CD82 acts as a tumor suppressor in a series of steps in malignant progression. Here, we identified a novel function of CD82 on posttranslational regulating E-cadherin in prostate cancer. In our study, the declined expression of CD82 was verified in prostate cancer tissues and cell lines compared with normal tissue and cell lines. Functionally, CD82 inhibited cell migration and E-cadherin cleavage from the cell membrane in prostate cancer cell. Further study proved that a disintegrin and metalloproteinase ADAM17 as an executor of E-cadherin cleavage mediated the inhibitory regulation of CD82 in E-cadherin shedding in prostate cancer. Specifically, CD82 interacted with ADAM17 and inhibited its metalloprotease activity, which led to the descent of E-cadherin shedding. These results show a nuanced but important role of CD82 in nontranscriptional regulation of E-cadherin, which may help to understand the intricate regulation of dysfunctional adhesion molecule in cancer progression.

中文翻译：

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CD82 抑制前列腺癌中 ADAM17 依赖的 E-钙粘蛋白裂解和细胞迁移

CD82 在恶性进展的一系列步骤中充当肿瘤抑制因子。在这里，我们确定了 CD82 在前列腺癌中对 E-钙粘蛋白的翻译后调节的新功能。在我们的研究中，与正常组织和细胞系相比，前列腺癌组织和细胞系中 CD82 的表达下降。在功能上，CD82 抑制细胞迁移和 E-钙粘蛋白从前列腺癌细胞的细胞膜上裂解。进一步的研究证明，作为 E-cadherin 切割的执行者，解整合素和金属蛋白酶 ADAM17 介导了前列腺癌中 E-cadherin 脱落中 CD82 的抑制调节。具体而言，CD82 与 ADAM17 相互作用并抑制其金属蛋白酶活性，从而导致 E-钙粘蛋白脱落的下降。