Br J Cancer: APC deficiency induces the Warburg effect of colorectal cancer cells by mediating the Wnt/β-catenin/PKM2 path.

Compared with normal cells, cancer cells showed changes in metabolism, increased aerobic sugar enzymes, and decreased oxidation phosphate.
increase in glucose intake and lactic acid production, which are not related to oxygen supply, are known as aerobic glycolysis or warburg effects and are a major feature of most cancer cells.
this reprogrammed metabolic form is necessary for cancer cells to grow, multiply and survive, and promote the development of tumors.
, however, the mechanisms by which cancer genes and tumor suppressors control tumor cell metabolism vary among different tumor types, and in most cases little is known about the molecular mechanisms associated with changes in metabolic enzyme expression.
addition, although cell metabolic reprogramming is considered to be a key event in tumor development, the regulatory mechanisms and signal-transducting mechanisms that initiate and control this reprogramming role are still unknown.
KYA1797K inhibits the expression of metabolic enzymes Wnt/β-catenin signaling path, which is the primary path path path through which important biological processes, including normal development and tumor occurrence, are regulated.
the study sheds light on the key link between the Warburg effect and the abnormally activated Wnt/β-catenin signal transductive path, particularly in colorectal cancer (CRC), where APC (adenoma-related gene associated with colon pliosarcoma) is defunct.
the expression levels of PKM2 and LDHA in CRC were positively related to the Wnt/catenin signal, the researchers evaluated the overall effect of the Wnt/β-catenin signal inhibitor KYA1797K on cell proteins in CRC through proteomic analysis.
results show that PKM2 and LDHA are identified as key molecules regulated by the Wnt/β-catenin signal.
further studies have found that APC deficiency leads to higher levels of expression of metabolic genes, including PKM2 and LDHA, as well as increased glucose consumption and lactic acid secretion.
the relationship between Wnt/β-catenin signal activation and tumor metabolism was analyzed in the Warburg effect and tumor occurrence by analyzing the effects of PKM2 on warburg effects and tumor occurrence in Apcmin/mouse models and tumor tissue in CRC patients.
the role of PKM2 in tumor metabolism in transplant tumor models.
researchers found elevated levels of expression between the glycolysis gene and the Wnt target gene in mouse models and tumor tissue.
researchers found that knocking out PKM2 inhibited the warburg effect and the growth of transplanted tumors induced by APC mutant CRC cells.
, the results reveal that the APC's missing induced β-catenin/PKM2 adjustment path activates the Warburg effect in CRC.
.