Article(id=1292130429168022300, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.05.008, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1768147200000, receivedDateStr=2026-01-12, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997500935, onlineDateStr=2026-08-06, pubDate=1773676800000, pubDateStr=2026-03-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997500935, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997500935, creator=13701087609, updateTime=1785997500935, updator=13701087609, issue=Issue{id=1292130254689165893, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='5', pageStart='601', pageEnd='750', issueExtLink='null', onlineDate='null', pubDate='1773676800000', pubDateStr='2026-03-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785997459337, creator='13701087609', updateTime=1786014469153, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201599108141219, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201599108141220, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=686, endPage=692, ext={EN=ArticleExt(id=1292130431122567965, articleId=1292130429168022300, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of bicalutamide affecting the malignant biological behaviors of prostate cancer LNCaP cells by regulating the MAPK-ERK signaling pathway through CDH7, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effects of bicalutamide (BIC) on the malignant biological behavior of prostate cancer LNCaP cells through cadherin 7 (CDH7), and to explore its possible mechanism of action.
Methods This study was divided into two parts, animal experiment and cell experiment. In animal experiment, 30 Balb/c male nude mice were randomly divided into animal blank control group (daily gavage of 10 mL·kg-1 0.5% carboxymethyl cellulose sodium solution), animal positive control group (daily gavage of 10 mL·kg-1 enzalutamide) and animal experimental group (daily gavage of 25 mg·kg-1 BIC), with 10 nude mice in each group. All mice were treated with subcutaneous injection of LNCaP cell suspension to establish a xenograft model and each group was continuously treated for 28 days. The tumor volume of nude mice in each group was recorded every 7 days; tumor tissues were collected 24 h after drug withdrawal; the expression of proliferating cell nuclear antigen (PCNA) protein was detected by immunohistochemistry. In cell experiment, LNCaP cells were divided into cell blank control group (normal culture, no treatment), cell positive control group (treated with enzalutamide 1 μM), cell experimental group (treated with BIC 50 μM), oe-NC group (transfected with oe-NC plasmid and then treated with BIC 50 μM), and oe-CDH7 group (transfected with oe-CDH7 plasmid and then treated with BIC 50 μM). The relative expression levels of CDH7 mRNA in cells was detected by real-time fluorescence quantitative polymerase chain reaction method. The cell invasion ability and apoptosis rate were detected by Transwell assay and terminal-deoxynucleotidyl transferase mediated nick end labeling method, respectively. The activities of superoxide dismutase (SOD) and the levels of malondialdehyde (MDA) were detected by enzyme-linked immunosorbent assay. The relative expression levels of CDH7 and proteins related to relevant pathways were detected by Western blot.
Results In animal experiments, the tumor volume on day 21 of animal blank control group, animal positive control group and animal experimental group were (622.30±131.15), (411.90±72.07) and (467.40±63.92) mm3, respectively; the tumor volumes on day 28 were (1 189.50±225.95), (729.40±142.90) and (688.60±89.07) mm3, respectively; and the relative expression levels of PCNA protein were 1.00±0.11, 0.28±0.09 and 0.33±0.07, respectively. There were statistically significant differences compared animal positive control group or animal experimental group with the control group (all P<0.001). In cell experiments, the relative expression levels of CDH7 mRNA in the cell blank control group, cell positive control group, cell experimental group, oe-NC group and oe-CDH7 group were 1.00±0.16, 0.35±0.07, 0.40±0.05, 0.37±0.05 and 3.12±0.34, respectively; the number of cell invasions were (134.26±24.97), (57.63±11.53), (66.34±11.84), (61.17±9.12) and (98.08±15.88) pieces, respectively; the MDA levels were (126.94±20.81), (257.63±46.19), (239.21±29.32), (244.35±38.46) and (187.79±25.35) pg·mL-1, respectively; the apoptosis rates were (4.54±0.87)%, (53.27±6.14)%, (47.13±7.15)%, (51.76±9.59)% and (17.49±3.48) %, respectively; the relative expression levels of extracellular signal-regulated kinase 1/2 (ERK1/2) protein were 1.00±0.12, 0.44±0.06, 0.39±0.05, 0.41±0.03 and 0.67±0.11, respectively. Compared cell positive control group, or cell experimental group with cell blank control group, compared oe-CDH7 group with oe-NC group, the above indicators were all statistically significantly different (all P<0.001).
