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2018 | 67 | 2 | 361-373
Article title

Receptory aktywowane przez proliferatory peroksysomów w procesie nowotworzenia - fakty i kontrowersje

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EN
Peroxisome proliferator-activated receptors in carcinogenesis - facts and controversies
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PL EN
Abstracts
PL
Receptory aktywowane przez proliferatory peroksysomów (PPAR) należą do rodziny receptorów jądrowych. Dotychczas scharakteryzowano ich trzy izoformy: alfa, beta i gamma, które jako ligando-zależne czynniki transkrypcyjne zaangażowane są w regulację różnych procesów fizjologicznych w organizmie. Ich podstawową funkcją jest udział w metabolizmie lipidów i glukozy. PPAR uczestniczą również w reakcji zapalnej oraz w kontroli proliferacji i różnicowania komórek, a także w regulowaniu procesów rozrodczych. Wyniki wielu badań wskazują, że receptory te zaangażowane są w proces nowotworzenia, chociaż rola poszczególnych izoform nie jest jednoznacznie zdefiniowana. Izoforma alfa uczestniczy w powstawaniu raka wątrobowokomórkowego u gryzoni, jednak w przypadku ludzkich hepatocytów długotrwała aktywacja tej izoformy nie wywołuje zmian nowotworowych. Udział PPARβ/δ w procesie kancerogenezy jest najbardziej niesprecyzowany spośród wszystkich izoform PPAR. Istnieją przypuszczenia, że pełni ona ważną rolę w powstawaniu raka jelita grubego. Z kolei, ekspresję PPARγ obserwuje się w wielu typach komórek nowotworowych, a rola tej izoformy w powstawaniu nowotworów jest najbardziej złożona. Wykazuje ona m. in. właściwości anty-proliferacyjne i proapoptotyczne, hamuje angiogenezę oraz indukuje końcowe różnicowanie komórek. W niniejszej pracy przedstawiono istniejące poglądy i kontrowersje na temat udziału trzech izoform PPAR w procesie nowotworzenia.
EN
Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear receptor family. So far, three isoforms of PPARs: alpha, beta and gamma have been described. As ligand-dependent transcription factors, they participate in the regulation of diverse physiological processes. PPARs are involved in the regulation of lipid and glucose metabolism. They also control inflammatory processes or cell proliferation and differentiation. PPARs are also implicated in the regulation of reproductive functions. Furthermore, results of several studies clearly indicate, that PPARs are involved in carcinogenesis. PPARα mediates in hepatocellular tumor growth in rodents, but its role in human hepatocytes is not so obvious as in rodents. The role of PPARβ/δ in carcinogenesis still remains unclear. It is believed, that PPARβ/δ has important function in colorectal tumor growth. In turn, the expression of PPARγ has been demonstrated in different types of tumor cells and its role in carcinogenesis seems the most complex. There are reports that indicate antiproliferative and proapoptotic effects of PPARγ activation. It has been also demonstrated that PPARγ ligands inhibit angiogenesis and induce terminal differentiation. In this review, we summarize current findings regarding the involvement of the three PPAR isoforms in carcinogenesis.
