LDL cholesterol promotes the proliferation of prostate and pancreatic cancer cells by activating the STAT3 pathway.
Young Yun JungJeong-Hyeon KoJae-Young UmArunachalam ChinnathambiSulaiman Ali AlharbiGautam SethiYeong Shik KimPublished in: Journal of cellular physiology (2020)
Hypercholesterolemia has been found to be closely linked with a significant increase in both cancer incidence and mortality. However, the exact correlation between serum cholesterol levels and cancer has not been completely deciphered. Here we analyzed the effect of low-density lipoprotein (LDL) cholesterol on prostate and pancreatic cancer cells. We noted that LDL induced a substantial STAT3 activation and JAK1, JAK2, Src activation in diverse prostate and pancreatic tumor cells. Moreover, LDL promoted cancer cell proliferation, migration, and invasion as well as upregulated the expression of diverse oncogenic gene products. However, deletion of LDL-activated STAT3 in LNCaP and PANC-1 cells and reduced LDL-induced cell viability. Simvastatin (SV) treatment also alleviated LDL-induced cell viability and migration ability in both the prostate and pancreatic tumor cells. These results demonstrate that LDL-induced STAT3 activation may exert a profound effect on the proliferation and survival of tumor cells.
Keyphrases
- low density lipoprotein
- cell proliferation
- prostate cancer
- high glucose
- diabetic rats
- papillary thyroid
- signaling pathway
- benign prostatic hyperplasia
- induced apoptosis
- squamous cell
- risk factors
- transcription factor
- cell death
- type diabetes
- coronary artery disease
- endothelial cells
- cardiovascular disease
- poor prognosis
- oxidative stress
- cardiovascular events
- dna methylation
- tyrosine kinase
- intellectual disability
- young adults
- molecular dynamics
- cell cycle arrest