敲低B7-H4对MFC细胞增殖和肿瘤形成的影响及其机制

doi:10.3969/j.issn.1004-616x.2026.01.001

摘要/Abstract

摘要： 目的：探究协同共刺激分子B7-H4对小鼠胃癌MFC细胞增殖和肿瘤形成的影响及其可能的作用机制。方法：试验设B7-H4敲低组(转染B7-H4敲低慢病毒)和对照组(转染空载慢病毒)，通过慢病毒转染MFC细胞后分别采用逆转录实时荧光定量PCR (RT-PCR)和Western blot法检测转染后MFC细胞中B7-H4 mRNA和蛋白的表达。然后采用CCK-8和细胞划痕实验检测敲低B7-H4对MFC细胞增殖和迁移的影响。再将B7-H4敲低组和对照组MFC细胞注射到小鼠左侧上肢腋下皮下，通过成瘤实验探究B7-H4敲低对移植瘤形成的影响。分别采用RT-qPCR和Western blot法检测B7-H4、WNT家族成员7A (WNT7A)、STAT3在敲低的MFC细胞和小鼠移植瘤组织中表达水平的变化。结果： RT-qPCR和Western blot检测结果显示，与对照组比较，敲低组MFC细胞中B7-H4 mRNA和蛋白的表达水平均显著降低(P<0.01)，说明B7-H4敲低细胞株构建成功。敲低B7-H4后，与对照组相比，敲低组MFC细胞增殖和迁移能力均明显下降(P<0.01)；小鼠皮下成瘤实验中，敲低组小鼠的肿瘤体积和质量均明显降低(P<0.01)。RT-qPCR和Western blot实验结果表明，相较于对照组，敲低组B7-H4、WNT7A、p-STAT3的mRNA和蛋白表达水平在细胞和组织中均降低(均为P<0.01)，而总STAT3的表达水平无显著变化(P>0.05)。结论：敲低B7-H4可以抑制MFC细胞的增殖、迁移和肿瘤形成能力，其机制可能为B7-H4低表达时抑制WNT7A表达进而抑制STAT3的活化。

关键词: B7-H4, 细胞增殖, 细胞迁移, 肿瘤形成, WNT7A

Abstract: OBJECTIVE： To investigate effects of the co-stimulatory molecule B7-H4 on MFC cell proliferation and tumor formation， and to explore its potential mechanisms. METHODS： MFC cells were transfected with lentiviruses to knock down B7-H4 expression，and stable transfection cell lines were screened. The cells were divided into a knockdown group (transfected with B7-H4 knockdown lentivirus) and a control group (transfected with the empty vector lentivirus). Expression levels of B7-H4 mRNA and protein in MFC cells were detected using RT-qPCR and Western blot to evaluate knockdown effects. Impact of B7-H4 knockdown on MFC cell proliferation and migration was assessed through CCK-8 assay and cell scratch experiments. The stably transfected cells from both groups were then injected subcutaneously into mice， and tumor formation was evaluated through tumor transplantation experiments. Expression levels of B7-H4，WNT7A，and STAT3 in MFC cells and mouse tumor tissues were analyzed using RT-qPCR and Western blot. RESULTS： RT-qPCR and Western blot results showed that compared to the control group，expression levels of B7-H4 in the knockdown group were significantly reduced (P<0.01)，indicating successful construction of B7-H4 knockdown cell lines. In MFC cells， B7-H4 knockdown significantly reduced both proliferation and migration capacity compared to the control group (P<0.01). In subcutaneous tumor formation experiments， the tumor volume and mass in the knockdown group were significantly smaller than those in the control group (P<0.01). RT-qPCR and Western blot results demonstrated that expression levels of B7-H4， WNT7A， and p-STAT3 in the knockdown group were significantly lower than those in the control group (P<0.01). In contrast， total STAT3 expression showed no significant change (P>0.05). CONCLUSION： B7-H4 knockdown inhibited MFC cell proliferation and migration and affected tumor formation in MFC cells. Low expression of B7-H4 inhibited expression of WNT7A and STAT3.

Key words: B7-H4, cell proliferation, cell migration, tumor formation, WNT7A

中图分类号:

R735.2

郭雅, 郭腾, 刘明峰, 杜丽英, 问天娇, 陈欣然. 敲低B7-H4对MFC细胞增殖和肿瘤形成的影响及其机制[J]. 癌变·畸变·突变, 2026, 38(1): 1-6.

GUO Ya, GUO Teng, LIU Mingfeng, DU Liying, WEN Tianjiao, CHEN Xinran. The effect of B7-H4 knockdown on MFC cell proliferation and tumor formation[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2026, 38(1): 1-6.

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