Journal
Year
Volume
67
Issue
2
Pages
361-373
Physical description
Dates
published
2018
Contributors
  • Katedra Anatomii i Fizjologii Zwierząt, Wydział Biologii i Biotechnologii, Uniwersytet Warmińsko-Mazurski w Olsztynie, Oczapowskiego 1A, 10-718 Olsztyn, Polska
  • Department of Animal Anatomy and Physiology, Faculty of Biology and Biotechnology, University of Warmia and Mazury in Olsztyn, 1A Oczapowskiego Str., 10-718 Olsztyn, Poland
  • Katedra Anatomii i Fizjologii Zwierząt, Wydział Biologii i Biotechnologii, Uniwersytet Warmińsko-Mazurski w Olsztynie, Oczapowskiego 1A, 10-718 Olsztyn, Polska
  • Department of Animal Anatomy and Physiology, Faculty of Biology and Biotechnology, University of Warmia and Mazury in Olsztyn, 1A Oczapowskiego Str., 10-718 Olsztyn, Poland
  • Katedra Anatomii i Fizjologii Zwierząt, Wydział Biologii i Biotechnologii, Uniwersytet Warmińsko-Mazurski w Olsztynie, Oczapowskiego 1A, 10-718 Olsztyn, Polska
  • Department of Animal Anatomy and Physiology, Faculty of Biology and Biotechnology, University of Warmia and Mazury in Olsztyn, 1A Oczapowskiego Str., 10-718 Olsztyn, Poland
author
  • Katedra Anatomii i Fizjologii Zwierząt, Wydział Biologii i Biotechnologii, Uniwersytet Warmińsko-Mazurski w Olsztynie, Oczapowskiego 1A, 10-718 Olsztyn, Polska
  • Department of Animal Anatomy and Physiology, Faculty of Biology and Biotechnology, University of Warmia and Mazury in Olsztyn, 1A Oczapowskiego Str., 10-718 Olsztyn, Poland
References
  • Abu Aboud O., Donohoe D., Bultman S., Fitch M., Riiff T., Hellerstein M., Weiss R. H., 2015. PPARα inhibition modulates multiple reprogrammed metabolic pathways in kidney cancer and attenuates tumor growth. Am. J. Physiol. Cell Physiol. 308, C890-C898.
  • Akinyeke T. O., Stewart L. V., 2011. Troglitazone suppresses c-Myc levels in human prostate cancer cells via a PPARγ-independent mechanizm. Cancer Biol. Ther. 11, 1046-1058.
  • Banno K., Iida M., Yanokura M., Irie H., Masuda K., Kobayashi Y., Tominaga E., Aoki D., 2015. Drug respositioning for gynecologic tumors: a new therapeutic strategy of cancer. Sci. World J., doi: 10.1155/2015/341362.
  • Benedetti E., D'Angelo M., Ammazzalorso A., Gravina G. L., Laezza C., Antonosante A., Panella G., Cinque B., Cristiano L., Dhez A.C., Astarita C., Galzio R., Cifone M. G., Ippoliti R., Amoroso R., Di Cesare E., Giordano A., Cimini A., 2016. PPARα antagonist AA452 triggers metabolic reprogramming and increases sensitivity to radiation therapy in human glioblastoma primary cells. J. Cell Physiol. 13, doi: 10.1002/jcp.25648.
  • Bieri F., Bentley P., Waechter F., Stäubli W., 1984. Use of primary cultures of adult rat hepatocytes to investigate mechanisms of action of nafenopin, a hepatocarcinogenic peroxisome proliferator. Carcinogenesis 5, 1033-1039.
  • Bogacka I., Kurzyńska A., Bogacki M., Chojnowska K., 2015. Peroxisome proliferator-activated receptors in the regulation of female reproductive functions. Folia Histochem. Cytobiol. 53, 189-200.
  • Cao L. Q., Shao Z. L., Liang H. H., Zhang D. W., Yang X. W., Jiang X. F., Xue P., 2015. Activation of peroxisome proliferator-activated receptor-γ (PPARγ) inhibits hepatoma cell growth via downregulation of SEPT2 expression. Cancer Lett. 359, 127-135.
  • Cao L. Q., Shao Z. L., Peng H. P., Xiao J. B., Xia T., 2010. Rosiglitazone enhances 5-fluorouracil-induced cell growth inhibition in hepatocellular carcinoma cell line Hep3B. Chin. J. Cancer. 29, 741-746.
  • Chan G., Boyle J. O., Yang E. K., Zhang F., Sacks P. G., Shah J. P., Edelstein D., Soslow R. A., Koki A. T., Woerner B. M., Masferrer J. L., Dannenberg A. J., 1999. Cyclooksygenase-2 expression is up-regulated in squamous cell carcinoma of the head and neck. Cancer Res. 59, 991-994.
  • Chintalgattu V., Harris G. S., Akula S. M., Katwa L. C., 2007. PPAR-gamma agonists induce the expression of VEGF and its receptors in cultured cardiac myofibroblasts. Cardiovasc. Res. 74, 140-150.
