Tubeimoside-1 up-regulates p21 expression and induces apoptosis and G2/M phase cell cycle arrest in human bladder cancer T24 cells

Authors

  • Azhar Rasul State Key Laboratory of Electroanalytical Chemistry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China; The Key Laboratory of Molecular Epigenetics of MOE, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China
  • Xiaoyan Shen The Key Laboratory of Molecular Epigenetics of MOE, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China
  • Bingyu Wang The Key Laboratory of Molecular Epigenetics of MOE, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China
  • Bao Liu The Key Laboratory of Molecular Epigenetics of MOE, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China
  • Xiaomeng Li The Key Laboratory of Molecular Epigenetics of MOE, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China
  • Jilin Tang State Key Laboratory of Electroanalytical Chemistry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China

DOI:

https://doi.org/10.3329/bjp.v9i4.19989

Keywords:

Apoptosis, Bladder cancer, Cell cycle arrest, Tubeimoside-1

Abstract

Tubeimoside-1 (TBMS1) is a triterpenoid saponin with potent anticancer properties. In this study, for the first, we examined the anti-proliferative effects of TBMS1 in human bladder cancer T24 cells and its ability to induce apoptosis and cell cycle arrest. Our results demonstrated that TBMS1 decreased the cell viability of bladder cancer T24 cells in a dose-dependent manner. Flow cytometric analysis showed that TBMS1 significantly triggered apoptosis in T24 cells and arrested cell cycle at G2/M phase in a dose-dependent manner. Further characterization demonstrated that TBMS1-induced apoptosis is associated with dissipation in mitochondrial membrane potential (??m), down-regulation of Bcl-2, and up-regulation of Bax and p21 in TBMS1-treated T24 cells. These in vitro results suggested that TBMS1 is an effective anti-bladder cancer natural compound that worth further mechanistic and therapeutic studies in human bladder cancer.

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Author Biography

Jilin Tang, State Key Laboratory of Electroanalytical Chemistry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China

Professor

References

Adams JM, Cory S. The Bcl-2 apoptotic switch in cancer development and therapy. Oncogene 2007; 26: 1324-37.

Amin AR, Kucuk O, Khuri FR, Shin DM. Perspectives for cancer prevention with natural compounds. J Clin Oncol. 2009; 27: 2712-25.

Boulaire J, Fotedar A, Fotedar R. The functions of the cdk-cyclin kinase inhibitor p21WAF1. Pathol Biol (Paris). 2000; 48: 190-202.

Burlacu A. Regulation of apoptosis by Bcl-2 family proteins. J Cell Mol Med. 2003; 7: 249-57.

Buytaert E, Dewaele M, Agostinis P. Molecular effectors of multiple cell death pathways initiated by photodynamic therapy. Biochim Biophys Acta. 2007; 1776: 86-107.

Chi XZ, Yang JO, Lee KY, Ito K, Sakakura C, Li QL, Kim HR, Cha EJ, Lee YH, Kaneda A, Ushijima T, Kim WJ, Ito Y, Bae SC. RUNX3 suppresses gastric epithelial cell growth by inducing p21(WAF1/Cip1) expression in cooperation with transforming growth factor {beta}-activated SMAD. Mol Cell Biol. 2005; 25: 8097-107.

Danial NN. BCL-2 family proteins: Critical checkpoints of apoptotic cell death. Clin Cancer Res. 2007; 13: 7254-63.

Derynck R, Akhurst RJ, Balmain A. TGF-beta signaling in tumor suppression and cancer progression. Nat Genet. 2001; 29: 117-29.

Elmore S. Apoptosis: A review of programmed cell death. Toxicol Pathol. 2007; 35: 495-516.

Feng P, Li TL, Guan ZX, Franklin RB, Costello LC. Direct effect of zinc on mitochondrial apoptogenesis in prostate cells. Prostate 2002; 52: 311-18.

