PMID: 25788262Mar 20, 2015Paper

Caffeic acid phenethyl ester induced cell cycle arrest and growth inhibition in androgen-independent prostate cancer cells via regulation of Skp2, p53, p21Cip1 and p27Kip1

Oncotarget
Hui-Ping LinChih-pin Chuu

Abstract

Prostate cancer (PCa) patients receiving the androgen ablation therapy ultimately develop recurrent castration-resistant prostate cancer (CRPC) within 1-3 years. Treatment with caffeic acid phenethyl ester (CAPE) suppressed cell survival and proliferation via induction of G1 or G2/M cell cycle arrest in LNCaP 104-R1, DU-145, 22Rv1, and C4-2 CRPC cells. CAPE treatment also inhibited soft agar colony formation and retarded nude mice xenograft growth of LNCaP 104-R1 cells. We identified that CAPE treatment significantly reduced protein abundance of Skp2, Cdk2, Cdk4, Cdk7, Rb, phospho-Rb S807/811, cyclin A, cyclin D1, cyclin H, E2F1, c-Myc, SGK, phospho-p70S6kinase T421/S424, phospho-mTOR Ser2481, phospho-GSK3α Ser21, but induced p21Cip1, p27Kip1, ATF4, cyclin E, p53, TRIB3, phospho-p53 (Ser6, Ser33, Ser46, Ser392), phospho-p38 MAPK Thr180/Tyr182, Chk1, Chk2, phospho-ATM S1981, phospho-ATR S428, and phospho-p90RSK Ser380. CAPE treatment decreased Skp2 and Akt1 protein expression in LNCaP 104-R1 tumors as compared to control group. Overexpression of Skp2, or siRNA knockdown of p21Cip1, p27Kip1, or p53 blocked suppressive effect of CAPE treatment. Co-treatment of CAPE with PI3K inhibitor LY294002 or Bcl-2 inhibitor ABT737 showed syne...Continue Reading

References

Mar 9, 1984·Science·A L Murphree, W F Benedict
May 1, 1995·Molecular and Cellular Biology·C L WuJ A Lees
Mar 9, 1995·Nature·D O Morgan
Apr 2, 1996·Proceedings of the National Academy of Sciences of the United States of America·K A CimprichS L Schreiber
Aug 20, 1996·Proceedings of the National Academy of Sciences of the United States of America·K NatarajanB B Aggarwal
Dec 6, 1996·Science·C J Sherr
Jan 23, 1999·Oncogene·C E Canman, D S Lim
Apr 14, 1999·Proceedings of the National Academy of Sciences of the United States of America·L C Cantley, B G Neel
Apr 12, 2001·Genes & Development·A C GingrasN Sonenberg
May 19, 2001·European Journal of Biochemistry·K ItahanaJ Campisi
Nov 3, 2001·Science·P B DennisG Thomas
Mar 20, 2002·Nature Reviews. Cancer·B J Feldman, D Feldman
May 23, 2002·CA: a Cancer Journal for Clinicians·Beth A Hellerstedt, Kenneth J Pienta
Jun 28, 2002·Cancer Cell·Dinesh SinghWilliam R Sellers
Sep 17, 2002·Urology·Timothy Gilligan, Philip W Kantoff
Jan 31, 2003·Nature·Christopher J Bakkenist, Michael B Kastan
Mar 12, 2003·Genes & Development·Eric J Brown, David Baltimore
Mar 19, 2003·Lancet·Henrik Grönberg
Jun 7, 2003·Science·Lee Zou, Stephen J Elledge
Aug 7, 2003·Current Opinion in Pharmacology·Shile Huang, Peter J Houghton
Nov 20, 2003·Nature Reviews. Molecular Cell Biology·Steven I Reed
Jan 2, 2004·Nature Medicine·Charlie D ChenCharles L Sawyers
Feb 5, 2004·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·James L MohlerFrank S French
Oct 12, 2004·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Gustavo AyalaWade Harper
Feb 19, 2005·Science·D D SarbassovDavid M Sabatini
Aug 6, 2005·Current Opinion in Genetics & Development·Michael Korenjak, Alexander Brehm

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Citations

Jun 8, 2017·International Journal of Molecular Sciences·Liviuta BudisanIoana Berindan-Neagoe
Dec 6, 2017·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Giorgio Ivan RussoGiuseppe Morgia
Dec 3, 2016·Nutrition Journal·Preethi G AnantharajuSubbaRao V Madhunapantula
Jul 12, 2017·Cancer Biology & Therapy·Archana MukhopadhyayJane V Aldrich
Jun 16, 2016·Oncotarget·Margrethe StormFahri Saatcioglu
Jan 12, 2021·Frontiers in Cell and Developmental Biology·Se-Ra ParkHwa-Yong Lee
Sep 20, 2017·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Wen LiDaqing Song
May 2, 2018·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Ge-Lin LiuShi-Shun Liu

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