  • Chittiboyina A. G., Venkatraman M. S., Mizuno C. S., Desai P. V., Patny A., Benson S. C., Ho C. I., Kurtz T. W., Pershadsingh H. A., Avery M. A., 2006. Design and synthesis of the first generation of dithiolane thiazolidinedione- and phenylacetic acid-based PPAR gamma agonists. J. Med. Chem. 49, 4072-4084.
  • Colin-Cassin C., Yao X., Cerella C., Chbicheb S., Kuntz S., Mazerbourg S., Boisburn M., Chapleur Y., Diederich M., Flament S., Grillier-Vuissoz I., 2015. PPARγ-inactive Δ2-troglitazone independently triggers ER stress and apoptosis in breast cancer cells. Mol. Carcinog. 54, 393-404.
  • Day C., 1999. Thiazolidinediones: a new class of antidiabetic drugs. Diabet. Med. 16, 179-192.
  • Demetri G. D., Fletcher C. D. M., Mueller E., Sarraf P., Naujoks R., Campbell N., Spiegelman B. M., Singer S., 1999. Induction of solid tumor differentation by the peroxisome proliferator-activated receptor-γ ligand troglitazone in patients with liposarcoma. Proc. Natl. Acad. Sci. USA. 96, 3951-3956.
  • Donald S. P., Sun X. Y., Hu C. A., Yu J., Mei J. M., Valle D., Phang J. M., 2001. Proline oxidase, encoded by p53-induced gene-6, catalyzes the generation of proline-dependent reactive oxygen species. Cancer Res. 1, 1810-1815.
  • Dong Y. W., Wang X. P., Wu K., 2009. Suppression of pancreatic carcinoma growth by activating peroxisome proliferator-activated receptor gamma involves angiogenesis inhibition. World J. Gastroenterol. 15, 441-448.
  • Fajas L., Auboeuf D., Raspé E., Schoonjans K., Lefebvre A. M., Saladin R., Najib J., Laville M., Fruchart J. C., Deeb S., Vidal-Puig A., Flier J., Briggs M. R., Staels B., Vidal H. i współaut., 1997. The organization, promoter analysis, and expression of the human PPARγ gene. J. Biol. Chem. 272, 18779-18789.
  • Forman B. M., Chen J., Evans R. M., 1997. Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors alpha and delta. Proc. Natl. Acad. Sci. USA. 94, 4312-4317.
  • Freeman S. R., Drake A. L., Heilig L. F., Graber M., McNealy K., Schilling L. M., Dellavalle R. P., 2006. Statins, fibrates, and melanoma risk: a systematic review and meta-analysis. J. Natl. Cancer Inst. 98, 1538-1546.
  • Fröhlich E., Wahl R., 2015. Chemotherapy and chemoprevention by thiazolidinediones. Biomed. Res. Int., 10.1155/2015/845340.
  • Gardette V., Bongard V., Dallongeville J., Arveiler D., Bingham A., Ruidavets J. B., Amouyel P., Haas B., Ducimetiére P., Ferriéres J., 2009.Ten-year all-cause mortality in preusmably health subjects on lipid-lowering drugs (from the Prospective Epidemiological Study of Myocardial Infarction [PRIME] prospective cohort). Am. J. Cardiol. 103, 381-386.
  • Giometti C. S., Liang X., Tollaksen S. L., Wall D. B., Lubman D. M., Subbarao V., Rao M. S., 2000. Mouse liver selenium-binding protein decreased in abundance by peroxisome proliferators. Electrophoresis. 21, 2162-2169.
  • Grommes C., Landreth G. E., Sastre M., Beck M., Feinstein D. L., Jacobs A. H., Schlegel U., Heneka M. T., 2006. Inhibition of in vivo glioma growth and invasion by peroxisome proliferator-activated receptor gamma agonist treatment. Mol. Pharmacol. 70, 1524-1533.
  • Guan Y. F., Zhang Y. H., Breyer R. M., Davis L., Breyer M. D., 1999. Expression of peroxisome proliferator-activated receptor γ (PPARγ) in human transitional bladder cancer and its role in inducing cell death. Neoplasia 1, 330-339.
  • Gupta R. A., DuBois R. N., 2001. Colorectal cancer prevention and treatment by inhibition of cyclooxygenase-2. Nat. Rev. Cancer. 1, 11-21.
