Potential anti-cervical carcinoma drugs with agonist and antagonist AhR/PXR activities
Main Article Content
Abstract
Cervical cancer (CC) is responsible of higher morbidity and mortality in the world. To understand the pharmacologic drugs’ efficacy in CC therapy, we investigated the ability of some widely used or potential anti-cancer drugs (alpha- and beta-naphthoflavone, clotrimazole, dimethoxybenzoquinone, paclitaxel, rifampicin, and RU-486) to agonize or antagonize with nuclear receptors: aryl hydrocarbon receptors (AhR) and pregnane X receptors (PXR). To achieve this goal, we performed our study on positive transfected HeLa cell lines, a representative cell line model for CC. In this paper, a study of the recent patents for the importance of these drugs as AhR or PXR agonists or antagonists was evaluated. Because little is known about the implication of AhR and PXR in cancer therapy, our results could be helpful for the design of future CC therapeutics. Future studies could lead to a better understanding of AhR and PXR transactivation/inhibition implication in CC; and lead to a better knowledge of CC therapy.
Article Details
How to Cite
MNIF, wissem; ZIDI, Ines; BALAGUER, Patrick.
Potential anti-cervical carcinoma drugs with agonist and antagonist AhR/PXR activities.
Medical Research Archives, [S.l.], v. 4, n. 8, dec. 2016.
ISSN 2375-1924.
Available at: <https://esmed.org/MRA/mra/article/view/899>. Date accessed: 24 nov. 2024.
Keywords
Cervical cancer; therapy; AhR; PXR; anti-cancer drugs.
Section
Research Articles
The Medical Research Archives grants authors the right to publish and reproduce the unrevised contribution in whole or in part at any time and in any form for any scholarly non-commercial purpose with the condition that all publications of the contribution include a full citation to the journal as published by the Medical Research Archives.
References
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[19] Huang H, Wang H, Sinz M, Zoeckler M, Staudinger J, Redinbo MR, Teotico DG, Locker J, Kalpana GV, Mani S. Inhibition of drug metabolism by blocking the activation of nuclear receptors by ketoconazole. Oncogene 2007; 26: 258-68.
[20] Venkatesh M, Wang H, Cayer J, Leroux M, Salvail D, Das B, Wrobel JE. Mani S: In vivo and in vitro characterization of a first-in-class novel azole analog that targets pregnane X receptor activation. Mol Pharmacol 2011; 80: 124-35.
[21] Hosaka M, Watari H, Kato T, Odagiri T, Konno Y, Endo D, Mitamura T, Kikawa S, Suzuki Y, Sakuragi N. Clinical efficacy of paclitaxel/cisplatin as an adjuvant chemotherapy for patients with cervical cancer who underwent radical hysterectomy and systematic lymphadenectomy. J Surg Oncol 2012; 105(6): 612-6.
[22] Qiao WJ, Cheng HY, Li CQ, Jin H, Yang SS, Li X, Zhang YY. Identification of pathways involved in paclitaxel activity in cervical cancer. Asian Pac J Cancer Prev 2011; 12: 99-102.
[23] Huang TC, Campbell TC. Comparison of weekly versus every 3 weeks paclitaxel in the treatment of advanced solid tumors: A meta-analysis. Cancer Treat Rev, 2011.
[24] Mense SM, Singh B, Remotti F, Liu X, Bhat HK. Vitamin C and alpha-naphthoflavone prevent estrogen-induced mammary tumors and decrease oxidative stress in female ACI rats. Carcinogenesis 2009; 30: 1202-8.
[25] Meira DD, Marinho-Carvalho MM, Teixeira CA, Veiga VF, Da Poian AT, Holandino C, de Freitas MS, Sola-Penna M. Clotrimazole decreases human breast cancer cells viability through alterations in cytoskeleton-associated glycolytic enzymes. Mol Genet Metab 2005; 84: 354-362.
[26] Rodriguez-Enriquez S, Marin-Hernandez A, Gallardo-Perez JC, Carreno-Fuentes L, Moreno-Sanchez R. Targeting of cancer energy metabolism. Mol Nutr Food Res 2009; 53: 29-48.
[27]27 Liu H, Li Y, Raisch KP. Clotrimazole induces a late G1 cell cycle arrest and sensitizes glioblastoma cells to radiation in vitro. Anticancer Drugs 2010; 21: 841-9.
[28] Ahmad M. Study on cytochrome P-450 dependent retinoic acid metabolism and its Inhibitors as potential agents for cancer therapy. Sci Pharm 2011; 79: 921-35.
[29] Ramondetta LM, Johnson AJ, Sun CC, Atkinson N, Smith JA, Jung MS, Broaddus R, Iyer RB, Burke T. Phase 2 trial of mifepristone (RU-486) in advanced or recurrent endometrioid adenocarcinoma or low-grade endometrial stromal sarcoma. Cancer 2009; 115: 1867-74.
