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Pioglitazone inhibits the proliferation and metastasis of human pancreatic cancer cells.

Ninomiya I, Yamazaki K, Oyama K, Hayashi H, Tajima H, Kitagawa H, Fushida S, Fujimura T, Ohta T - Oncol Lett (2014)

Bottom Line: Proliferator-activated receptor-γ (PPAR-γ) is a nuclear receptor that acts as a transcription factor in several types of tissue.Pioglitazone also reduced BxPC-3 cell lymph node and lung metastasis in the rectal xenograft model.These results suggest that pioglitazone treatment inhibited the proliferation and metastasis of pancreatic cancer cells through the induction of differentiation and the inhibition of angiogenesis-associated protein expression.

View Article: PubMed Central - PubMed

Affiliation: Gastroenterologic Surgery, Department of Oncology, Division of Cancer Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa, Japan.

ABSTRACT
Proliferator-activated receptor-γ (PPAR-γ) is a nuclear receptor that acts as a transcription factor in several types of tissue. PPAR-γ ligands are known to inhibit numerous cancer cell processes, including pancreatic cancer cell proliferation through terminal differentiation. Previous studies concerning the inhibitory effect of PPAR-γ ligands derived from thiazolidinediones (TZDs) on the metastatic potential of cancer cells have been reported. The present study aimed to investigate whether pioglitazone, a prescription TZD class drug and a ligand of PPAR-γ, inhibits the proliferation and metastasis of pancreatic cancer cells. The inhibitory effect of pioglitazone on the proliferation of the Capan-1, Aspc-1, BxPC-3, PANC-1 and MIApaCa-2 pancreatic cancer cell lines was analyzed. Alterations in carcinoembryonic antigen (CEA), interleukin-8 (IL-8) and cyclooxygenase-2 (COX-2) mRNA expression levels subsequent to pioglitazone treatment were examined in BxPC-3 cells by quantitative reverse transcription polymerase chain reaction. In addition, whether the oral administration of pioglitazone prevents tumorigenesis and spontaneous BxPC-3 cell lymph node and lung metastases was investigated using a rectal xenograft model. Pioglitazone treatment resulted in the inhibition of proliferation in all five pancreatic cancer cell lines in vitro. Pioglitazone induced CEA mRNA expression, suppressed IL-8 and COX-2 mRNA expression in vitro, and inhibited BxPC-3 xenograft growth. Pioglitazone also reduced BxPC-3 cell lymph node and lung metastasis in the rectal xenograft model. These results suggest that pioglitazone treatment inhibited the proliferation and metastasis of pancreatic cancer cells through the induction of differentiation and the inhibition of angiogenesis-associated protein expression.

No MeSH data available.


Related in: MedlinePlus

Kinetics of mRNA expression subsequent to pioglitazone treatment. The relative expression level ratio of (A) carcinoembryonic antigen (CEA), (B) interleukin-8 (IL-8) and (C) cyclooxygenase-2 (COX-2) mRNA in pioglitazone-treated BxPC-3 cells was calculated with respect to untreated cells. Statistical analysis was conducted using Student’s t-test. *P<0.05 vs. untreated cells.
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f2-ol-08-06-2709: Kinetics of mRNA expression subsequent to pioglitazone treatment. The relative expression level ratio of (A) carcinoembryonic antigen (CEA), (B) interleukin-8 (IL-8) and (C) cyclooxygenase-2 (COX-2) mRNA in pioglitazone-treated BxPC-3 cells was calculated with respect to untreated cells. Statistical analysis was conducted using Student’s t-test. *P<0.05 vs. untreated cells.

Mentions: The kinetics of mRNA expression subsequent to pioglitazone treatment in the BxPC-3 cells was analyzed by quantitative RT-PCR. Exposure for 24 h to 10 μM pioglitazone induced significant overexpression of CEA mRNA compared with that observed in the untreated cells (P<0.05; Fig. 2A). Furthermore, 10 μM pioglitazone significantly suppressed IL-8 mRNA expression after 24 h of exposure (P<0.05; Fig. 2B) and COX-2 mRNA expression after 18 h of exposure (P<0.05; Fig. 2C).