  • Gupta R. A., Tan J., Krause W. F., Geraci W. W., Willson T. M., Dey S. K., DuBois R. N., 2000. Prostacyclin-mediated activation of peroxisome proliferator-activated receptor delta in colorectal cancer. Proc. Natl. Acad. Sci. USA. 97, 13275-13280.
  • Han S., Roman J., 2006. Rosiglitazone suppresses human lung carcinoma cell growth through PPAR gamma-dependent and PPAR gamma-independent signal pathways. Mol. Cancer. Ther. 5, 430-437.
  • Hasegawa K., Ohashi Y., Ishikawa K., Yasue A., Kato R., Achiwa Y., Nishio E., Udagawa Y., 2005. Expression of cyclooxygenase-2 in uterine endometrial cancer and anti-tumor effects of a selective COX-2 inhibitor. Int. J. Oncol. 26, 1419-1428.
  • Hashimoto K., Ethridge R. T., Evers B. M., 2002. Peroxisome proliferator-activated receptor gamma ligand inhibits cell growth and invasion of human pancreatic cancer cells. Int. J. Gastrointest. Cancer. 32, 7-22.
  • Hays T., Rusyn I., Burns A. M., Kennett M. J., Ward J. M., Gonzalez F. J., Peters J. M., 2005. Role of peroxisome proliferator-activated receptor-alpha (PPAR aplha) in bezafibrate-induced hepatocarcinogenesis and cholestasis. Carcinogenesis. 26, 219-227.
  • He Q., Pang R., Song X., Chen J., Chen H., Chen B., Hu P., Chen M., 2008. Rosiglitazone suppresses the growth and invasiveness od SGC-7901 gastric cancer cells and angiogenesis in vitro via PPAR gamma dependent and independent mechanisms. PPAR Res., 10.1155/2008/649808.
  • He T. C., Chan T. A., Vogelstein B., Kinzler K. W., 1999. PPARδ is an APC-regulated target of nonsteroidal anti-inflammatory drugs. Cell 99, 335-345.
  • Hida T., Yatabe Y., Achiwa H., Muramatsu H., Kozaki K., Nakamura S., Ogawa M., Mitsudomi T., Sugiura T., Takahashi T., 1998. Increased expression of cyclooxygenase 2 occurs frequently in human lung cancers, specifically in adenocarcinomas. Cancer Res. 58, 3761-3764.
  • Hojka A., Rapak A., 2011. Receptory aktywowane proliferatorami peroksysomów (PPAR). Właściwości anty-proliferacyjne. Post. Hig. Med. Dosw. 65, 404-413.
  • Isseman I., Green S., 1990. Activation of a member of the steroid hormone receptor superfamily by peroxisome proliferators. Nature 347, 645-650.
  • Kasai H., Okada Y., Nishimura S., Rao M. S., Reddy J. K., 1989. Formation of 8-hydroksydeoxyguanosine in liver DNA of rats following long-term exposure to a peroxisome proliferator. Cancer Res.49, 2603-2605.
  • Kim J., Song J., Park K. W., 2015. The multifaceted factor peroxisome proliferator-activated receptor γ (PPARγ) in metabolism, immunity and cancer. Arch. Pharm. Res. 38, 302-312.
  • Kim K. Y., Ahn J. H., Cheon H. G., 2007. Apoptotic action of peroxisome proliferator-activated receptor-gamma activation in human non-small-cell lung cancer is mediated via proline oxidase-induced reactive oxygen species formation. Mol. Pharmacol. 72, 674-685.
  • Krey G., Braissant O., L'Horset F., Kalkhoven E., Perroud M., Parker M.G., Wahli W. 1997. Fatty acids, eicosanoids, and hypolipidemic agents indetified as ligands of peroxisome proliferator-activated receptors by coactivator-dependent receptor ligand assay. Mol. Endocrinol. 11, 779-791.
  • Lee N. J., Oh J. H., Ban J. O., Shim J. H., Lee H. P., Jung J. K., Ahn B. W., Yoon D. Y., Han S. B., Ham Y. W., Hong J. T., 2013. 4-O-methylhonokiol, a PPARγ agonist, inhibits prostate tumor growth: p21-mediated suppression of NF-κB activity. Br. J. Pharmacol. 168, 1133-1145.
