CLC number:
On-line Access: 2021-02-07
Received: 2020-08-07
Revision Accepted: 2022-04-22
Crosschecked: 2021-01-06
Cited: 0
Clicked: 3268
Aiysvariyah RAJEDADRAM, Kar Yong PIN, Sui Kiong LING, See Wan YAN, Mee Lee LOOI. Hydroxychavicol, a polyphenol from Piper betle leaf extract, induces cell cycle arrest and apoptosis in TP53-resistant HT-29 colon cancer cells[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org/10.1631/jzus.B2000446 @article{title="Hydroxychavicol, a polyphenol from Piper betle leaf extract, induces cell cycle arrest and apoptosis in TP53-resistant HT-29 colon cancer cells", %0 Journal Article TY - JOUR
从花椒叶中提取的羟基胡椒酚可以诱导耐TP53的HT-29结肠癌细胞的细胞周期阻滞和凋亡方法:从蒌叶(PBL)中分离出HC,经高效液相色谱(HPLC)、核磁共振(NMR)和气相色谱-质谱(GC-MS)进行检测。在处理24、48和72 h后,检测标准药物5-氟尿嘧啶(5-FU)、PBL水提物和HC对HT-29细胞的细胞毒性作用。检测30 h内5-FU和HC处理对细胞周期和凋亡的调控作用。同时检测18 h内磷酸化JNK(pJNK)和磷酸化P38(pP38)MAPK的表达变化。 结果:HC(30μg/ mL)和PBL水提物(380μg/ mL)的半数最大抑制浓度(IC50)值在24 h时达到,而5-FU(50μmol/ L)的IC50值在72 h时达到。从12h开始HC处理的细胞停滞在细胞周期的G0/G1期。与5-FU处理的细胞相比,HC处理的细胞凋亡率更高(P<0.05)。在HC处理的细胞中,pJNK和pP38 MAPK在12 h时出现高表达,而在5-FU处理的HT-29细胞中则没有(P<0.05)。 结论:由此可见,HC可诱导HT-29细胞的细胞周期阻滞和凋亡,这些作用可能由JNK和P38 MAPK介导。 关键词组: Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article
Reference[1]Abrahim NN, Kanthimathi MS, Abdul-Aziz A, 2012. Piper betle shows antioxidant activities, inhibits MCF-7 cell proliferation and increases activities of catalase and superoxide dismutase. BMC Complement Altern Med, 12:220. [2]Amin A, Gali-Muhtasib H, Ocker M, et al., 2009. Overview of major classes of plant-derived anticancer drugs. Int J Biomed Sci, 5(1):1-11. [3]Angulo P, Kaushik G, Subramaniam D, et al., 2017. Natural compounds targeting major cell signaling pathways: a novel paradigm for osteosarcoma therapy. J Hematol Oncol, 10:10. [4]Batra P, Sharma AK, 2013. Anti-cancer potential of flavonoids: recent trends and future perspectives. 3 Biotech, 3(6):439-459. [5]Bhanot A, Sharma R, Noolvi MN, 2011. Natural sources as potential anti-cancer agents: a review. Int J Phytomed, 3(1):9-26. [6]Bossi G, Lapi E, Strano S, et al., 2006. Mutant p53 gain of function: reduction of tumor malignancy of human cancer cell lines through abrogation of mutant p53 expression. Oncogene, 25(2):304-309. [7]Boyer J, McLean EG, Aroori S, et al., 2004. Characterization of p53 wild-type and null isogenic colorectal cancer cell lines resistant to 5-fluorouracil, oxaliplatin, and irinotecan. Clin Cancer Res, 10(6):2158-2167. [8]Brown CJ, Cheok CF, Verma CS, et al., 2011. Reactivation of p53: from peptides to small molecules. Trends Pharmacol Sci, 32(1):53-62. [9]Chakraborty JB, Mahato SK, Joshi K, et al., 2012. Hydroxychavicol, a Piper betle leaf component, induces apoptosis of CML cells through mitochondrial reactive oxygen species-dependent JNK and endothelial nitric oxide synthase activation and overrides imatinib resistance. Cancer Sci, 103(1):88-99. [10]Chang MC, Uang BJ, Wu HL, et al., 2002. Inducing the cell cycle arrest and apoptosis of oral KB carcinoma cells by hydroxychavicol: roles of glutathione and reactive oxygen species. Br J Pharmacol, 135(3):619-630. [11]Chang MC, Uang BJ, Tsai CY, et al., 