Conclusion BIC could inhibit the invasion of prostate cancer LNCaP cells and promote their apoptosis through CDH7, and the mechanism of action may be related to the inhibition of mitogen-activated protein kinase (MAPK)-ERK signaling pathway activation.
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目的 探究比卡鲁胺（BIC）通过钙黏蛋白7（CDH7）对前列腺癌LNCaP细胞恶性生物学行为的影响，并探讨其可能的作用机制。
方法 本研究分为动物实验和细胞实验2部分。在动物实验部分，将30只Balb/c雄性裸鼠随机分为动物空白对照组（每日灌胃10 mL·kg-1 0.5%羧甲基纤维素钠溶液）、动物阳性对照组（每日灌胃10 mg·kg-1恩杂鲁胺）和动物实验组（每日灌胃25 mg·kg-1 BIC），每组10只裸鼠。所有裸鼠均用皮下注射LNCaP细胞悬液的方法建立移植瘤模型，各组持续处理28 d，每7 d记录各组裸鼠肿瘤体积；停药24 h后收集肿瘤组织，用免疫组化法检测增殖细胞核抗原（PCNA）蛋白表达。在细胞实验部分，将LNCaP细胞分为细胞空白对照组（正常培养，不做处理）、细胞阳性对照组（恩杂鲁胺1 μM处理）、细胞实验组（BIC 50 μM处理）、oe-NC组（转染oe-NC质粒+BIC 50 μM处理）和oe-CDH7组（转染oe-CDH7质粒+BIC 50 μM处理）。用实时荧光定量聚合酶链式反应法检测细胞CDH7 mRNA表达水平，用Transwell和原位末端标记法分别检测细胞侵袭能力和凋亡率，用酶联免疫吸附法检测超氧化物歧化酶活性（SOD）和丙二醛（MDA）水平，用蛋白免疫印迹法检测CDH7和丝裂原活化蛋白激酶（MAPK）-细胞外信号调节激酶（ERK）相关通路蛋白表达水平。
结果 在动物实验部分，动物空白对照组、动物阳性对照组和动物实验组第21天的肿瘤体积分别为（622.30±131.15）、（411.90±72.07）和（467.40±63.92）mm3，第28天的肿瘤体积分别为（1 189.50±225.95）、（729.40±142.90）和（688.60±89.07）mm3，PCNA蛋白相对表达水平分别为1.00±0.11、0.28±0.09和0.33±0.07。动物阳性对照组和动物实验组的上述指标与动物空白对照组比较，在统计学上差异均有统计学意义（均P<0.001）。在细胞实验部分，细胞空白对照组、细胞阳性对照组、细胞实验组、oe-NC组和oe-CDH7组的CDH7 mRNA相对表达水平分别为1.00±0.16、0.35±0.07、0.40±0.05、0.37±0.05和3.12±0.34，细胞侵袭数分别为（134.26±24.97）、（57.63±11.53）、（66.34±11.84）、（61.17±9.12）和（98.08±15.88）个，MDA水平分别为（126.94±20.81）、（257.63±46.19）、（239.21±29.32）、（244.35±38.46）和（187.79±25.35）pg·mL-1，细胞凋亡率分别为（4.54±0.87）%、（53.27±6.14）%、（47.13±7.15）%、（51.76±9.59）%和（17.49±3.48）%，ERK1/2分别为1.00±0.12、0.44±0.06、0.39±0.05、0.41±0.03和0.67±0.11。上述指标在细胞阳性对照组、细胞实验组与细胞空白对照组之间比较，在oe-CDH7组与oe-NC组之间比较，在统计学上差异均有统计学意义（均P<0.001）。
结论 BIC能够抑制前列腺癌LNCaP细胞的侵袭并促进凋亡，其机制可能与下调CDH7抑制MAPK-ERK信号通路激活有关。
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