  • Misra P., Reddy J. K., 2014. Peroxisome proliferator-activated receptor-α activation and excess energy burning in hepatocarcinogenesis. Biochimie. 98, 63-74.
  • Motomura W., Okumura T., Takahashi N., Obara T., Kohgo Y., 2000. Activation of peroxisome proliferator-activated receptor γ by troglitazone inhibits cell growth through the increase of p27Kip1 in human pancreatic carcinoma cells. Cancer Res. 60, 5558-5564.
  • Mrówka M., Głodkowska-Mrówka E., 2011. Struktura, działanie i rola receptora-gamma peroksysomów aktywowanego przez proliferatory - PPARγ. Post. Biol. Kom. 38, 629-652.
  • Müller R. 2016. PPARβ/δ in human cancer. Biochimie. 2, pii: S0300-9084(16)30193-6.
  • Nickkho-Amiry M., McVey R., Holland C., 2012. Peroxisome proliferator-activated receptors modulate proliferation and angiogenesis in human endometrial carcinoma. Mol. Cancer. Res.10, 441-453.
  • Ogino S., Shima K., Baba Y., Nosho K., Irahara N., Kure S., Chen L., Toyoda S., Kirkner G. J., Wang Y. L., Giovannucci E. L., Fuchs C. S., 2009. Colorectal cancer expression of peroxisome proliferator-activated receptor gamma (PPARG, PPAR gamma) is associated with good prognosis. Gastroenterology 136, 1242-1250.
  • Ohta K., Endo T., Haraguchi K., Hershman J. M., Onaya T., 2001. Ligands for peroxisome proliferator-activated receptor gamma inhibit growth and induce apoptosis of human papillary thyroid carcinoma cells. J. Clin. Endocrinol. Metab. 86, 2170-2177.
  • Oliver W. R., Shenk J. L., Snaith M. R., Russell C. S., Plunket K. D., Bodkin N. L., Lewis M. C., Winegar D. A., Sznaidman M. L., Lambert M. H., Xu H. E., Sternbach D. D., Kliewer S. A., Hansen B. C., Wilson T. M., 2001. A selective peroxisome proliferator-activated receptor delta agonist promotes reverse cholesterol transport. Proc. Natl. Acad. Sci. USA. 98, 5306-5311.
  • Palmer C. N., Hsu M. H., Griffin K. J., Raucy J. L., Johnson E. F., 1998. Peroxisome proliferator-activated receptor-α expression in human liver. Mol. Pharmacol. 53, 14-22.
  • Pandhare J., Cooper S. K., Phang J. M., 2006. Proline oxidase, a proapoptotic gene, is induced by troglitazone: evidence for both peroxisome proliferator-activated receptor gamma-dependent and -independent mechanisms. J. Biol. Chem. 281, 2044-52.
  • Peters J. M., Cattley R. C., Gonzalez F. J., 1997. Role of PPAR Ralpha in the mechanism of action of the nongenotoxic carcinogen and peroxisome proliferator Wy-14,643. Carcinogenesis 18, 2029-2033.
  • Peters J. M., Shah Y. M., Gonzalez F. J., 2012. The role of peroxisome proliferator-activated receptors in carcinogenesis and chemoprevention. Nat. Rev. Cancer. 12, 181-195.
  • Peters J. M., Gonzales F. J., Müller R., 2015. Establishing the role of PPARβ/δ in carcinogenesis. Trends Endocrinol. Metabol. 26, 595-607.
  • Polyak K., Xia Y., Zweier J. L., Kinzler K. W., Vogelstein B., 1997. A model for p53-induced apoptosis. Nature 389, 300-305.
  • Raman P., Koenig R. J., 2014. PAX8-PPARγ fusion protein in thyroid carcinoma. Nat. Rev. Endocrinol. 10, 616-623.
  • Saidi S. A., Holland C. M., Charnock-Jones D. S., Smith S. K., 2006. In vitro and in vivo effects of the PPARα agonists fenofibrate and retinoic acid in endometrial cancer. Mol. Cancer. 5, 13.