[30] Ørbo A, Moe BT, Grønaas H, Paulssen RH. Early effects of high concentrations of progesterone and mifepristone A gene expression study of endometrial cancer cells (Ishikawa). J Steroid Biochem Mol Biol 2009; 113: 139-49.
[31] Fjelldal R, Moe BT, Ørbo A, Sager G. MCF-7 cell apoptosis and cell cycle arrest: non-genomic effects of progesterone and mifepristone (RU-486). Anticancer Res 2010; 30: 4835-40.
[32] Benad P, Rauner M, Rachner TD, Hofbauer LC. The anti-progestin RU-486 inhibits viability of MCF-7 breast cancer cells by suppressing WNT1. Cancer Lett 2011; 312: 101-8.
[33] Chen J, Raymond K. Roles of rifampicin in drug-drug interactions: underlying molecular mechanisms involving the nuclear pregnane X receptor. Ann Clin Microbiol Antimicrob 2006; 5: 3.
[2] Jhingran A, Levenback C. Malignant diseases of the cervix. Microinvasive and invasive carcinoma: diagnosis and management, In Katz: Comprehensive Gynecology (Katz, V. L., Lentz, G. M., and Lobo, R. A., Eds.). Mosby: Elsevier 2007; 759-780.
[3] Jhingran A, Russell A, Seiden M, Duska L, Goodman A, Lee S, Digumarthy S, Fuller A. Cancers of the cervix, vulva, and vagina, In Abeloff: Abeloff's Clinical Oncology (Abeloff, M. D., Armitage, J. O., Niederhuber, J. E., Kastan, M. B., and McKenna, W. G., Eds.) 4 ed., Churchill Livingstone: Elsevier 2008; 1745-1791.
[4] Balaguer P, Boussioux AM, Demirpence E, Nicolas JC. Reporter cell lines are useful tools for monitoring biological activity of nuclear receptor ligands. Luminescence 2001; 16: 153-8.
[5] Pillon A, Boussioux AM, Escande A, Ait-Aissa S, Gomez E, Fenet H, Ruff M, Moras D, Vignon F, Duchesne MJ, Casellas C, Nicolas JC, Balaguer P. Binding of estrogenic compounds to recombinant estrogen receptor-alpha: application to environmental analysis. Environ Health Perspect 2005; 113: 278-84.
[6] Lemaire G, Mnif W, Pascussi JM, Pillon A, Rabenoelina F, Fenet H, Gomez E, Casellas C, Nicolas JC, Cavailles V, Duchesne MJ, Balaguer P. Identification of new human pregnane X receptor ligands among pesticides using a stable reporter cell system. Toxicol Sci 2006; 91: 501-9.
[7] Ma C, Marlowe JL, Puga A. The aryl hydrocarbon receptor at the crossroads of multiple signaling pathways, In Molecular, Clinical and Environmental Toxicology (Luch, A., Ed.), Birkhäuser Verlag. Switzerland: 2009; 231-257.
[8] Romagnolo DF, Degner SC, Selmin O. Aryl hydrocarbon receptor-mediated carcinogenesis and modulation by dietary xenobiotic and natural ligands, In Bioactive Compounds and Cancer (Milner, J. A., and Romagnolo, D. F., Eds.), Humana Press: 2010; 761-782.
[9] Goergens A, Frericks M, Esser C. The arylhydrocarbon receptor is only marginally involved in the antileukemic effects of its ligand curcumin. Anticancer Res 2009; 29: 4657-64.
[10] Masuyama H, Suwaki N, Tateishi Y, Nakatsukasa H, Segawa T, Hiramatsu Y. The pregnane X receptor regulates gene expression in a ligand- and promoter-selective fashion. Mol Endocrinol 2005; 19: 1170-80.
[11] Masuyama H, Nakatsukasa H, Takamoto N, Hiramatsu Y. Down-regulation of pregnane X receptor contributes to cell growth inhibition and apoptosis by anticancer agents in endometrial cancer cells. Mol Pharmacol 2007; 72: 1045-53.
[12] Biswas A, Mani S, Redinbo MR, Krasowski MD, Li H, Ekins S. Elucidating the `Jekyll and Hyde' nature of PXR: The case for discovering antagonists or allosteric antagonists. Pharm Res 2009; 26: 1807-15.
[13] Jiang H, Chen K, He J, Pan F, Li J, Chen J, Chen W, Liang H. Association of pregnane X receptor with multidrug resistance-related protein 3 and its role in human colon cancer chemoresistance. J Gastrointest Surg 2009; 13: 1831-8.
[14] Zhang B, Cheng Q, Ou Z, Lee JH, Xu M, Kochhar U, Ren S, Huang M, Pflug BR, Xie W. Pregnane X receptor as a therapeutic target to inhibit androgen activity. Endocrinology 2010; 151: 5721-29.
[15] Verma S, Tabb MM, Blumberg B. Activation of the steroid and xenobiotic receptor, SXR, induces apoptosis in breast cancer cells. BMC Cancer 2009; 9: 3.
