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| Effect of YWHAZ Gene on the Proliferation and Pigration of Prostate Cancer 22RV1 Cells |
| LI Yong1, ZHAO Jia-Fu2, LUO Bin-Jie1, CHEN Chen2, SONG Lin-Jin2, XU Hou-Qiang1,2,* |
1 Key laboratory of Plant Resource Conservation and Germplasm Innovation in Mountainous Region (Ministry of Education), Collaborative Innovation Center for Mountain Ecology & Agro-Bioengineering (CICMEA), Institute of Agro-bioengineering/College of Life Sciences, Guizhou University, Guiyang 550025, China;
2 Key Laboratory of Plateau Mountain Animal Genetics, Breeding and Reproduction, Ministry of Education, Guizhou University, Guiyang 550025, China |
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Abstract Prostate cancer is a heterogeneous disease with a high degree of clinical and genetic heterogeneity, thus providing multiple therapeutic targets.To investigate the expression profiles of 14-3-3 protein family isoforms in different cell lines of prostate cancer and to search for specific drug targets for the treatment of prostate cancer.The expression patterns of each isoform of the 14-3-3 protein family in different prostate cancer cell lines were analyzed by qPCR (real-time fluorescence quantitative PCR) in combination with the UALCAN-TCGA database. The effects of different expression levels on the proliferation and migration ability of 22RV1 cells were demonstrated by up- and down-regulating the expression of tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta (YWHAZ) gene using CCK-8 and cell scratch assay. It was found that the expression of YWHAZ in cancer tissues was lower than that in normal tissues when GLEASON SCORE was lower than 8, while the relative expression of YWHAZ in prostate cancer cell lines showed a significant upward trend in the middle and late stages as Gleason score (GS) was elevated. The results of CCK-8 assay and cell scratch assay revealed that the interference and overexpression of 14-3-3ζ expression levels in 22RV1 cells severely affected the proliferation and migration ability of the cells YWHAZ. The above results implied that YWHAZ may play a role as a proto-oncogene in the middle and late stages of prostate cancer development. The related results provide a theoretical basis and experimental ideas for the subsequent study of drugs targeting this gene.
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Received: 07 July 2021
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Corresponding Authors:
*gzdxxhq@163.com
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[1] 董正远, 杨清玲, 陈昌杰. 2020. 14-3-3ζ蛋白在乳腺癌发生发展中的作用研究进展[J]. 分子诊断与治疗杂志, 12(04): 538-541.
(Dong Z Y, Yang Q L, Chen C J.2020. Advances in the role of 14-3-3ζ proteins in the development of breast cancer[J]. Journal of Molecular Diagnosis and Therapy, 12(04): 538-541.)
[2] 韩雪娇, 李艳春, 孙立春, 等. 2017. 14-3-3ζ与恶性肿瘤关系的研究进展[J]. 实用肿瘤学杂志, 31(06): 543-547.
(Han X J, Li Y C, Sun L C, et al.2017. Advances in the relationship between 14-3-3ζ and malignant tumors[J]. Journal of Practical Oncology, 31(06): 543-547.)
[3] 简如丽, 刘霆. 2020. 14-3-3ζ蛋白在肝细胞癌发生发展中的作用及研究进展[J]. 中国普通外科杂志, 29(07): 884-889.
(Jian R L, Liu T.2020. 14-3-3ζ protein in the development of hepatocellular carcinoma[J]. Chinese Journal of General Surgery, 29(07): 884-889.)
[4] 李新军. 2020. MiR-30a通过靶向MYBL2、FOXD1和SOX4抑制前列腺癌雄激素非依赖性增殖的作用和机制研究[D].博士学位论文. 山东大学,导师: 韩博. pp. 129.
(Li X J.2020. Study of the role and mechanism of MiR-30a in inhibiting androgen-independent proliferation in prostate cancer by targeting MYBL2, FOXD1 and SOX4[D]. Thesis for Ph.D., Shandong University, Supervisor: Han B., pp. 129.)
[5] 梁蓉, 陈协群, 王哲, 等. 2013. 14-3-3ζ对HL-60和HL-60/VCR细胞增殖的抑制作用[J]. 中国实验血液学杂志, 21(04): 866-871.
(Liang R, Chen X Q, Wang Z.et al.2013. 14-Suphibition of 3-3 ζ on HL-60 and HL-60/VCR cell proliferation[J]. Chinese Journal of Experimental Haematology, 21(04): 866-871.)
[6] 凌人, 凌今, 陈仲华, 等. 2017. 14-3-3 zeta蛋白过表达与他莫昔芬治疗乳腺癌耐药的关系[J]. 温州医科大学学报, 47(03): 192-196.
(Ling R, Ling J, Chen Z H, et al.2017. Relationship between overexpression of 14-3-3 zeta protein and resistance to tamoxifen in the treatment of breast cancer[J]. Proceedings of Wenzhou Medical University, 47(03): 192-196.)
[7] 齐凤杰, 邸金娜, 赵树鹏. 2011. 乳腺癌中组织14-3-3σ和cyclin B1的表达及其临床意义[J]. 中国肿瘤生物治疗杂志, 18(02): 211-215.
