An ornamental plant targets epigenetic signaling to block cancer stem cell-driven colon carcinogenesis

Carcinogenesis
Ishfaq AhmedShahid Umar

Abstract

Phytochemicals modulate key cellular signaling pathways and have proven anticancer effects. Alcea rosea(AR; Hollyhock) is an ornamental plant with known anti-inflammatory properties. This study explored its role as an anticancer agent. The AR seed extract (AR extract) inhibited proliferation and colony formation in a dose- and time-dependent manner and promoted apoptosis as was evidenced by cleavage of PARP and increased expression of Bax accompanying reduced levels of BCL-xl protein in HCT116 and SW480 cells, respectively. In addition, AR extract-arrested cells at Go/G1 phase of cell cycle and exhibited decreases in Cyclin D1. AR extract-treated cells exhibited reduced number and size of colonospheres in a dose-dependent manner concomitant with decreases in cancer stem cell (CSC) markers ALDH1A1 and Dclk1. Relative levels of β-catenin, Notch-ICD, Hes1 and EZH2 were also attenuated by AR extract. TOP-flash reporter activity, a measure of Wnt signaling, decreased significantly in response to treatment while overexpression of wild type but not mutant EZH2, reversed the inhibitory effects. Moreover, WIF1 (a Wnt antagonist) promoter activity increased dramatically following treatment with AR extract which phenocopied increases in W...Continue Reading

References

Jun 1, 1990·Cell·E R Fearon, B Vogelstein
Dec 3, 2003·Proceedings of the National Academy of Sciences of the United States of America·Houman D HemmatiHarley I Kornblum
Jun 4, 2004·The New England Journal of Medicine·Thierry AndréUNKNOWN Multicenter International Study of Oxaliplatin/5-Fluorouracil/Leucovorin in the Adjuvant Treatment of Colon Cancer (MOSAIC)
Jul 1, 2005·Breast Cancer Research : BCR·Suling LiuMax S Wicha
Mar 15, 2006·American Journal of Surgery·Sergio HuertaEdward H Livingston
Apr 5, 2007·Nature Protocols·Nicolaas A P FrankenChris van Bree
Jun 6, 2007·Proceedings of the National Academy of Sciences of the United States of America·Piero DalerbaMichael F Clarke
Jul 11, 2007·The Cancer Journal·Ki Young Chung, Leonard B Saltz
Sep 18, 2007·Biochemical Pharmacology·Valentina CecchinatoPaola Comi
Jun 10, 2008·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Bruce M Boman, Max S Wicha
Nov 13, 2008·Biochemical and Biophysical Research Communications·Min-Jung RyuSangtaek Oh
Apr 14, 2009·Trends in Molecular Medicine·Shi Yu YangMarc C Winslet
Aug 12, 2009·The International Journal of Biochemistry & Cell Biology·Franziska Arlt, Ulrike Stein
Apr 15, 2010·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Yanyan LiDuxin Sun
Aug 5, 2010·Current Gastroenterology Reports·Shahid Umar
Aug 10, 2010·Molecular Cancer·Shailender S KanwarAdhip P N Majumdar
Mar 1, 2011·European Journal of Pharmaceutical Sciences : Official Journal of the European Federation for Pharmaceutical Sciences·Xiong ZhangYu Li
Jun 21, 2011·CA: a Cancer Journal for Clinicians·Rebecca SiegelAhmedin Jemal
Oct 19, 2011·Biochemical Pharmacology·Kentaro JingushiToshiyuki Sasaguri
Dec 14, 2011·Cell Cycle·Alix Scholer-Dahirel, Margaret E McLaughlin
Feb 10, 2012·Molecular Cancer Therapeutics·Sivapriya PonnurangamShrikant Anant
Jun 16, 2012·Indian Journal of Pharmacology·Marzieh AhmadiNafiseh Sadat Tabasi
Sep 11, 2012·Cell Biochemistry and Function·Bethany M BushTakita Felder Sumter
Sep 24, 2013·Molecular Cell·Hae-Yun JungJae-Il Park
Dec 25, 2013·Cancer Biology & Therapy·Amelie Boquoi
May 3, 2014·American Journal of Physiology. Gastrointestinal and Liver Physiology·Allen K GreinerShahid Umar
May 14, 2014·Frontiers in Oncology·Dharmalingam SubramaniamShrikant Anant
Sep 10, 2014·Nature Reviews. Microbiology·Petra LouisHarry J Flint
Nov 15, 2014·Current Colorectal Cancer Reports·Suman SumanChendil Damodaran
Apr 29, 2015·Journal of Cellular Biochemistry·Alexander W FenderGeorge Sigounas
May 6, 2015·International Journal of Molecular Sciences·Soo Jin MinYuri Kim

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