Oral squamous cell carcinoma (OSCC) is a significant global health concern. Epstein–Barr virus (EBV) infection as well as long non-coding RNA (lncRNAs) associated EBV infection, have been linked to OSCC development and are known to influence cancer progression.LINC00944is associated with various cancers and immune cells, but its role in oral cancer remains underexplored. This study investigated the role of EBV-inducedLINC00944in OSCC and its impact on the tumor microenvironment. TheLINC00944expression was analyzed from a database of head and neck squamous cell carcinoma (HNSCC) tissues, and its expression in EBV-positive and EBV-negative OSCC cell lines was examined via qRT-PCR. We overexpressedLINC00944in SCC25 and ORL-48T oral cancer cell lines and evaluated its impact on migration and invasion ability using wound healing and transwell experiments. Additionally, we studied its influence on macrophage differentiation. The results showed thatLINC00944expression was higher in HNSCC than in normal tissues and was linked to EBV-positive OSCC cell lines.LINC00944overexpressed-OSCC cell lines significantly increased cellular motility and invasiveness. Additionally,LINC00944was secreted in a cultured medium, delivered to macrophages, and promoted macrophage differentiation into the M1 subtype. Predicted interactions suggested thatLINC00944targets miRNAs that regulateNFKB1andRELA. In conclusion, EBV-inducedLINC00944contributes to OSCC progression by enhancing tumor cell migration, invasion, and macrophage differentiation, potentially regulating these processes throughNFKB1andRELA. These findings provide valuable directions forLINC00944’s future studies on its mechanisms and suggest that it could be a target of study in EBV-associated OSCC.
口腔鳞状细胞癌（OSCC）是全球范围内重要的健康问题。爱泼斯坦-巴尔病毒（EBV）感染及其相关的长链非编码RNA（lncRNAs）已被证实与OSCC的发生发展相关，并影响癌症进展。LINC00944与多种癌症及免疫细胞存在关联，但其在口腔癌中的作用尚未充分阐明。本研究探讨了EBV诱导的LINC00944在OSCC中的作用及其对肿瘤微环境的影响。通过头颈部鳞状细胞癌（HNSCC）组织数据库分析LINC00944表达水平，并采用qRT-PCR技术检测其在EBV阳性和EBV阴性OSCC细胞系中的表达。我们在SCC25和ORL-48T口腔癌细胞系中过表达LINC00944，通过划痕愈合实验和Transwell实验评估其对细胞迁移和侵袭能力的影响，同时研究其对巨噬细胞分化的调控作用。结果显示，LINC00944在HNSCC组织中的表达高于正常组织，且与EBV阳性OSCC细胞系密切相关。过表达LINC00944的OSCC细胞系表现出显著增强的细胞运动能力和侵袭性。此外，LINC00944可分泌至培养基中，递送至巨噬细胞并促进其向M1亚型分化。预测相互作用分析表明LINC00944可能靶向调控NFKB1和RELA的miRNAs。综上所述，EBV诱导的LINC00944通过增强肿瘤细胞迁移、侵袭及巨噬细胞分化促进OSCC进展，这些过程可能通过NFKB1和RELA通路进行调控。本研究为LINC00944的作用机制研究提供了重要方向，并提示其可能成为EBV相关OSCC的潜在研究靶点。
肿瘤(癌症)患者之家