Growth factor receptor-bound protein 7 (GRB7) has been found closely related to the occurrence and development of various tumors, but its function in bladder cancer has not yet been elucidated. The study is aiming at investigating the expression and function of GRB7 in bladder cancer. The Cancer Genome Atlas (TCGA) database was selected to analyze mRNA levels of GRB7 in bladder cancer. RT-qPCR and Western blot were conducted to detect the expression of GRB7 in normal bladder epithelial cells, seven bladder cancer cell lines and eight pairs of malignant/nonmalignant bladder tissues. The role of GRB7 in tumor proliferation and tumorigenesis was explored by establishing stable cells, in vitro cell experiments and in vivo xenograft models. The molecular regulation mechanism of GRB7 in bladder cancer was investigated by treatment with AKT inhibitor. GRB7 mRNA was upregulated in bladder cancer samples compared with that in normal tissue samples. Overexpressing GRB7 significantly promoted the proliferation and tumorigenesis of bladder cancer. However, silencing GRB7 played the retarding part. GRB7 promoted G1/S transition by activating the AKT pathway. Our results indicate that GRB7 plays an important role in promoting proliferation and tumorigenesis of bladder cancer.

中文翻译：

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上调的 GRB7 通过 Phospho-AKT 通路促进膀胱癌的增殖和肿瘤发生

已经发现生长因子受体结合蛋白7（GRB7）与各种肿瘤的发生发展密切相关，但其在膀胱癌中的作用尚未阐明。该研究旨在研究 GRB7 在膀胱癌中的表达和功能。选择癌症基因组图谱（TCGA）数据库来分析膀胱癌中 GRB7 的 mRNA 水平。进行RT-qPCR和Western blot检测GRB7在正常膀胱上皮细胞、7个膀胱癌细胞系和8对恶性/非恶性膀胱组织中的表达。通过建立稳定细胞、体外细胞实验和体内实验探索GRB7在肿瘤增殖和肿瘤发生中的作用异种移植模型。通过AKT抑制剂治疗研究GRB7在膀胱癌中的分子调控机制。与正常组织样本相比，膀胱癌样本中的GRB7 mRNA上调。过表达 GRB7 显着促进膀胱癌的增殖和肿瘤发生。然而，沉默 GRB7 起到了阻碍作用。GRB7 通过激活 AKT 通路促进 G1/S 过渡。我们的研究结果表明，GRB7 在促进膀胱癌的增殖和肿瘤发生中起重要作用。