研究动态
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细胞因子自主幅动因子受体通过调控细胞迁移和侵袭来促进胶质母细胞瘤的恶性化。

Autocrine motility factor receptor promotes the malignancy of glioblastoma by regulating cell migration and invasion.

发表日期:2023 Sep 13
作者: Yao Zhang, Xiuping Wang, Guanghui Chen, Yajing Lu, Qiang Chen
来源: Cell Death & Disease

摘要:

癌症患者死亡的重要原因之一是恶性转移,肿瘤细胞的侵袭和转移。转移也是各种肿瘤的基本生理特征和发病机制。先前发表的研究表明,自分泌动因子受体(AMFR)是肿瘤细胞迁移和侵袭的关键调控因子。同时,AMFR在食管肿瘤、胃肠道肿瘤和膀胱癌中高度表达,并参与其发病机制。然而,在胶质母细胞瘤中,AMFR的作用尚未报道。为了研究AMFR在胶质母细胞瘤细胞迁移和侵袭中的作用,我们使用siRNA使AMFR静默,并利用cDNA过度表达。采用免疫印迹分析和实时定量聚合酶链反应(PCR)评估AMFR的表达。我们进行了划痕愈合实验、细胞迁移实验和肿瘤球形体形成实验,以检测胶质母细胞瘤的侵袭和转移能力。该研究发现AMFR表达水平与临床样本中胶质瘤组织的恶性程度显著相关。AMFR静默降低了LN229细胞的迁移和侵袭能力。AMFR的过度表达显著增加了U251细胞的迁移和侵袭能力。该研究表明AMFR可能作为胶质母细胞瘤的临床治疗策略。
One of the important causes of death in cancer patients is malignant metastasis, invasion, and metastasis of tumor cells. Metastasis is also the most basic physiological characteristics and pathogenesis of various tumors. Previously published studies have suggested that autocrine motor factor receptor (AMFR) is the key regulator of tumor cell migration and invasion. Meanwhile, AMFR is highly expressed in esophageal tumors, gastrointestinal tumors, and bladder cancer, and it is also involved in its pathogenesis. However, the role of AMFR in glioblastoma has not been reported.In order to study the role of AMFR in the cell migration and invasion of glioblastoma, AMFR was silenced using siRNA and overexpressed using cDNA. Immunoblotting analysis and real-time quantitative polymerase chain reaction (PCR) were employed to assess the expression of AMFR. We conducted wound healing assay, cell migration assay, and tumorsphere formation assay to detect the invasion and metastatic ability of glioblastoma.This study found that the level of AMFR expression was significantly correlated with the malignant degree of glioma tissue in clinic samples. AMFR silencing decreased cell migration and invasion of LN229. Overexpression of AMFR significantly increased cell migration and invasion of U251.This study suggests that AMFR could be used as a therapeutic strategy for the clinical treatment of glioblastoma.