(Qi F J, Di J N, Zhao S P.2011. Expression of tissue 14-3-3σand cyclin B1 in breast cancer and its clinical significance[J]. Chinese Journal of Tumor Biotherapy, 18(02): 211-215.)
[8] 王慧香, 翟建军. 2015. 凋亡抑制蛋白14-3-3ζ与肿瘤的关系[J]. 医学综述, 21(13): 2370-2373.
(Wang H X, Zhai J J.2015. Association of the apoptotic inhibitory protein 14-3-3ζ and the tumor[J]. Medical Review, 21(13): 2370-2373.)
[9] 袁亚丽. 2011. 靶向14-3-3ζ基因siRNA的重组腺相关病毒载体的构建与表达[D].硕士学位论文. 华南理工大学,导师: 曹以诚. pp. 78.
( Yuan Y L.2011. Construction and expression of recombinant adeno-associated viral vectors targeting siRNA of the 14-3-3 ζ gene[D]. Thesis for M.S., South China University of Technology. Supervisor: Cao Y C. pp. 78.)
[10] 曾琴. 2012. 14-3-3蛋白亚型在人胃癌组织中的表达及意义[D]. 硕士学位论文. 南昌大学, 导师: 尹东. pp. 43.
(Ceng Q.2012. Expression and significance of the 14-3-3 protein isoform in human gastric cancer tissues[D]. Thesis for M.S., Nanchang University,Supervisor: Yin D, pp. 43.)
[11] 张志兴, 敏秀梅, 宋果, 等. 2021. 14-3-3蛋白在水稻籽粒灌浆过程中的互作靶蛋白鉴定及其对外源激素的响应[J]. 中国农业科学, 54(12): 2523-2537.
(Zhang Z.X., Min X M, Song G, et al.2021. Identification of reciprocal targets of 14-3-3 proteins in rice grain grouting and its response to exogenous hormones[J]. Agricultural Science of China, 54(12): 2523-2537.)
[12] Andrews R K, Du X, Berndt M C.2007. The 14-3-3zeta-GPIb-IX-V complex as an antiplatelet target[J]. Drug News & Perspectives, 20(5): 285-292.
[13] Du M, Wang X, Yue Y W, et al.2016. Selection of reference genes in canine uterine tissues[J]. Genetics and Molecular Research, 15(2): DOI:10.4238/gmr.15028138.
[14] Fan X, Cui L, Zeng Y, et al.2019. 14-3-3 proteins are on the crossroads of cancer, aging, and age-related neurodegenerative disease[J]. International Journal of Molecular Sciences, 20(14): 3518.
[15] Hoffman R M, Meisner A L, Arap W, et al.2016. Trends in United States prostate cancer incidence rates by age and stage, 1995-2012[J]. Cancer Epidemiology, Biomarkers and Prevention, 25(2): 259-263.
[16] Kobayashi P E, Fonseca-Alves C E, Rivera-Calderon L G, et al.2018. Deregulation of E-cadherin, beta-catenin, APC and caveolin-1 expression occurs in canine prostate cancer and metastatic processes[J]. Research in Veterinary Science, 118: 254-261.
[17] Matta A, Masui O, Siu K W, et al.2016. Identification of 14-3-3zeta associated protein networks in oral cancer[J]. Proteomics, 16(7): 1079-1089.
[18] Matta A, Siu K W, Ralhan R.2012. 14-3-3 zeta as novel molecular target for cancer therapy[J]. Expert Opinion on Therapeutic Targets, 16(5): 515-523.
[19] Murata T, Takayama K, Urano T, et al.2012. 14-3-3zeta, a novel androgen-responsive gene, is upregulated in prostate cancer and promotes prostate cancer cell proliferation and survival[J]. Clin Cancer Research, 18(20): 5617-5627.
[20] Root A, Beizaei A, Ebhardt H A.2018. Structure-based assessment and network analysis of targeting 14-3-3 proteins in prostate cancer[J]. Molecular Cancer, 17: 156.
[21] Simooka H, Oyama T, Sano T, et al.2004. Immunohistochemical analysis of 14-3-3 sigma and related proteins in hyperplastic and neoplastic breast lesions, with particular reference to early carcinogenesis[J]. Pathology International, 54(8): 595-602.
[22] Stassen Q E M, Riemers F M, Reijmerink H, et al.2015. Reference genes for reverse transcription quantitative PCR in canine brain tissue[J]. BMC Research Notes, 8: 761.
[23] Waters D J, Chiang E C.2018. Five threads: How U-shaped thinking weaves together dogs, men, selenium, and prostate cancer risk[J]. Free Radical Biology And Medicine, 127: 36-45.
[24] Waters D J, Shen S, Glickman L T, et al.2005. Prostate cancer risk and DNA damage: Translational significance of selenium supplementation in a canine model[J]. Carcinogenesis, 26(7): 1256-1262.
[25] Zhao J, Xu H, Duan Z, et al.2020. miR-31-5p regulates 14-3-3 varepsilon to inhibit prostate cancer 22RV1 cell survival and proliferation via PI3K/AKT/Bcl-2 signaling pathway[J]. Cancer Management and Research, 12: 6679-6694. |
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