Bladder cancer (BLCA) is a prevalent malignancy of the urinary system, associated with a high recurrence rate and poor prognosis.FAM111B, which encodes a protein containing a trypsin-like cysteine/serine peptidase domain, has been implicated in the progression of various human cancers; however, its involvement in BLCA remains unclear. In this study, we investigated the expression ofFAM111Bgene in tumor tissues compared to para-tumor tissues using immunohistochemistry and observed a significantly higherFAM111Bgene expression in tumor tissues. Furthermore, analysis of clinical characteristics indicated that the increasedFAM111Bgene expression correlated with lymphatic metastasis and reduced overall survival. To investigate its functional role, we employedFAM111B-knockdown BLCA cell models and performed cell proliferation, wound-healing, transwell, and flow cytometry assays. The results showed that decreasedFAM111Bgene expression inhibited proliferation and migration but induced apoptosis in BLCA cells. In vivo experiments further validated thatFAM111Bknockdown suppressed tumor growth. Overall, our findings suggest thatFAM111Bacts as an oncogene in BLCA, playing a critical role in tumorigenesis, progression, and metastasis of BLCA. In conclusion, we have demonstrated a strong correlation between the expression ofFAM111Bgene and the development, progression, and metastasis of bladder cancer (BLCA). Thus,FAM111Bis an oncogene associated with BLCA and holds promise as a molecular target for future treatment of this cancer.
膀胱癌（BLCA）是泌尿系统常见的恶性肿瘤，具有高复发率和不良预后。FAM111B基因编码一种含有胰蛋白酶样半胱氨酸/丝氨酸肽酶结构域的蛋白，已被证实参与多种人类癌症的进展，但其在膀胱癌中的作用尚不明确。本研究通过免疫组化检测发现，与癌旁组织相比，膀胱癌组织中FAM111B基因表达显著升高。临床特征分析进一步表明，FAM111B高表达与淋巴结转移及患者总生存期缩短相关。为探究其功能作用，我们构建了FAM111B敲低的膀胱癌细胞模型，并通过细胞增殖、划痕愈合、Transwell及流式细胞术实验发现，降低FAM111B表达可抑制膀胱癌细胞的增殖与迁移，并诱导细胞凋亡。体内实验进一步证实，敲低FAM111B能够抑制肿瘤生长。综上所述，我们的研究结果表明FAM111B在膀胱癌中发挥癌基因功能，对膀胱癌的发生、进展及转移具有重要作用。因此，FAM111B是与膀胱癌相关的癌基因，有望成为未来治疗该癌症的分子靶点。
肿瘤(癌症)患者之家