Knocking down Cavin1 can suppress cell proliferation, lipid metabolism and accelerate cell apoptosis in pancreatic cancer.

Pancreatic cancer is a highly aggressive malignancy with serious threat to human health and survival. Cavin1, a caveolin-associated protein, has recently been identified as a differentially expressed gene linked to lipid droplet formation, suggesting its potential involvement in pancreatic cancer biology. However, the significance and underlying mechanisms of Cavin1 in the progression of pancreatic cancer remain poorly understood. In this present study, we demonstrated that Cavin1 expression was significantly elevated in pancreatic cancer, its knockdown significantly inhibited cell proliferation, and its suppression enhanced apoptotic activity in pancreatic cancer cells. In addition, inhibition of Cavin1 impaired lipid metabolism, and silencing of Cavin1 activated the adenosine 5'-monophosphate-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) signaling pathway. In conclusion, Cavin1 depletion was found to impair tumor cell growth by inhibiting proliferation and lipid metabolism while promoting apoptosis, supporting Cavin1 as a potential therapeutic target for pancreatic cancer management.