Fulda S. Evasion of apoptosis as a cellular stress response in cancer. Int J Cell Biol. 2010; 2010: 370835.

Grana X, Reddy EP. Cell cycle control in mammalian cells: Role of cyclins, cyclin dependent kinases (CDKs), growth suppressor genes and cyclin-dependent kinase inhibitors (CKIs). Oncogene 1995; 11: 211-19.

Hengartner MO. The biochemistry of apoptosis. Nature 2000; 407: 770-76.

Kanduc D, Mittelman A, Serpico R, Sinigaglia E, Sinha AA, Natale C, Santacroce R, Di Corcia MG, Lucchese A, Dini L, Pani P, Santacroce S, Simone S, Bucci R, Farber E. Cell death: Apoptosis versus necrosis (review). Int J Oncol. 2002; 21: 165-70.

Kerr JF, Wyllie AH, Currie AR. Apoptosis: A basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer. 1972; 26: 239-57.

Khan M, Rasul A, Yi F, Zhong L, Ma T. Jaceosidin induces p53-dependent G2/M phase arrest in U87 glioblastoma cells. Asian Pac J Cancer Prev. 2011; 12: 3235-38.

Khan M, Yu B, Rasul A, Al Shawi A, Yi F, Yang H, Ma T. Jaceosidin Induces Apoptosis in U87 Glioblastoma Cells through G2/M Phase Arrest. Evidence-based complementary and alternative medicine: eCAM 2012; 2012: 703034.

Kintzios SE, Barberaki MG. Plants that fight cancer. CRC Press: Boca Raton, 2004.

Kluck RM, Bossy-Wetzel E, Green DR, Newmeyer DD. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis. Science 1997; 275: 1132-36.

Lawen A. Apoptosis: An introduction. BioEssays 2003; 25: 888-96.

Lee SH, Lee MY, Kang HM, Han DC, Son KH, Yang DC, Sung ND, Lee CW, Kim HM, Kwon BM. Anti-tumor activity of the farnesyl-protein transferase inhibitors arteminolides, isolated from Artemisa. Bioorg Med Chem. 2003; 11: 4545-49.

Leist M, Jaattela M. Four deaths and a funeral: From caspases to alternative mechanisms. Nature Rev Mol Cell Biol. 2001; 2: 589-98.

Ma R, Song G, You W, Yu L, Su W, Liao M, Zhang Y, Huang L, Zhang X, Yu T. Anti-microtubule activity of tubeimoside I and its colchicine binding site of tubulin. Cancer Chemother Pharmacol. 2008; 62: 559-68.

Magadula JJ, Erasto P. Bioactive natural products derived from the East African flora. Nat Prod Reports. 2009; 26: 1535-54.

Mallat Z, Tedgui A. Apoptosis in the vasculature: Mechanisms and functional importance. Br J Pharmacol. 2000; 130: 947-62.

Mashima T, Tsuruo T. Defects of the apoptotic pathway as therapeutic target against cancer. Drug Resist Updat. 2005; 8: 339-43.

Pardali K, Kowanetz M, Heldin CH, Moustakas A. Smad pathway-specific transcriptional regulation of the cell cycle inhibitor p21(WAF1/Cip1). J Cell Physiol. 2005; 204: 260-72.

Ploeg M, Aben KK, Kiemeney LA. The present and future burden of urinary bladder cancer in the world. World J Urol. 2009; 27: 289-93.

Pommier Y, Sordet O, Antony S, Hayward RL, Kohn KW. Apoptosis defects and chemotherapy resistance: Molecular interaction maps and networks. Oncogene 2004; 23: 2934-49.

Rasul A, Ding C, Li X, Khan M, Yi F, Ali M, Ma T. Dracorhodin perchlorate inhibits PI3K/Akt and NF-kappaB activation, up-regulates the expression of p53, and enhances apoptosis. Apoptosis 2012a; 17: 1104-19.