[16] Nwankwo JO. Significant transcriptional down-regulation of the human MDR1 gene by beta-naphthoflavone: a proposed hypothesis linking potent CYP gene induction to MDR1 inhibition. Med Hypotheses 2007; 68: 661-9.
[17] Stoner GD, Adam-Rodwell G, Morse MA. Lung tumors in strain A mice: application for studies in cancer chemoprevention. J Cell Biochem 1993; Suppl 17F: 95-103.
[18] Malejka-Giganti D, Bennett KK, Culp SJ, Beland FA, Shinozuka H and Bliss RL. Suppression of 7,12-dimethylbenz[a]anthracene-induced mammary carcinogenesis by pre-initiation treatment of rats with beta-naphthoflavone coincides with decreased levels of the carcinogen-derived DNA adducts in the mammary gland. Cancer Detect Prev 2005; 29: 338-47.
[19] Huang H, Wang H, Sinz M, Zoeckler M, Staudinger J, Redinbo MR, Teotico DG, Locker J, Kalpana GV, Mani S. Inhibition of drug metabolism by blocking the activation of nuclear receptors by ketoconazole. Oncogene 2007; 26: 258-68.
[20] Venkatesh M, Wang H, Cayer J, Leroux M, Salvail D, Das B, Wrobel JE. Mani S: In vivo and in vitro characterization of a first-in-class novel azole analog that targets pregnane X receptor activation. Mol Pharmacol 2011; 80: 124-35.
[21] Hosaka M, Watari H, Kato T, Odagiri T, Konno Y, Endo D, Mitamura T, Kikawa S, Suzuki Y, Sakuragi N. Clinical efficacy of paclitaxel/cisplatin as an adjuvant chemotherapy for patients with cervical cancer who underwent radical hysterectomy and systematic lymphadenectomy. J Surg Oncol 2012; 105(6): 612-6.
[22] Qiao WJ, Cheng HY, Li CQ, Jin H, Yang SS, Li X, Zhang YY. Identification of pathways involved in paclitaxel activity in cervical cancer. Asian Pac J Cancer Prev 2011; 12: 99-102.
[23] Huang TC, Campbell TC. Comparison of weekly versus every 3 weeks paclitaxel in the treatment of advanced solid tumors: A meta-analysis. Cancer Treat Rev, 2011.
[24] Mense SM, Singh B, Remotti F, Liu X, Bhat HK. Vitamin C and alpha-naphthoflavone prevent estrogen-induced mammary tumors and decrease oxidative stress in female ACI rats. Carcinogenesis 2009; 30: 1202-8.
[25] Meira DD, Marinho-Carvalho MM, Teixeira CA, Veiga VF, Da Poian AT, Holandino C, de Freitas MS, Sola-Penna M. Clotrimazole decreases human breast cancer cells viability through alterations in cytoskeleton-associated glycolytic enzymes. Mol Genet Metab 2005; 84: 354-362.
[26] Rodriguez-Enriquez S, Marin-Hernandez A, Gallardo-Perez JC, Carreno-Fuentes L, Moreno-Sanchez R. Targeting of cancer energy metabolism. Mol Nutr Food Res 2009; 53: 29-48.
[27]27 Liu H, Li Y, Raisch KP. Clotrimazole induces a late G1 cell cycle arrest and sensitizes glioblastoma cells to radiation in vitro. Anticancer Drugs 2010; 21: 841-9.
[28] Ahmad M. Study on cytochrome P-450 dependent retinoic acid metabolism and its Inhibitors as potential agents for cancer therapy. Sci Pharm 2011; 79: 921-35.
[29] Ramondetta LM, Johnson AJ, Sun CC, Atkinson N, Smith JA, Jung MS, Broaddus R, Iyer RB, Burke T. Phase 2 trial of mifepristone (RU-486) in advanced or recurrent endometrioid adenocarcinoma or low-grade endometrial stromal sarcoma. Cancer 2009; 115: 1867-74.
[30] Ørbo A, Moe BT, Grønaas H, Paulssen RH. Early effects of high concentrations of progesterone and mifepristone A gene expression study of endometrial cancer cells (Ishikawa). J Steroid Biochem Mol Biol 2009; 113: 139-49.
[31] Fjelldal R, Moe BT, Ørbo A, Sager G. MCF-7 cell apoptosis and cell cycle arrest: non-genomic effects of progesterone and mifepristone (RU-486). Anticancer Res 2010; 30: 4835-40.
[32] Benad P, Rauner M, Rachner TD, Hofbauer LC. The anti-progestin RU-486 inhibits viability of MCF-7 breast cancer cells by suppressing WNT1. Cancer Lett 2011; 312: 101-8.
[33] Chen J, Raymond K. Roles of rifampicin in drug-drug interactions: underlying molecular mechanisms involving the nuclear pregnane X receptor. Ann Clin Microbiol Antimicrob 2006; 5: 3.