转录因子 KLF7 高表达与前列腺癌发生的 相关性及其靶基因预测

李雪 , 唐慧, , 桑海明 , 李伟 , 王竞州 , 庞槐 , 张君

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石河子大学学报 ›› 2021, Vol. 39 ›› Issue (1) : 92-101. DOI: 10. 13880 /j. cnki. 65-1174 /n. 2021. 22. 002
医学·药学

转录因子 KLF7 高表达与前列腺癌发生的 相关性及其靶基因预测

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Correlation between overexpression of KLF7 and carcinogenesis of prostate cancer and its target gene prediction

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摘要

目的 探讨 KLF7 高表达与前列腺癌( PCa) 发生的相关性,并对其可能的下游靶基因进行筛选。方法 比较前 列腺增生( BPH) 患者( n = 22) 以及 PCa 患者( n = 30) 血糖、血脂及一般资料的差异; 调取石蜡包埋的前列腺组织标 本,运用免疫组织化学法检测组织中 KLF7 及其下游因子 IL-6,以及肿瘤发生相关因子 E-钙粘蛋白、Ki67 的表达 量。运用统计学方法,比较各因子在 BPH 和 PCa 患者前列腺组织中的表达差异,并分析 KLF7 表达与各因子之间 的相关性。运用 Cistrome Data Browser 数据库对 KLF7 可能的下游靶基因进行预测。结果 PCa 患者血清中总前列 腺特异性抗原( TPSA) 含量显著高于正常体检及 BPH 个体( P<0. 001) ; PCa 患者前列腺组织中 KLF7 及 IL-6 表达 量显著高于 BPH 患者前列腺组织( P<0. 05) ,肿瘤发生相关因子 Ki67 表达量显著高于 BPH 患者前列腺组织( P< 0. 05) ,E-钙粘蛋白的表达量在两组间无显著差异。相关性分析结果显示: 前列腺癌组织中 KLF7 的表达与患者血 清中 TPSA 含量显著正相关( r = 0. 465,P= 0. 001) ,与癌组织中 IL-6 的表达显著正相关( r = 0. 437,P = 0. 014) ,与癌 组织中 Ki67 的表达显著正相关( r = 0. 434,P = 0. 002) ,与癌组织中 E-钙粘蛋白的表达显著正相关( r = 0. 473,P = 0. 009) 。生物信息学分析结果显示: 转录因子 KLF7 可能通过调控肿瘤相关基因 STAT3,DDX20,ZNF233,ZNF581, ZNF487,ZNF580,ZNF391,ZNF793,HMGB1,DMAP1,CTNNB1,ZBTB45 等参与肿瘤的发生发展。结论 KLF7 高表达 可能是前列腺癌发生的危险因素,前列腺癌组织中 KLF7 的表达与 IL-6、Ki67 以及 E-钙粘蛋白的表达显著正相 关。KLF7 可能通过调控一系列肿瘤相关基因的表达参与肿瘤发生发展的过程

Abstract

Objective To investigate the correlation between KLF7 overexpression and the occurrence of prostate cancer ( PCa) ,and to screen and verify its potential downstream target genes. Methods Compare the differences of blood glucose,blood lipid and general data between BPH( Benign prostatic hyperplasia) patients ( n = 22) and patients with PCa ( n = 30) ; The paraffin-embedded prostate tissue samples were collected,and the expression levels of KLF7 and its downstream factors IL-6,and tumor-associated factors E-cadherin and Ki67 were detected by immunohistochemistry. Using statistical methods to compare the expression differences of various factors in pa- tients with BPH and PCa. Using bioinformatics methods to predict possible downstream target genes of KLF7. Results The serum TPSA content of PCa patients was significantly higher than that of normal physical examination and BPH individuals ( P<0. 001) ; The expression of KLF7 and IL-6 in prostate cancer tissues of PCa patients was significantly higher than that of prostate tissues of BPH patients ( P<0. 05) ,the expression level of Ki67 was significantly higher than that of prostate tissue in patients with BPH ( P<0. 05) ,and the expression level of E-cadherin was not significantly different between the two groups. The results of correlation analysis showed that the expression of KLF7 in prostate cancer tissue was significantly positively correlated with the TPSA( r = 0. 465,P = 0. 001) ,IL-6( r = 0. 437,P= 0. 014) ,Ki67( r = 0. 434,P= 0. 002) ,and E-cadherin( r = 0. 473,P = 0. 009) . The results of bioinformatics analysis showed that the transcription factor KLF7 may be involved in the occurrence and development of tumors by regulating tumor-related genes STAT3,DDX20,ZNF233,ZNF581,ZNF487,ZNF580,ZNF391,ZNF793,HMGB1,DMAP1,CTNNB1,ZBTB45 and so on. Conclusion High expression of KLF7 may be a risk factor for prostate cancer. The expression of KLF7 in prostate cancer tissue is significantly positively correlated with the expression of IL-6,Ki67 and E-cadherin. KLF7 may participate in the process of tumorigenesis by regulating the expression of a series of tumor-related genes.

关键词

KLF7 / IL-6 / Ki67 / E 钙粘蛋白 / 前列腺癌

Key words

KLF7 / IL-6 / Ki67 / E-cadherin / prostate cancer

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李雪 , 唐慧, , 桑海明 , 李伟 , 王竞州 , 庞槐 , 张君. 转录因子 KLF7 高表达与前列腺癌发生的 相关性及其靶基因预测. 石河子大学学报. 2021, 39(1): 92-101 https://doi.org/10. 13880 /j. cnki. 65-1174 /n. 2021. 22. 002
LI Xue , TANG Hui , , SANG Haiming , LI Wei , WANG Jingzhou , PANG Huai , ZHANG Jun . Correlation between overexpression of KLF7 and carcinogenesis of prostate cancer and its target gene prediction. Journal of Shihezi University. 2021, 39(1): 92-101 https://doi.org/10. 13880 /j. cnki. 65-1174 /n. 2021. 22. 002

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基金

国家自然科学基金项目( 81760518,81900707) ,新疆兵团重点领域创新团队项目( 2018CB002) ,新疆兵团国际合作 项目( 2016AH005) ,石河子大学科研项目( ZZZC201817A)
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