogenases (LDHs) and monocarboxylate transporters (MCTs) on the metabolic interplay between tumour cells and CAFs under hypoxia compared to normoxia. Tumour cells adapt to rapid environmental changes from normoxia to hypoxia through metabolic interplay with CAFs. CAFs, the most abundant cells in tumour stroma, secrete growth factors that play pivotal roles in tumour cell proliferation, metabolism, angiogenesis and metastasis. The growth of tumour cells is closely related to cancer-associated fibroblasts (CAFs) present within their microenvironment.
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