  • Salvo F., Bazin F., Robinson P., Moore N. D., 2014. Fibrates and risk of cancer in tissues with high PPAR-α concentration: A nested case-control study. Drug Saf. 37, 361-368.
  • Schoojans K., Watanabe M., Suzuki H., Mahfoudi A., Krey G., Wahli W., Grimaldi P., Staeis B., Yamamoto T., Auwerx J., 1995. Induction of the acyl-coenzyme A synthetase gene by fibrates and fatty acids in mediated by a peroxisome proliferator response element in the C promoter. J. Biol. Chem. 270, 19269-19276.
  • Schwab M., Reynders V., Loitsch S., Shastri Y. M., Steinhilber D., Schröder O., Stein J., 2008. PPARgamma is involved in mesalazine-mediated induction of apoptosis and inhibition of cell growth in colon cancer cells. Carcinogenesis 29, 1407-1414.
  • Shah Y. M., Morimura K., Yang Q., Tanabe T., Takagi M., Gonzalez F. J., 2007. Peroxisome proliferator-activated receptor alpha regulates a microRNA-mediated signaling cascade responsible for hepatocellular proliferation. Mol. Cell. Biol. 27, 4238-4247.
  • Shapaz A., Önal B., Yesilyurt A., Han Ü., Delibasi T., 2015. BRAF(V600E) mutation, RET/PTC1 and PAX8-PPAR gamma rearrangements in follicular epithelium derived thyroid lesions - institutional experience and literature review. Balkan Med. J. 32, 156-166.
  • Shureiqi I., Jiang W., Zuo X., Wu Y., Stimmel J. B., Leesnitzer L. M., Morris J. S., Fan H., Fischer S. M., Lippman S. M., 2003. The 15-lipooxygenase-1 product 13-S-hydroxyoctadecadienoic acid down-regulates PPAR-δ to induce apoptosis in colorectal cancer cells. Proc. Natl. Acad. Sci. USA. 100, 9968-9973.
  • Soslow R. A., Dannenberg A. J., Rush D., Woerner B. M., Khan K. N., Masferrer J., Koki A. T., 2000.COX-2 is expressed in human pulmonary, colonic, and mammary tumors. Cancer 89, 2637-2645.
  • Strakova N., Ehrmann J., Bartos J., Malikova J., Dolezel J., Kolar Z., 2005. Peroxisome proliferator-activated receptors (PPAR) agonists affect cell viability, apoptosis and expression of cell cycle related proteins in cell lines of glial brain tumors. Neoplasma 52, 126-136.
  • Sunami E., Tsuno N. H., Kitayama J., Saito S., Osada T., Yamaguchi H., Tomozawa S., Tsuruo T., Shibata Y., Nagawa H., 2002. Decreased synthesis of matrix metalloproteinase-7 and adhesion to the extracellular matrix proteins of human colon cancer cells treated with troglitazone. Surg. Today. 32, 343-350.
  • Tachibana K., Yamasaki D., Ishimoto K., Doi T., 2008. The role of PPARs in cancer. PPAR Res., doi:10.1155/2008/102.
  • Tontoz P., Spiegelman B. M., 2008. Fat and Beyond: The diverse biology of PPARγ. Ann. Rev. Biochem. 77, 289-312.
  • Tucker O. N., Dannenberg A. J., Yang E. K., Zhang F., Teng L., Daly J. M., Soslow R. A., Masferrer J. L., Woerner B. M., Koki A. T., Fahey T. J., 1999. Cyclooxygenase-2 expression is up -regulated in human pancreatic cancer. Cancer Res. 59, 987-990.
  • Vu-Phan D., Grachtchouk V., Yu J., Colby L. A., Wicha M. S., Koenig R. J., 2013. The thyroid cancer PAX8-PPARG fusion protein activates Wnt/TCF-responsive cells that have a transformer phenotype. Endocr. Relat. Cancer 20, 725-739.
  • Wan Z., Shi W., Shao B., Shi J., Shen A., Ma Y., Chen J., Lan Q., 2011. Peroxisome proliferator-activated receptor γ agonist pioglitazone inhibits β-catenin-mediated glioma cell growth and invasion. Mol. Cell. Biochem. 349, 1-10.