Pioglitazone inhibits the proliferation and metastasis of human pancreatic cancer cells.

Ninomiya I, Yamazaki K, Oyama K, Hayashi H, Tajima H, Kitagawa H, Fushida S, Fujimura T, Ohta T - Oncol Lett (2014)

Kinetics of mRNA expression subsequent to pioglitazone treatment. The relative expression level ratio of (A) carcinoembryonic antigen (CEA), (B) interleukin-8 (IL-8) and (C) cyclooxygenase-2 (COX-2) mRNA in pioglitazone-treated BxPC-3 cells was calculated with respect to untreated cells. Statistical analysis was conducted using Student’s t-test. *P<0.05 vs. untreated cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4214501&req=5

f2-ol-08-06-2709: Kinetics of mRNA expression subsequent to pioglitazone treatment. The relative expression level ratio of (A) carcinoembryonic antigen (CEA), (B) interleukin-8 (IL-8) and (C) cyclooxygenase-2 (COX-2) mRNA in pioglitazone-treated BxPC-3 cells was calculated with respect to untreated cells. Statistical analysis was conducted using Student’s t-test. *P<0.05 vs. untreated cells.
Mentions: The kinetics of mRNA expression subsequent to pioglitazone treatment in the BxPC-3 cells was analyzed by quantitative RT-PCR. Exposure for 24 h to 10 μM pioglitazone induced significant overexpression of CEA mRNA compared with that observed in the untreated cells (P<0.05; Fig. 2A). Furthermore, 10 μM pioglitazone significantly suppressed IL-8 mRNA expression after 24 h of exposure (P<0.05; Fig. 2B) and COX-2 mRNA expression after 18 h of exposure (P<0.05; Fig. 2C).

Bottom Line: Proliferator-activated receptor-γ (PPAR-γ) is a nuclear receptor that acts as a transcription factor in several types of tissue.Pioglitazone also reduced BxPC-3 cell lymph node and lung metastasis in the rectal xenograft model.These results suggest that pioglitazone treatment inhibited the proliferation and metastasis of pancreatic cancer cells through the induction of differentiation and the inhibition of angiogenesis-associated protein expression.

View Article: PubMed Central - PubMed

Affiliation: Gastroenterologic Surgery, Department of Oncology, Division of Cancer Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa, Japan.

ABSTRACT
Proliferator-activated receptor-γ (PPAR-γ) is a nuclear receptor that acts as a transcription factor in several types of tissue. PPAR-γ ligands are known to inhibit numerous cancer cell processes, including pancreatic cancer cell proliferation through terminal differentiation. Previous studies concerning the inhibitory effect of PPAR-γ ligands derived from thiazolidinediones (TZDs) on the metastatic potential of cancer cells have been reported. The present study aimed to investigate whether pioglitazone, a prescription TZD class drug and a ligand of PPAR-γ, inhibits the proliferation and metastasis of pancreatic cancer cells. The inhibitory effect of pioglitazone on the proliferation of the Capan-1, Aspc-1, BxPC-3, PANC-1 and MIApaCa-2 pancreatic cancer cell lines was analyzed. Alterations in carcinoembryonic antigen (CEA), interleukin-8 (IL-8) and cyclooxygenase-2 (COX-2) mRNA expression levels subsequent to pioglitazone treatment were examined in BxPC-3 cells by quantitative reverse transcription polymerase chain reaction. In addition, whether the oral administration of pioglitazone prevents tumorigenesis and spontaneous BxPC-3 cell lymph node and lung metastases was investigated using a rectal xenograft model. Pioglitazone treatment resulted in the inhibition of proliferation in all five pancreatic cancer cell lines in vitro. Pioglitazone induced CEA mRNA expression, suppressed IL-8 and COX-2 mRNA expression in vitro, and inhibited BxPC-3 xenograft growth. Pioglitazone also reduced BxPC-3 cell lymph node and lung metastasis in the rectal xenograft model. These results suggest that pioglitazone treatment inhibited the proliferation and metastasis of pancreatic cancer cells through the induction of differentiation and the inhibition of angiogenesis-associated protein expression.

No MeSH data available.


Related in: MedlinePlus