[1]严成梅　潘松英　陈子琪　石凤梅　梁彩月　何永华.阴离子通道CFTR在双酚A致前列腺癌细胞凋亡的机制研究[J].大众科技,2020,22(10):68-71.
　Study on the Mechanism of Anion Channel CFTR in Bisphenol A-induced Apoptosis of Prostate Cancer Cells[J].Popular Science & Technology,2020,22(10):68-71.
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阴离子通道CFTR在双酚A致前列腺癌细胞 凋亡的机制研究()
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《大众科技》[ISSN:1008-1151/CN:45-1235/N]

卷:
22
期数:
2020年10
页码:
68-71
栏目:
医药与卫生
出版日期:
2020-10-20

文章信息/Info

Title:
Study on the Mechanism of Anion Channel CFTR in Bisphenol A-induced Apoptosis of Prostate Cancer Cells
作者:
严成梅　潘松英　陈子琪　石凤梅　梁彩月　何永华
（桂林医学院公共卫生学院，广西 桂林 541100）
关键词:
囊性纤维化跨膜传导调节蛋白; 双酚A; 前列腺癌; 细胞凋亡
Keywords:
cystic fibrosis transmembrane conductance regulator bisphenol A prostate cancer cell apoptosis
文献标志码:
A
摘要:
目的：探讨阴离子通道囊性纤维化跨膜传导调节蛋白（CFTR）表达水平与双酚A致前列腺癌细胞系凋亡中的机制。方法：将前列腺癌细胞系PC-3和LNCaP按染毒剂量分为DMSO溶剂对照组、0 µM组、低、中、高剂量组，分别暴露于含不同染毒剂量的溶液24 h。用MTT和酶联免疫吸附法（ELISA）检测BPA对细胞的毒性反应；采用酶标仪检测ATP的浓度；ELISA法检测经细胞系中cAMP和CFTR的表达水平；Western-blotting法检测MAPKα、BCl-2和Bax的浓度；Annexin-FITC与PI染色-流式细胞仪定量检测细胞凋亡水平。用单因素方差分析比较组间差异。结果：经不同浓度BPA染毒24 h后，PC-3和LNCaP细胞的细胞存活率随着BPA浓度的增加而降低；cAMP、CFTR和ATP的表达水平降低；Bax蛋白表达增加而Bcl-2蛋白表达减少，AMPKα激酶表达增加，细胞凋亡数目增加。结论：BPA诱导的前列腺癌可能与离子通道CFTR影响ATP合成、细胞凋亡途径有关。
Abstract:
Objective: To explore the mechanism of anion channel cystic fibrosis transmembrane conductance regulator (CFTR) expression and bisphenol A-induced apoptosis in prostate cancer cell lines. Methods: The prostate cancer cell lines PC-3 and LNCaP were divided into DMSO solvent control group, 0 μM group, low, medium, and high dose groups according to the exposure dose. They were respectively exposed to solutions containing different doses for 24 hours. MTT and ELISA were used to detect the toxicity of BPA on cells. ATP concentration was measured by a microplate reader. ELISA was used to detect the expression levels of cAMP and CFTR in cell lines. Western-blotting was used to detect MAPKα and Bcl-2 and Bax concentrations. Annexin V-FITC staining and flow cytometry was applied to quantitatively determine apoptosis levels. Variation between groups was compared with one-way analysis of variance. Results: After treated with different concentrations of BPA for 24 hours, the cell viability of PC-3 and LNCaP cells was decreased with increasing BPA concentration. The expression levels of cAMP, CFTR, ATP decreased Bax protein expression increased while Bcl-2 protein expression decreased, AMPKα expression increased, and the number of apoptosis increased. Conclusion: BPA-induced prostate cancer perhaps is possibly relevant with the anion channel CFTR by affecting ATP synthesis and cell apoptosis.

参考文献/References:

[1]　韩仁强，武鸣，陈万青，等. 2003－2007年中国前列腺癌发病与死亡分析[J]. 中国肿瘤，2012(11): 805-811. [2]　吴同俊，石峻岭，周志俊. 双酚A的人群接触与生物监测[J]. 中国职业医学，2006，33(2): 132-134. [3]　Seachrist D D, Bonk K W, Ho S M, et al. A review of the carcinogenic potential of bisphenol A[J]. Reproductive Toxicology, 2016, 59: 167-182. [4]　Kim K, Lee H, Choi K. Bisphenol A and phthalate stimulated the growth of human prostate cancer cells and altered downstream target genes of ras signaling pathway[J]. Endocrine, 2012, 29:751. [5]　Pardo L A, Stühmer W. The roles of K(+) channels in cancer[J]. Nature Reviews. Cancer, 2014, 14(1): 39-48. [6]　Tomaskova Z, Ondrias K. Mitochondrial chloride channels- What are they for?[J]. FEBS Letters, 2010, 584: 2085-2092. [7]　Zhu Q, Li H, Liu Y, et al. Knockdown of CFTR enhances sensitivity of prostate cancer cells to cisplatin via inhibition of autophagy[J]. Neoplasma, 2017, 64(5): 709-717. [8]　万洪磊，谭超，刘升学，等. 阴离子通道CFTR表达水平与双酚A损伤小鼠精子活性的关系[J]. 毒理学杂志，2017，31(6): 471-473. [9]　Insel P A, Zhang L, Murray F, et al. Cyclic AMP is both a pro-apoptotic and anti-apoptotic second messenger[J]. Acta Physiologica , 2011, 204(2): 277-287. [10] Hardie D G, Ross F A, Hawley S A. AMPK: a nutrient and energy sensor that maintains energy homeostasis[J]. Nature Reviews Molecular Cell Biology, 2012, 13: 251-262. [11] Lieberthal W, Zhang L, Patel V A, et al. AMPK protects proximal tubular cells from stress-induced apoptosis by an ATP-independent mechanism: potential role of Akt activation[J]. American Journal of Physiology Renal Physiology, 2011, 301(6): F1177-F1192. [12] Lin V C H, Tsai Y C, Lin J N, et al. Activation of AMPK by pterostilbene suppresses lipogenesis and cell-cycle progression in p53 positive and negative human prostate cancer cells[J]. Journal of Agricultural and Food Chemistry, 2012, 60(25): 6399-6407. [13] Desiniotis A, Schafer G, Klocker H, et al. Enhanced antiproliferative and proapoptotic effects on prostate cancer cells by simultaneously inhibiting androgen receptor and cAMP-dependent protein kinase A[J]. International Journal of Cancer, 2010, 126(3): 775-789. [14] 李广博，张淑君，姚婕，等. 程序性细胞死亡机制的研究进展[J]. 现代生物医学进展，2017，17(35): 6992-6996.

备注/Memo

备注/Memo:
【收稿日期】2020-08-06 【作者简介】严成梅（1997－），女，广西岑溪人，桂林医学院公共卫生学院学生，研究方向为环境与职业医学。 【通信作者】何永华（1969－），桂林医学院公共卫生学院教授，博士，研究方向为环境与职业医学。
更新日期/Last Update: 2020-11-20