lncRNAs are related to the progression of various diseases, including oral squamous cell carcinoma (OSCC), which is a common squamous cell carcinoma of the head and neck. Tumor-associated macrophages and tumor cells are significant components of tumor microenvironment. M2 polarization of tumor-associated macrophages is a crucial actor in tumor malignancy and metastasis. In this study, we studied the molecular mechanism of lncRNA DCST1-AS1 in OSCC. Here, we reported that DCST1-AS1 was significantly increased in OSCC cells. We found that loss of DCST1-AS1 obviously inhibited the proliferation, migration, and invasion of OSCC cells and xenograft tumor growth. Meanwhile, silencing of DCST1-AS1 also repressed the percentage of macrophages expressing M2 markers CD206 and CD11b. DCST1-AS1 shRNA enhanced the percentage of macrophages expressing M1 markers CD80 and CD11c. Then, we observed that loss of DCST1-AS1 suppressed OSCC progression via inactivating NF-κB signaling. As well established, NF-κB signaling exerts critical roles in tumor progression, and our study proved that DCST1-AS1 could regulate NF-κB signaling. We proved that blocking the NF-κB pathway using antagonists greatly downregulated OSCC progression and M2 macrophage polarization induced by the overexpression of DCST1-AS1. To sum up, we reported that DCST1-AS1 plays an important role in modulating OSCC tumorigenicity and M2 macrophage polarization through regulating the NF-κB pathway.

中文翻译：

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lncRNA DCST1-AS1通过激活NF-κB信号促进M2巨噬细胞极化促进口腔鳞状细胞癌

lncRNA与多种疾病的进展有关，包括口腔鳞状细胞癌（OSCC），这是一种常见的头颈部鳞状细胞癌。肿瘤相关巨噬细胞和肿瘤细胞是肿瘤微环境的重要组成部分。肿瘤相关巨噬细胞的 M2 极化是肿瘤恶性和转移的关键因素。在本研究中，我们研究了 lncRNA DCST1-AS1 在 OSCC 中的分子机制。在这里，我们报道了 DCST1-AS1 在 OSCC 细胞中显着增加。我们发现 DCST1-AS1 的缺失明显抑制了 OSCC 细胞的增殖、迁移和侵袭以及异种移植肿瘤的生长。同时，DCST1-AS1 的沉默也抑制了巨噬细胞表达 M2 标记 CD206 和 CD11b 的百分比。DCST1-AS1 shRNA 提高了巨噬细胞表达 M1 标记 CD80 和 CD11c 的百分比。然后，我们观察到 DCST1-AS1 的缺失通过灭活 NF-抑制 OSCC 进展。κB信号传导。作为非常成熟，NF- κ b信号发挥在肿瘤进展的关键角色，而我们的研究证明，DCST1-AS1能够调节NF- κ κB信号。我们证明，使用拮抗剂阻断 NF- κ B 通路可大大下调 DCST1-AS1 过表达诱导的 OSCC 进展和 M2 巨噬细胞极化。综上所述，我们报道了DCST1-AS1起着通过调节NF-调节口腔鳞状细胞癌致瘤性和M2巨噬细胞极化的重要作用κ乙途径。