Department of Oncology, Guizhou Provincial People's Hospital, Guiyang City, Guizhou Province, China.
Department of Oncology, Zheng'an People's Hospital Feng Yi Zhen, Zunyi City, Guizhou Province, China.
Allergol Immunopathol (Madr). 2022 Sep 1;50(5):68-74. doi: 10.15586/aei.v50i5.659. eCollection 2022.
Lung cancer is a common malignancy. Non-small cell lung cancer (NSCLC) is divided into lung squamous cancer (LUSC), large cell carcinoma, and adenocarcinoma. More than 85% of lung cancer cases are NSCLC patients. Further exploration of the pathogenesis of lung cancer is of great significance. In this study, functions of far upstream element-binding protein 1 (FUBP1) on the proliferation and tumor immunity of LUSC cells were evaluated.
The Cancer Genome Atlas (TCGA) database, Western blot analysis, and immunohistochemistry (IHC) analysis were used to examine the overexpression levels of FUBP1 in LUSC and paracancerous tissues, LUSC cell line, and human normal lung cell line. Then, Western blot assay was employed to validate the transfection efficiency of FUBP1 knockdown in SK-MES-1 cells. Cell counting kit-8 and colony formation assays were used to detect the viability and proliferation of SK-MES-1 cells. Transwell assay was used to examine the migrative and invasive abilities of SK-MES-1 cells. Finally, the xenograft tumor mice model was applied to explore the role of FUBP1 . IHC assay was used to determine the expression levels FUBP1, PD-L1, and Ki-67. Flow cytometry technology was employed to detect the proportion of CD4 and CD8 cells in short sequence negative control (sh-NC) and sh-FUBP1 groups.
Collectively, the results first indicated that FUBP1 was up-regulated in LUSC tissues and cells. It was also demonstrated that knockdown of FUBP1 suppressed cell migration, invasion, and proliferation in lung squamous carcinoma cells. Finally, knockdown of FUBP1 regulated tumor immunity .
This research suggested that FUBP1 promotes the proliferation of LUSC cells and regulates tumor immunity through programmed death-ligand 1 (PD-L1).
肺癌是一种常见的恶性肿瘤。非小细胞肺癌（NSCLC）分为肺鳞癌（LUSC）、大细胞癌和腺癌。超过 85%的肺癌病例为 NSCLC 患者。进一步探索肺癌的发病机制具有重要意义。本研究评估了远上游元件结合蛋白 1（FUBP1）对 LUSC 细胞增殖和肿瘤免疫的功能。
使用癌症基因组图谱（TCGA）数据库、Western blot 分析和免疫组织化学（IHC）分析检测 FUBP1 在 LUSC 和癌旁组织、LUSC 细胞系和人正常肺细胞系中的过表达水平。然后，Western blot 检测用于验证 SK-MES-1 细胞中 FUBP1 敲低的转染效率。细胞计数试剂盒-8 和集落形成实验用于检测 SK-MES-1 细胞的活力和增殖。Transwell 实验用于检测 SK-MES-1 细胞的迁移和侵袭能力。最后，应用异种移植肿瘤小鼠模型探讨 FUBP1 的作用。IHC 检测用于确定 FUBP1、PD-L1 和 Ki-67 的表达水平。流式细胞术技术用于检测短序列阴性对照（sh-NC）和 sh-FUBP1 组中 CD4 和 CD8 细胞的比例。
结果表明，FUBP1 在 LUSC 组织和细胞中上调。此外，敲低 FUBP1 抑制了肺鳞癌细胞的迁移、侵袭和增殖。最后，敲低 FUBP1 调节肿瘤免疫。
本研究表明，FUBP1 通过程序性死亡配体 1（PD-L1）促进 LUSC 细胞的增殖并调节肿瘤免疫。
