Mechanism Of Caveolin-1-mediated Metabolic Reprogramming In Breast Cancer

Breast cancer is the most common type of tumor among Chinese women which shows high proliferative and metastatic ability.All the malignant behaviors that breast cancer shows require a supply of energy.The type of cancer cell metabolism is different from the type of ordinary cells,and its metabolic imbalance is mainly manifested as enhancing glycolysis level,promoting glucose transport,increasing oxidative stress response,and inhibiting the tricarboxylic acid cycle.These metabolic alterations cause cancer cells to produce large amounts of ATP through glycolysis and provide energy for other biological processes in the body.Since Otto Warburg discovered that cancer cells exhibit extremely high levels of glycolysis,this has prompted laboratories around the world to search for glycolysis inhibitors as potential anti-cancer drugs,and studies have shown that expression levels of Caveolin-1(CAV-1)are associated with metabolic disorders in breast cancer.Evidence from various studies suggests that CAV-1 affects glucose metabolism by regulating multiple glucose uptake transporters.Therefore,the role of CAV-1 in breast cancer metabolism has attracted much attention and may become a new target for breast cancer treatment.Future research needs to delve deeper into the mechanisms of CAV-1 metabolism in breast cancer and how this understanding can be used to develop more effective treatment strategies.Based on this,this paper first conducted extensive search and collation of related studies,and then used LC-MS,QPCR,WB,IF,ELISA and other experimental techniques to explore the effect of CAV-1 on the energy metabolism of breast cancer cells(MDA-MB-231),and explored the potential regulatory mechanism,and finally verified the role of CAV-1 in regulating tumor glycolysis in mice,with the intention of understanding the specific role of CAV-1 in breast cancer energy metabolism.The experimental results showed that silencing CAV-1 can significantly promote the uptake of glucose and lactic acid production by breast cancer cells,in addition,we also found that silencing CAV-1 can significantly inhibit the level of oxidative phosphorylation.The relevant mechanism was explored and it was found that CAV-1 in breast cancer could regulate the distribution and activity of ALDA through the arrangement of the skeleton,thereby affecting the glycolysis level.The effects of in vivo CAV-1 on glycolysis and oxidative phosphorylation of mouse tumors were also consistent with the conclusions at the cellular level.Starting from CAV-1,this paper studies its relationship with breast cancer metabolic reprogramming and its underlying mechanism,and better understands the changes in breast cancer metabolism,which can help identify enzymes or carry out combination interventions,which can provide guidance for more effective anti-cancer drug development.