دورية أكاديمية

Indole-3-carbinol and its N-alkoxy derivatives preferentially target ERα-positive breast cancer cells.

التفاصيل البيبلوغرافية
العنوان: Indole-3-carbinol and its N-alkoxy derivatives preferentially target ERα-positive breast cancer cells.
المؤلفون: Caruso JA; a Department of Experimental Radiation Oncology ; University of Texas MD Anderson Cancer Center ; Houston , TX USA., Campana R, Wei C, Su CH, Hanks AM, Bornmann WG, Keyomarsi K
المصدر: Cell cycle (Georgetown, Tex.) [Cell Cycle] 2014; Vol. 13 (16), pp. 2587-99.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Taylor & Francis Country of Publication: United States NLM ID: 101137841 Publication Model: Print Cited Medium: Internet ISSN: 1551-4005 (Electronic) Linking ISSN: 15514005 NLM ISO Abbreviation: Cell Cycle Subsets: MEDLINE
أسماء مطبوعة: Publication: 2015- : Philadelphia, PA : Taylor & Francis
Original Publication: Georgetown, TX : Landes Bioscience, c2002-
مواضيع طبية MeSH: Alcohols/*pharmacology , Antineoplastic Agents/*pharmacology , Breast Neoplasms/*metabolism , Estrogen Receptor alpha/*metabolism , Indoles/*pharmacology , Metabolic Networks and Pathways/*drug effects, Alcohols/chemistry ; Antineoplastic Agents/chemistry ; Apoptosis/drug effects ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cyclin E/metabolism ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Indoles/chemistry ; Leukocyte Elastase/metabolism ; Receptors, Aryl Hydrocarbon/metabolism ; Signal Transduction/drug effects
مستخلص: Indole-3-carbinol (I3C) is a natural anti-carcinogenic compound found at high concentrations in Brassica vegetables. I3C was recently reported to inhibit neutrophil elastase (NE) activity, while consequently limiting the proteolytic processing of full length cyclin E into pro-tumorigenic low molecular weight cyclin E (LMW-E). In this study, we hypothesized that inhibition of NE activity and resultant LMW-E generation is critical to the anti-tumor effects of I3C. LMW-E was predominately expressed by ERα-negative breast cancer cell lines. However, ERα-positive cell lines demonstrated the greatest sensitivity to the anti-tumor effects of I3C and its more potent N-alkoxy derivatives. We found that I3C was incapable of inhibiting NE activity or the generation of LMW-E. Therefore, this pathway did not contribute to the anti-tumor activity of I3C. Gene expression analyzes identified ligand-activated aryl hydrocarbon receptor (AhR), which mediated sensitivity to the anti-tumor effects of I3C in ERα-positive MCF-7 cells. In this model system, the reactive oxygen species (ROS)-induced upregulation of ATF-3 and pro-apoptotic BH3-only proteins (e.g. NOXA) contributed to the sensitivity of ERα-positive breast cancer cells to the anti-tumor effects of I3C. Overexpression of ERα in MDA-MB-231 cells, which normally lack ERα expression, increased sensitivity to the anti-tumor effects of I3C, demonstrating a direct role for ERα in mediating the sensitivity of breast cancer cell lines to I3C. Our results suggest that ERα signaling amplified the pro-apoptotic effect of I3C-induced AhR signaling in luminal breast cancer cell lines, which was mediated in part through oxidative stress induced upregulation of ATF-3 and downstream BH3-only proteins.
References: Int J Cancer. 2013 Dec 15;133(12):2769-80. (PMID: 23733406)
Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19750-5. (PMID: 19064917)
Cancer Res. 1999 Mar 15;59(6):1244-51. (PMID: 10096555)
Cancer Res. 2011 May 1;71(9):3377-86. (PMID: 21385896)
Carcinogenesis. 1991 Sep;12(9):1571-4. (PMID: 1893517)
Mol Cancer Ther. 2006 Oct;5(10):2512-21. (PMID: 17041095)
Nutr Cancer. 1991;16(1):59-66. (PMID: 1656396)
Mol Cell Biol. 2003 Mar;23(6):1843-55. (PMID: 12612060)
Cell Cycle. 2005 Sep;4(9):1201-15. (PMID: 16082211)
Oncogene. 2001 May 24;20(23):2927-36. (PMID: 11420705)
J Nutr Biochem. 2006 Oct;17(10):659-64. (PMID: 16488130)
