Protein- or peptide-based therapeutics have emerged as an innovative strategy for the treatment of cancer. Our previous research demonstrated that tripartite motif 9 short isoform (TRIM9s) is a tumor suppressor in glioma. In this report, we investigated whether a new peptide derived from TRIM9s, named T9sP, inhibits glioma progression and determined the possible molecular mechanism. The CCK-8 proliferation assay was performed in LN229 and U251 glioma cells. The scratch-wound assay was used to determine the migration of the cells. Apoptosis was assessed by flow cytometry using Annexin V-FITC/PI double staining method. The relative protein expression levels were detected by immunoblot analysis. The cell-penetrating peptide TAT was fused with T9sP to form TAT-T9sP. TAT-T9sP efficiently penetrated through the cell membrane of both LN229 and U251 cells. TAT-T9sP inhibited proliferation and migration and promoted apoptosis of glioma cells. TAT-T9sP activated p38 signaling by upregulating MKK6, and a p38 inhibitor, SB203580, reversed the inhibitory effects of TAT-T9sP on glioma cells. These results indicated the potential of TAT-T9sP for the development of a new anti-glioma medicine.

中文翻译：

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一种新型抗肿瘤肽通过调节 MKK6/p38 信号通路抑制胶质瘤细胞增殖和迁移并促进细胞凋亡。

基于蛋白质或肽的疗法已成为治疗癌症的创新策略。我们之前的研究表明，三联基序 9 短同种型 (TRIM9s) 是神经胶质瘤的肿瘤抑制因子。在本报告中，我们研究了一种名为 T9sP 的源自 TRIM9s 的新肽是否抑制胶质瘤进展并确定了可能的分子机制。CCK-8 增殖试验在 LN229 和 U251 神经胶质瘤细胞中进行。划伤试验用于确定细胞的迁移。使用膜联蛋白 V-FITC/PI 双染色法通过流式细胞术评估细胞凋亡。通过免疫印迹分析检测相对蛋白质表达水平。细胞穿透肽TAT与T9sP融合形成TAT-T9sP。TAT-T9sP 有效地穿透 LN229 和 U251 细胞的细胞膜。TAT-T9sP抑制胶质瘤细胞的增殖和迁移并促进其凋亡。TAT-T9sP 通过上调 MKK6 激活 p38 信号传导，并且 p38 抑制剂 SB203580 逆转了 TAT-T9sP 对神经胶质瘤细胞的抑制作用。这些结果表明 TAT-T9sP 具有开发新的抗神经胶质瘤药物的潜力。