  • Wang G., Cao R., Wang Y., Qian G., Dan H.C., Jiang W., Ju L., Wu M., Xiao Y., Wang X., 2016. Simvastatin induces cell cycle arrest and inhibits proliferation of bladder cancer cells via PPARγ signalling pathway. Sci Rep. 25, 35783.
  • Willson T. M., Brown P. J., Strenbach D. D., Henke B. R., 2000. The PPARs: from orphan receptors to drug discovery. J. Med. Chem. 43, 527-550.
  • Winczyk K., 2008. Znaczenie receptorów gamma aktywowanych proliferatorami peroksysomów (PPARγ) w nowotworach gruczołów dokrewnych. Endokrynol. Pol. 59, 156-166.
  • Wood W. M., Sharma V., Bauerle K. T., Pike L. A., Zhou Q., Fretwell D. L., Schweppe R. E., Haugen B. P., 2011. PPARγ promotes growth and invasion of thyroid cancer cells. PPAR Res., doi:10.1155/2011/171765.
  • Wu T. T., Niu H. S., Chen L. J., Cheng J. T., Tong Y. C., 2016. Increase of human prostate cancer cell (DU145) apoptosis by telmisartan through PPAR-delta pathway. Eur. J. Pharmacol. 775, 35-42.
  • Yang L., Zhang H., Zhou Z. G., Yan H., Adell G., Sun X. F., 2011. Biological function and prognostic significance of peroxisome proliferator-activated receptor δ in rectal cancer. Clin. Cancer Res. 17, 3760-3770.
  • Yang Q., Nagano T., Shah Y., Cheung C., Ito S., Gonzalez F. J., 2008. The PPARα-humanized mouse: a model to investigate species differences in liver toxicity Mediatel by PPARα. Toxicol. Sci. 101, 132-139.
  • Yang W. L., Frucht H., 2001. Activation of the PPAR pathway induces apoptosis and COX-2 inhibition in HT-29 human colon cancer cells. Carcinogenesis 22, 1379-1383.
  • Yokoyama Y., Xin B., Shigeto T., Mizunuma H., 2011. Combination of ciglitazone, a peroxisome proliferator-activated receptor gamma ligand, and cisplatin enhances the inhibition of growth of human ovarian cancers. J. Cancer Res. Clin. Oncol. 137, 1219-1228.
  • Yokoyama Y., Xin B., Shigeto T., Umemoto M., Kasai-Sakamoto A., Futagami M., Tsuchida S., Al-Mulla F., Mizunuma H., 2007.Clofibric acid, a peroxisome proliferator-activated receptor alpha ligand, inhibits growth of human ovarian cancer. Mol. Cancer Ther. 6, 1379-1386.
  • Yoshinaga M., Kitamura Y., Chaen T., Yamashita S., Tsuruta S., Hisano T., Ikeda Y., Sakai H., Nakamura K., Takayanagi R., Muto Y., 2009. The simultaneous expression of peroxisome proliferator-activated receptor delta and cyklooxygenase-2 may enhance angiogenesis and tumor venous invasion in tissues of colorectal cancers. Dig. Dis. Sci. 54, 1108-1114.
  • Yousefi B., Samadi N., Baradaran B., Shafiei-Irannejad V., Zarghami N., 2016. Peroxisome proliferator-activated receptor ligands and their role in chronic myeloid leucemia: therapeutic strategies. Chem. Biol. Drug Des. 88,17-25.
  • Yu H. N., Lee Y. R., Noh E. M., Lee K. S., Kim J. S., Song E. K., Han M. K., Lee Y. C., Kwon K. B., Lee S. J., Youn H. J., Jung S. H., 2008. Induction of G1 phase arrest and apoptosis in MDA-MB-231 breast cancer cells by troglitazone, a synthetic peroxisome proliferator-activated receptor gamma (PPAR gamma) ligand. Cell Biol. Int. 32, 906-912.
  • Zaveri N. T., Sato B. G., Jiang F., Calaoagan J., Laderoute K. R., Murphy B. J., 2009. A novel peroxisome proliferator-activated receptor delta antagonist, SR13904, Has anti-proliferative activity in human cancer cells. Cancer Biol. Ther. 8, 1252-1261.
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