Association between the peroxisome proliferator-activated receptor gammaPro12Ala variant and haplotype and pancreatic cancer in a high-risk cohort of smokers: a pilot study.
We genotyped 7 single-nucleotide polymorphisms (SNPs) in PPARG2 (rs1801282), ADIPOQ (rs1501299), ADRB3 (rs4994), KCNQ1 (rs2237895), KCNJ11 (rs5219), TCF7L2 (rs7903146), and CDKAL1 (rs2206734), and examined their associations with pancreatic cancer risk in a multi-institute case-control study including 360 cases and 400 controls in Japan.
In previous years, with increasing studies focusing on tumor pathogenesis, it has been revealed that peroxisome proliferator‑activated receptor‑γ (PPARγ) and phosphatase and tensin homolog (PTEN) are closely associated with the occurrence and development of pancreatic cancer.
Reverse transcription-PCR and Northern blot analysis demonstrated that all four tested human pancreatic cancer cell lines, PK-1, PK-8, PK-9, and MIA Paca-2, expressed PPARgamma mRNA.
A severe combined immunodeficiency xenograft metastasis model was used to examine the in vivo effect of PPARgamma inhibition on pancreatic cancer metastasis.
Reverse transcription-PCR and Northern blot analysis demonstrated that all four tested human pancreatic cancer cell lines, PK-1, PK-8, PK-9, and MIA Paca-2, expressed PPARgamma mRNA.
Taken together, our results suggest that activation of PPARgamma may represent a novel approach for the treatment of pancreatic cancer by increasing PTEN levels and inhibiting PI3K activity.