Rasul A, Song R, Wei W, Nishino Y, Tsuji I, Li X, Li J. Tubeimoside-1 inhibits growth via the induction of cell cycle arrest and apoptosis in human melanoma A375 cells. Bangladesh J Pharmacol. 2012b; 7: 150-56.

Rasul A, Bao R, Malhi M, Zhao B, Tsuji I, Li J, Li X. Induction of apoptosis by costunolide in bladder cancer cells is mediated through ROS generation and mitochondrial dysfunction. Molecules 2013a; 18: 1418-33.

Rasul A, Di J, Millimouno FM, Malhi M, Tsuji I, Ali M, Li J, Li X. Reactive oxygen species mediate isoalantolactone-induced apoptosis in human prostate cancer cells. Molecules 2013b; 18: 9382-96.

Reed JC. Bcl-2 family proteins. Oncogene 1998; 17: 3225-36.

Reed JC. Apoptosis-based therapies. Nat Rev Drug Discov. 2002; 1: 111-21.

Saramaki A, Banwell CM, Campbell MJ, Carlberg C. Regulation of the human p21(waf1/cip1) gene promoter via multiple binding sites for p53 and the vitamin D3 receptor. Nucleic Acids Res. 2006; 34: 543-54.

Tan RX, Zheng WF, Tang HQ. Biologically active substances from the genus Artemisia. Planta Med. 1998; 64: 295-302.

Vermeulen K, Van Bockstaele DR, Berneman ZN. The cell cycle: A review of regulation, deregulation and therapeutic targets in cancer. Cell Prolif. 2003; 36: 131-49.

Wang X. The expanding role of mitochondria in apoptosis. Genes Dev. 2001; 15: 2922-33.

Weng XY, Ma RD, Yu LJ. [Apoptosis of human nasopharyngeal carcinoma CNE-2Z cells induced by tubeimoside I]. Chinese J Cancer. 2003; 22: 806-11.

Woldemichael GM, Wink M. Identification and biological activities of triterpenoid saponins from Chenopodium quinoa. J Agric Food Chem. 2001; 49: 2327-32.

Xu Y, Chiu JF, He QY, Chen F. Tubeimoside-1 exerts cytotoxi-city in HeLa cells through mitochondrial dysfunction and endoplasmic reticulum stress pathways. J Proteome Res. 2009; 8: 1585-93.

Yu L, Ma R, Yu T. Induction of morphological and functional differentiation of human promyelocytic leukemia cells (HL-60) by tubeimoside 1. Planta Medica. 1996; 62: 119-21.

Yu LJ, Ma RD, Wang YQ, Nishino H, Takayasu J, He WZ, Chang M, Zhen J, Liu WS, Fan SX. Potent anti-tumorigenic effect of tubeimoside 1 isolated from the bulb of Bolbostemma paniculatum (Maxim) Franquet. Int J Cancer J Int du Cancer. 1992; 50: 635-38.

Yu LJ, Ma RD, Jiang SB. Effects of tubeimoside-1 on HIV core protein p24 and cytopathogenesis in vitro. Zhongguo Yao Li Xue Bao (Acta Pharmacologica Sinica). 1994; 15: 103-06.

Zhang Y, Xu X, He P. Tubeimoside-1 inhibits proliferation and induces apoptosis by increasing the Bax to Bcl-2 ratio and decreasing COX-2 expression in lung cancer A549 cells. Mol Med Rep. 2011; 4: 25-29.

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Published

2014-11-18

How to Cite

Rasul, A., X. Shen, B. Wang, B. Liu, X. Li, and J. Tang. “Tubeimoside-1 up-Regulates p21 Expression and Induces Apoptosis and G2/M Phase Cell Cycle Arrest in Human Bladder Cancer T24 Cells”. Bangladesh Journal of Pharmacology, vol. 9, no. 4, Nov. 2014, pp. 595-03, doi:10.3329/bjp.v9i4.19989.

Issue

Vol. 9 No. 4 (2014)

Section

Research Articles

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