Department of Medical Oncology, Taihe County People's Hospital, Fuyang, Anhui 236600, P.R. China.
Mol Med Rep. 2025 Jan;31(1). doi: 10.3892/mmr.2024.13376. Epub 2024 Oct 25.
Lung adenocarcinoma (LUAD) is highly associated with lung cancer‑associated mortality. Notably, S100 calcium‑binding protein A16 (S100A16) has been increasingly considered to have prognostic value in LUAD; however, the underlying mechanism remains unknown. In the present study, S100A16 expression levels in LUAD tissues and cells were respectively analyzed by the UALCAN database and western blotting. Cell Counting Kit‑8 and 5‑ethynyl‑2'‑deoxyuridine assays were used to examine cell proliferation, whereas wound healing, Transwell and tube formation assays were used to assess cell migration, invasion and angiogenesis, respectively. Western blotting was also used to examine the expression levels of proteins associated with metastasis, angiogenesis, focal adhesion and the extracellular matrix (ECM)‑receptor interaction pathways. The relationship between S100A16 and Mov10 RNA helicase (MOV10) was predicted by bioinformatics tools, and was verified using a co‑immunoprecipitation assay. Furthermore, the interaction between MOV10 and integrin α3 (ITGA3) was verified by RNA immunoprecipitation assay, and the actinomycin D assay was used to detect ITGA3 mRNA stability. The results demonstrated that S100A16 expression was increased in LUAD tissues and cell lines, and was associated with unfavorable outcomes. Knocking down S100A16 expression hindered the proliferation, migration, invasion and angiogenesis of LUAD cells. Furthermore, S100A16 was shown to bind to MOV10 and positively modulate MOV10 expression in LUAD cells, while MOV10 overexpression partially reversed the suppressive role of S100A16 knockdown on the aggressive phenotypes of LUAD cells. Furthermore, it was demonstrated that S100A16 regulated the stability of ITGA3 mRNA via MOV10 to mediate ECM‑receptor interactions. In conclusion, S100A16 may bind to MOV10 to stabilize ITGA3 mRNA and regulate ECM‑receptor interactions, hence contributing to the malignant progression of LUAD.
肺腺癌 (LUAD) 与肺癌相关死亡率高度相关。值得注意的是，S100 钙结合蛋白 A16 (S100A16) 在 LUAD 中被认为具有预后价值；然而，其潜在机制尚不清楚。在本研究中，分别通过 UALCAN 数据库和 Western blot 分析 LUAD 组织和细胞中的 S100A16 表达水平。使用细胞计数试剂盒 -8 和 5-乙炔基-2'-脱氧尿苷测定法检测细胞增殖，而划痕愈合、Transwell 和管形成测定法分别用于评估细胞迁移、侵袭和血管生成。Western blot 还用于检测与转移、血管生成、焦点黏附以及细胞外基质 (ECM)-受体相互作用途径相关的蛋白表达水平。生物信息学工具预测 S100A16 与 Mov10 RNA 解旋酶 (MOV10) 之间的关系，并通过共免疫沉淀测定法进行验证。此外，通过 RNA 免疫沉淀测定法验证 MOV10 与整合素 α3 (ITGA3) 之间的相互作用，并使用放线菌素 D 测定法检测 ITGA3 mRNA 稳定性。结果表明，S100A16 在 LUAD 组织和细胞系中表达增加，与不良预后相关。敲低 S100A16 表达抑制 LUAD 细胞的增殖、迁移、侵袭和血管生成。此外，S100A16 被证明与 MOV10 结合并正向调节 LUAD 细胞中的 MOV10 表达，而 MOV10 过表达部分逆转了 S100A16 敲低对 LUAD 细胞侵袭表型的抑制作用。此外，研究表明 S100A16 通过 MOV10 调节 ITGA3 mRNA 的稳定性，从而介导 ECM-受体相互作用。总之，S100A16 可能与 MOV10 结合以稳定 ITGA3 mRNA，并调节 ECM-受体相互作用，从而促进 LUAD 的恶性进展。
