Department of Thoracic Surgery and Lung Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Department of Thoracic Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, 646000, China.
Adv Biol (Weinh). 2024 Nov;8(11):e2400157. doi: 10.1002/adbi.202400157. Epub 2024 Aug 26.
FAM136A promotes the progression and metastasis of various tumors. However, there are few studies on the role of FAM136A in esophageal cancer (ESCA). The TCGA, GTEx, and GEO databases are employed to analyze the expression of FAM136A in ESCA, and qPCR and TMA experiments are performed for validation. Enrichment analyzes are performed to investigate the association of FAM136A expression with immune features, m6A modification, alternative splicing, cuproptosis, and the ceRNA network via bioinformatics analysis. FAM136A is highly expressed in ESCA and correlated with lymph node metastasis and overall survival (OS). Bioinformatics analysis suggested that FAM136A may participate in the following processes to promote ESCA development and progression: 1) Promotion of mast cells infiltration to influence the ESCA immune microenvironment, 2) HNRNPC upregulation to regulate m6A modification, 3) ALYREF upregulation to increase the occurrence of retained intron (RI) events, 4) CDK5RAP1 upregulation to achieve inhibition of tumor cell apoptosis, and 5) promotion of ESCA progression through the lncRNA SNHG15/hsa-miR-29c-3p/FAM136A ceRNA network. FAM136A is a potential biomarker for ESCA diagnosis and treatment response evaluation, and the underlying mechanisms may be associated with immune infiltration, m6A modification, alternative splicing, cuproptosis, and the ceRNA regulatory network.
FAM136A 促进了多种肿瘤的进展和转移。然而，目前关于 FAM136A 在食管癌（ESCA）中的作用的研究较少。本研究利用 TCGA、GTEx 和 GEO 数据库分析 ESCA 中 FAM136A 的表达，并通过 qPCR 和 TMA 实验进行验证。通过生物信息学分析，进行富集分析以研究 FAM136A 表达与免疫特征、m6A 修饰、可变剪接、铜死亡和 ceRNA 网络之间的关联。FAM136A 在 ESCA 中高表达，并与淋巴结转移和总生存期（OS）相关。生物信息学分析表明，FAM136A 可能通过以下方式参与促进 ESCA 发展和进展的过程：1）促进肥大细胞浸润以影响 ESCA 免疫微环境，2）上调 HNRNPC 以调节 m6A 修饰，3）上调 ALYREF 以增加内含子保留事件（RI）的发生，4）上调 CDK5RAP1 以抑制肿瘤细胞凋亡，5）通过 lncRNA SNHG15/hsa-miR-29c-3p/FAM136A ceRNA 网络促进 ESCA 进展。FAM136A 是 ESCA 诊断和治疗反应评估的潜在生物标志物，其潜在机制可能与免疫浸润、m6A 修饰、可变剪接、铜死亡和 ceRNA 调控网络有关。
