Alpha-2 Heremans Schmid Glycoprotein (AHSG) promotes the proliferation of bladder cancer cells by regulating the TGF-β signalling pathway.
Alpha-2 Heremans Schmid Glycoprotein (AHSG) promotes the proliferation of bladder cancer cells by regulating the TGF-β signalling pathway.
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DOI：
10.1080/21655979.2022.2081465
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发表时间：
2022-06
期刊：
影响因子：
4.9
通讯作者：
中科院分区：
文献类型：
--
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膀胱癌（BC）是最常见的泌尿道恶性肿瘤之一，并且是全球第十大最常见的癌症。α-2 Heremans Schmid糖蛋白（AHSG）是一种多功能蛋白，在多种肿瘤的进展中发挥不同的作用。然而，AHSG在BC发生和发展中的作用和机制尚不清楚。使用蛋白质印迹和免疫组织化学评估BC细胞和组织中的AHSG表达。利用质粒和siRNA构建了在BC细胞中过表达和敲低AHSG的载体。进行了一系列功能实验，包括CCK 8、平板克隆形成和流式细胞术，以评估细胞增殖和周期。AHSG在BC细胞和组织中的表达高于正常膀胱上皮细胞和非肿瘤组织。在功能上，AHSG的过表达可显著促进BC细胞的增殖，并使细胞从G1期进入S期，而AHSG的敲低则相反;此外，Western blot结果显示AHSG的表达水平与Smad 2/3蛋白的磷酸化水平呈负相关，Smad 2/3蛋白是传统TGF-β信号通路的关键下游分子，提示AHSG可拮抗传统的TGF-β信号通路。ELISA检测BC患者尿液中AHSG的表达水平明显高于健康人，具有特异性。结论AHSG可能是一种新的乳腺癌标志物，通过调节TGF-β信号通路促进乳腺癌细胞增殖。
Bladder cancer (BC) is one of the most common urinary tract malignancies and is the tenth most common cancer globally. Alpha-2 Heremans Schmid Glycoprotein (AHSG) is a multifunctional protein that plays different roles in the progression of multiple tumors. However, the role and mechanism of AHSG in the development and progression of BC are unknown. AHSG expression was assessed in BC cells and tissues using western blot and immunohistochemistry. Using plasmid and siRNA, overexpressed and knocked down AHSG in BC cells were constructed. A series of functional experiments, including CCK8, plate clone formation, and flow cytometry, were performed to evaluate cell proliferation and cycle. AHSG was expressed higher in BC cells and tissues than in normal bladder epithelial cells and non-tumor tissues. Functionally, the overexpression of AHSG significantly increased the proliferation of BC cells and promoted the cell cycle from G1 to the S phase, whereas the knockdown of AHSG gave the opposite result.Additionally, western blot results revealed that AHSG expression level was negatively correlated with the phosphorylation level of Smad2/3 protein, a key downstream molecule of the traditional TGF-β signaling pathway, suggesting that AHSG could antagonize the traditional TGF-β signaling pathway. Finally, the expression level of AHSG in the urine of BC patients was significantly higher than that of healthy subjects by ELISA, with specificity. Our study concluded that AHSG might be a novel marker of BC that promotes the proliferation of BC cells by regulating the TGF-β signaling pathway.
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