2007. Hydroxychavicol, a novel betel leaf component, inhibits platelet aggregation by suppression of cyclooxygenase, thromboxane production and calcium mobilization. Br J Pharmacol, 152(1):73-82. [12]Chen CL, Chi CW, Liu TY, 2000. Enhanced hydroxychavicol-induced cytotoxic effects in glutathione-depleted HepG2 cells. Cancer Lett, 155(1):29-35. [13]Chowdhury AA, Chaudhuri J, Biswas N, et al., 2013. Synergistic apoptosis of CML cells by buthionine sulfoximine and hydroxychavicol correlates with activation of aif and GSH-ROS-JNK-ERK-iNOS pathway. PLoS ONE, 8(9):e73672. [14]Dhanasekaran DN, Reddy EP, 2008. JNK signaling in apoptosis. Oncogene, 27(48):6245-6251. [15]Dhillon AS, Hagan S, Rath O, et al., 2007. MAP kinase signalling pathways in cancer. Oncogene, 26(22):3279-3290. [16]Garodia P, Ichikawa H, Malani N, et al., 2007. From ancient medicine to modern medicine: ayurvedic concepts of health and their role in inflammation and cancer. J Soc Integr Oncol, 5(1):25-37. [17]Garufi A, Pistritto G, Cirone M, et al., 2016. Reactivation of mutant p53 by capsaicin, the major constituent of peppers. J Exp Clin Cancer Rese, 35:136. [18]Gokare P, Finnberg NK, Abbosh PH, et al., 2017. P53 represses pyrimidine catabolic gene dihydropyrimidine dehydrogenase (DPYD) expression in response to thymidylate synthase (TS) targeting. Sci Rep, 7:9711. [19]Gundala SR, Aneja R, 2014. Piper betle leaf: a reservoir of potential xenohormetic nutraceuticals with cancer-fighting properties. Cancer Prev Res, 7(5):477-486. [20]Gundala SR, Yang CH, Mukkavilli R, et al., 2014. Hydroxychavicol, a betel leaf component, inhibits prostate cancer through ROS-driven DNA damage and apoptosis. Toxicol Appl Pharmacol, 280(1):86-96. [21]Hanahan D, Weinberg RA, 2011. Hallmarks of cancer: the next generation. Cell, 144(5):646-674. [22]Jeng JH, Ho YS, Chan CP, et al., 2000. Areca nut extract up-regulates prostaglandin production, cyclooxygenase-2 mRNA and protein expression of human oral keratinocytes. Carcinogenesis, 21(7):1365-1370. [23]Jeng JH, Chang MC, Hahn LJ, 2001. Role of areca nut in betel quid-associated chemical carcinogenesis: current awareness and future perspectives. Oral Oncol, 37(6):477-492. [24]Jeng JH, Chen SY, Liao CH, et al., 2002. Modulation of platelet aggregation by areca nut and betel leaf ingredients: roles of reactive oxygen species and cyclooxygenase. Free Radic Biol Med, 32(9):860-871. [25]Jeng JH, Wang YJ, Chang WH, et al., 2004. Reactive oxygen species are crucial for hydroxychavicol toxicity toward KB epithelial cells. Cell Mol Life Sci, 61(1):83-96. [26]Kitagishi Y, Kobayashi M, Matsuda S, 2012. Protection against cancer with medicinal herbs via activation of tumor suppressor. J Oncol, 2012:236530. [27]Kumar N, Misra P, Dube A, et al., 2010. Piper betle Linn. a maligned Pan-Asiatic plant with an array of pharmacological activities and prospects for drug discovery. Curr Sci, 99(7):922-932. [28]Longley DB, Harkin DP, Johnston PG, 2003. 