Peroxisome proliferator-activated receptor gamma (PPARγ) is a
nuclear receptor that plays a major regulatory role in metabolic function. It is overexpressed in many types of
cancer cells, suggesting that regulation of PPARγ may also affect
carcinogenesis. Our previous study suggested that
PTB-associated splicing factor (PSF) is a PPARγ-interacting
protein and growth regulator of
colon cancer cells. In addition, PSF has been shown to be involved in several important regulatory steps of
cancer cell proliferation. In this study, we aimed to investigate the relationships between PSF and PPARγ in
pancreatic cancer by evaluating the effects of PSF expression in
pancreatic cancer cell lines. PSF expression affected the expression of PPARγ, and knockdown of PSF using specific
small-interfering RNA (
siRNA) significantly suppressed the proliferation of
pancreatic cancer cells. Furthermore, PSF knockdown induced cell growth inhibition and autophagosome formation through inhibition of PPARγ. Interestingly, Panc-1 cells were more susceptible to PSF knockdown-induced autophagy than MIA-PaCa-2 cells. Thus, our data indicated that PSF was an important regulator of autophagy and played critical roles in the survival and growth of
pancreatic cancer cells. The PSF-PPARγ axis may play a role in the control of
pancreatic cancer pathogenesis. This study is the first to describe the effects of PSF on
pancreatic cancer cell growth and autophagy associated with PPARγ.