Glioblastoma (GBM) is a deadly brain tumor with a bleak prognosis. In recent years, the copine III (CPNE3) protein was discovered to be associated to metastasis across various types of malignancies. Nevertheless, its function has not been well documented in glioma. This study characterizes CPNE3 expression in GBM along with its impact and underlying molecular mechanism with regards to cellular migration, invasion and proliferation. Immunohistochemistry was used to characterizes CPNE3 expression in the glioma tissues. Then, knockdown of CPNE3 expression was used to analyze the role of CPNE3 in GBM cell viability, migration, invasion. Western blot analysis was performed to measure the protein levels of FAK signaling pathway. We found that GBM tissues had higher CPNE3 expressions as compared to those in normal brain tissues. CPNE3 silencing in GBM cells impaired the migratory, invasive and proliferative abilities of GBM cells that can be attributed to inactivation of the FAK signaling pathway. Collectively, these findings highlight the role of CPNE3 as a new biomarker, offering deeper insights into its carcinogenic role in GBM.

胶质母细胞瘤 (GBM) 是一种致命的脑肿瘤，预后不佳。近年来，人们发现 copine III (CPNE3) 蛋白与各种恶性肿瘤的转移有关。然而，其在胶质瘤中的功能尚未得到很好的记录。本研究表征了 GBM 中 CPNE3 的表达及其对细胞迁移、侵袭和增殖的影响和潜在分子机制。免疫组织化学用于表征神经胶质瘤组织中 CPNE3 的表达。然后，通过抑制 CPNE3 表达来分析 CPNE3 在 GBM 细胞活力、迁移、侵袭中的作用。进行蛋白质印迹分析以测量 FAK 信号通路的蛋白质水平。我们发现与正常脑组织相比，GBM 组织具有更高的 CPNE3 表达。GBM 细胞中 CPNE3 的沉默损害了 GBM 细胞的迁移、侵袭和增殖能力，这可归因于 FAK 信号通路的失活。总的来说，这些发现突出了 CPNE3 作为新生物标志物的作用，为其在 GBM 中的致癌作用提供了更深入的见解。