5-Fluorouracil: mechanisms of action and clinical strategies. Nat Rev Cancer, 3(5):330-338. [29]Majumdar AG, Subramanian M, 2019. Hydroxychavicol from Piper betle induces apoptosis, cell cycle arrest, and inhibits epithelial-mesenchymal transition in pancreatic cancer cells. Biochem Pharmacol, 166:274-291. [30]Martins CP, Brown-Swigart L, Evan GI, 2006. Modeling the therapeutic efficacy of p53 restoration in tumors. Cell, 127(7):1323-1334. [31]Ng PL, Rajab NF, Then SM, et al., 2014. Piper betle leaf extract enhances the cytotoxicity effect of 5-fluorouracil in inhibiting the growth of HT29 and HCT116 colon cancer cells. J Zhejiang Univ-Sci B (Biomed & Biotechnol), 15(8):692-700. [32]Ozaki T, Nakagawara A, 2011. Role of p53 in cell death and human cancers. Cancers, 3(1):994-1013. [33]Paranjpe R, Gundala SR, Lakshminarayana N, et al., 2013. Piper betel leaf extract: anticancer benefits and bio-guided fractionation to identify active principles for prostate cancer management. Carcinogenesis, 34(7):1558-1566. [34]Rahman AA, Jamal ARA, Harun R, et al., 2014. Gamma-tocotrienol and hydroxy-chavicol synergistically inhibits growth and induces apoptosis of human glioma cells. BMC Complement Altern Med, 14:213. [35]Sarkar FH, Li YW, Wang ZW, et al., 2009. Cellular signaling perturbation by natural products. Cell Signal, 21(11):1541-1547. [36]Slattery ML, Lundgreen A, Wolff RK, 2012. MAP kinase genes and colon and rectal cancer. Carcinogenesis, 33(12): 2398-2408. [37]Sui XB, Kong N, Wang X, et al., 2014. JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy. Sci Rep, 4:4694. [38]Sung B, Prasad S, Yadav VR, et al., 2012. Cancer cell signaling pathways targeted by spice-derived nutraceuticals. Nutr Cancer, 64(2):173-197. [39]Takayama T, Miyanishi K, Hayashi T, et al., 2006. Colorectal cancer: genetics of development and metastasis. J Gastroenterol, 41(3):185-192. [40]Thornton TM, Rincon M, 2009. Non-classical p38 MAP kinase functions: cell cycle checkpoints and survival. Int J Biol Sci, 5(1):44-51. [41]Trivedy CR, Craig G, Warnakulasuriya S, 2002. The oral health consequences of chewing areca nut. Addict Biol, 7(1):115-125. [42]Wagner EF, Nebreda ÁR, 2009. Signal integration by JNK and p38 MAPK pathways in cancer development. Nat Rev Cancer, 9(8):537-549. [43]Widowati W, Wijaya L, Wargasetia TL, et al., 2013. Antioxidant, anticancer, and apoptosis-inducing effects of Piper extracts in HeLa cells. J Exp Integr Med, 3(3):225-230. [44]Wigmore PM, Mustafa S, El-Beltagy M, et al., 2010. Effects of 5-FU. In: Raffa RB, Tallarida RJ (Eds.), Chemo Fog: Cancer Chemotherapy-Related Cognitive Impairment. Springer, New York, p.157-164. [45]Wiman KG, 2010. Pharmacological reactivation of mutant p53: from protein structure to the cancer patient. Oncogene, 29(30): 4245-4252. [46]Zawacka-Pankau J, Selivanova G, 2015. Pharmacological reactivation of p53 as a strategy to treat cancer. J Intern Med, 277(2):248-259. [47]Zhang N, Yin Y, Xu SJ, et al., 2008. 5-Fluorouracil: mechanisms of resistance and reversal strategies. Molecules, 13(8):1551-1569. Journal of Zhejiang University-SCIENCE, 38 Zheda Road, Hangzhou
310027, China
Tel: +86-571-87952783; E-mail: cjzhang@zju.edu.cn Copyright © 2000 - 2024 Journal of Zhejiang University-SCIENCE |
Open peer comments: Debate/Discuss/Question/Opinion
<1>