Inflammatory changes are involved in tumor cell proliferation, migration, and invasion. Tumor necrosis factor-α (TNF-α) and lipopolysaccharide (LPS) play important roles in inflammatory regulation during tumor development. Oct4 acts as a transcription factor that modulates inflammatory changes in mesenchymal stem cells. In this study, we explored the role of Oct4 in the invasion and migration of oral squamous cell carcinoma (OSCC) cells. LPS and TNF-α were used to treat the OSCC cell lines HN4 and CAL27 to induce inflammation. The generation of inflammatory cytokines, including TNF-α, interleukin (IL)-1β, and IL-6, was evaluated by enzyme-linked immunosorbent assay and real-time quantitative PCR. Western blot analysis was employed to detect the expression and phosphorylation of JNK1, p65, and STAT3, which are key modulators of inflammation. Wound scratch healing and transwell invasion assays were further used to determine the role of inflammation in the invasion and migration of OSCC cells. Robust inflammation was observed in HN4 and CAL27 cells treated with LPS and TNF-α. A marked increase in JNK1, p65, and STAT3 phosphorylation levels in OSCC cells was also detected after LPS and TNF-α treatment. The migration and invasion of HN4 and CAL27 cells were significantly boosted by stimulation with LPS and TNF-α. Furthermore, Oct4 mRNA and protein levels were significantly upregulated by stimulation with LPS and TNF-α. Silencing of Oct4 led to reduced inflammation and decreased levels of phosphorylated JNK1, p65, and STAT3 and impaired invasion and migration in LPS- and TNF-α-stimulated OSCC cells. Overall, LPS- and TNF-α-induced inflammation suppressed the migration and invasion of OSCC cells by upregulating Oct4 expression.

中文翻译：

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Oct4下调诱导的炎症增加了口腔鳞状细胞癌的迁移和侵袭率。

炎症变化与肿瘤细胞增殖、迁移和侵袭有关。肿瘤坏死因子-α（TNF-α）和脂多糖（LPS）在肿瘤发展过程中的炎症调节中起重要作用。Oct4 作为调节间充质干细胞炎症变化的转录因子。在这项研究中，我们探讨了 Oct4 在口腔鳞状细胞癌 (OSCC) 细胞侵袭和迁移中的作用。LPS 和 TNF-α 用于治疗 OSCC 细胞系 HN4 和 CAL27 以诱导炎症。通过酶联免疫吸附试验和实时定量 PCR 评估炎症细胞因子的产生，包括 TNF-α、白细胞介素 (IL)-1β 和 IL-6。Western印迹分析用于检测JNK1、p65和STAT3的表达和磷酸化，它们是炎症的关键调节剂。伤口划痕愈合和 transwell 侵袭试验进一步用于确定炎症在 OSCC 细胞侵袭和迁移中的作用。在用 LPS 和 TNF-α 处理的 HN4 和 CAL27 细胞中观察到强烈的炎症。在 LPS 和 TNF-α 处理后，还检测到 OSCC 细胞中 JNK1、p65 和 STAT3 磷酸化水平的显着增加。LPS 和 TNF-α 刺激显着促进了 HN4 和 CAL27 细胞的迁移和侵袭。此外，通过 LPS 和 TNF-α 刺激，Oct4 mRNA 和蛋白质水平显着上调。Oct4 的沉默导致炎症减少，磷酸化 JNK1、p65 和 STAT3 水平降低，并损害 LPS 和 TNF-α 刺激的 OSCC 细胞的侵袭和迁移。全面的，