Breast. 2013 Jun;22(3):309-13. (PMID: 22877795)
Toxicology. 1994 Sep 6;92(1-3):39-51. (PMID: 7940568)
Breast Cancer (Auckl). 2010 Dec 16;4:85-95. (PMID: 21234288)
Anticancer Res. 1995 May-Jun;15(3):709-16. (PMID: 7645947)
Biochem Pharmacol. 2002 Mar 15;63(6):1085-97. (PMID: 11931841)
Nutr Cancer. 2000;36(1):112-21. (PMID: 10798223)
Mol Cell Biol. 2005 Jul;25(13):5317-28. (PMID: 15964790)
Carcinogenesis. 1998 Sep;19(9):1631-9. (PMID: 9771935)
J Am Diet Assoc. 1996 Oct;96(10):1027-39. (PMID: 8841165)
Mol Cell Biol. 2006 Feb;26(3):1087-97. (PMID: 16428460)
N Engl J Med. 2002 Nov 14;347(20):1566-75. (PMID: 12432043)
Mol Biol Cell. 2010 Apr 1;21(7):1166-77. (PMID: 20130088)
Cancer Res. 2010 Sep 15;70(18):7125-36. (PMID: 20823156)
PLoS One. 2009;4(8):e6529. (PMID: 19657394)
Gene Expr. 1999;7(4-6):321-35. (PMID: 10440233)
Proc Natl Acad Sci U S A. 1990 Jan;87(1):463-7. (PMID: 2153303)
Cancer Res. 2007 Aug 1;67(15):7212-22. (PMID: 17671189)
Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2477-81. (PMID: 17164373)
Science. 1988 Jul 8;241(4862):218-21. (PMID: 3388033)
Nat Med. 2012 Jan;18(1):128-34. (PMID: 22179317)
Mol Cell Biol. 2001 Sep;21(18):6254-69. (PMID: 11509668)
Proc Natl Acad Sci U S A. 1989 Feb;86(4):1249-53. (PMID: 2919173)
JAMA. 2001 Feb 14;285(6):769-76. (PMID: 11176915)
Cancer Epidemiol Biomarkers Prev. 2005 Aug;14(8):1953-60. (PMID: 16103443)
Cell Cycle. 2003 Sep-Oct;2(5):461-6. (PMID: 12963845)
Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9543-7. (PMID: 1658785)
Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2200-5. (PMID: 19164757)
J Mol Med (Berl). 2000;78(3):155-65. (PMID: 10868478)
PLoS One. 2010;5(9):e12860. (PMID: 20877462)
Carcinogenesis. 1994 May;15(5):933-7. (PMID: 8200098)
Nature. 2012 Mar 29;483(7391):603-7. (PMID: 22460905)
Mol Endocrinol. 1989 Jan;3(1):157-64. (PMID: 2464754)
Chem Res Toxicol. 2003 Jul;16(7):807-16. (PMID: 12870882)
Mol Pharmacol. 1999 Sep;56(3):588-97. (PMID: 10462547)
Acta Biochim Pol. 2007;54(1):113-7. (PMID: 17311112)
Mol Cell Biol. 1999 Oct;19(10):6825-32. (PMID: 10490621)
J Biol Chem. 2005 Apr 15;280(15):15148-57. (PMID: 15708847)
J Biol Chem. 1998 Feb 13;273(7):3838-47. (PMID: 9461564)
Toxicol Sci. 2012 Feb;125(2):401-11. (PMID: 22071320)
Mol Endocrinol. 2006 Dec;20(12):3070-82. (PMID: 16901971)
J Biochem Mol Biol. 2005 Mar 31;38(2):167-76. (PMID: 15826493)
J Biol Chem. 1998 Apr 17;273(16):9357-60. (PMID: 9545256)
Toxicol Sci. 2009 Oct;111(2):254-66. (PMID: 19574409)
Breast Cancer Res Treat. 2012 Apr;132(2):575-88. (PMID: 21695458)
Oncol Rep. 1998 Mar-Apr;5(2):311-5. (PMID: 9468547)
Biochem Pharmacol. 2008 Feb 1;75(3):713-24. (PMID: 18023427)
J Nutr. 2000 Dec;130(12):2927-31. (PMID: 11110848)
معلومات مُعتمدة: P30 CA016672 United States CA NCI NIH HHS; R01 CA087548 United States CA NCI NIH HHS; R01 CA152228 United States CA NCI NIH HHS; T32 CA163185 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: AhR, aryl hydrocarbon receptor; CYP, cytochrome p450 oxidases; DIM, 3,3-diindoylmethane; ERα, estrogen receptor α; HMECs, human mammary epithelial cells; I3C, indole-3-carbinol; LMW-E, low molecular weight cyclin E; NE, neutrophil elastase; ROS, reactive oxygen species; RPPA, reverse phase protein array; TNBC, triple-receptor negative breast cancer; aryl hydrocarbon receptor; estrogen receptor α; indole-3-carbinol; neutrophil elastase
المشرفين على المادة: 0 (Alcohols)
0 (Antineoplastic Agents)
0 (Cyclin E)
0 (ESR1 protein, human)
0 (Estrogen Receptor alpha)
0 (Indoles)
0 (Receptors, Aryl Hydrocarbon)
0 (alkoxyl radical)
C11E72455F (indole-3-carbinol)
EC 3.4.21.37 (Leukocyte Elastase)
تواريخ الأحداث: Date Created: 20141209 Date Completed: 20150819 Latest Revision: 20210816
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC4614451
DOI: 10.4161/15384101.2015.942210
PMID: 25486199
قاعدة البيانات: MEDLINE
الوصف
تدمد:1551-4005
DOI:10.4161/15384101.2015.942210