基于生物信息学与实验验证探讨RELT在肾透明细胞癌中的预后评估及其免疫调控作用

宋佳丽; 李玉英; 胡燕; 缪小敏; 汪佳琪; 金波; 周晓芳; 邱月萍; 方罗

doi:10.13748/j.cnki.issn1007-7693.20252990

基于生物信息学与实验验证探讨RELT在肾透明细胞癌中的预后评估及其免疫调控作用

Exploring the Prognostic Value and Immunomodulatory Role of RELT in Kidney Renal Clear Cell Carcinoma Based on Bioinformatics and Experimental Validation

摘要

摘要:
目的系统评估淋巴组织表达的受体(receptor expressed in lymphoid tissues，RELT)在肾透明细胞癌(kidney renal clear cell carcinoma，KIRC)中的表达及预后相关性，探究其参与免疫调控和肿瘤进展的生物学功能。
方法从癌症基因组图谱计划数据库中获取了多个数据集，采用Kaplan-Meier曲线、Cox回归和ROC曲线评估RELT的预后意义。使用 ESTIMATE 和 X cell 算法量化免疫浸润，并通过 GSEA 识别RELT调控的通路。对180个病理组织样本进行免疫组织化学分析，检测RELT蛋白表达及其与生存期的相关性。此外，通过敲除人源肾癌细胞中的RELT基因，基于 qRT-PCR、Western blotting和免疫组化等生物学试验方法验证其对KIRC的影响。
结果 RELT在肿瘤组织中的高表达与KIRC患者的不良生存期密切相关。生物信息学和功能试验揭示RELT是KIRC进展的关键调节因子。RELT还通过促进 M2 型巨噬细胞、NKT 细胞和 B 细胞的增殖来影响免疫浸润。此外，RELT在肾癌细胞凋亡中起关键作用，沉默 RELT 可抑制细胞迁移并诱导凋亡。
结论 RELT 可调节肿瘤免疫微环境，促进肿瘤的恶性进展，其高表达提示不良预后。它有可能成为 KIRC 的预后生物标志物和新的治疗靶点，为提高KIRC患者生存期提供一种全新的策略。

Abstract:
OBJECTIVE To systematically evaluate the expression of receptor expressed in lymphoid tissues(RELT) in kidney renal clear cell carcinoma(KIRC) and its correlation with prognosis, and to explore its biological functions in immune regulation and tumor progression.
METHODS Obtained multiple datasets from the database of The Cancer Genome Atlas. The prognostic significance of RELT was evaluated by Kaplan-Meier curve, Cox regression and ROC curve. The ESTIMATE and X cell algorithms were used to quantify immune infiltration, and the pathways regulated by RELT were identified through GSEA. Immunohistochemical analysis was performed on 180 pathological tissue samples to detect the expression of RELT protein and its correlation with survival period. In addition, by knocking out the RELT gene in human renal cancer cells, the effect on KIRC was verified based on biological experimental methods such as qRT-PCR, Western blotting and immunohistochemistry.
RESULTS The high expression of RELT in tumor tissues was closely related to the poor survival period of patients with KIRC. Bioinformatics and functional experiments revealed that RELT was a key regulatory factor for the progression of KIRC. RELT also affected immune infiltration by promoting the proliferation of M2-type macrophages, NKT cells and B cells. In addition, RELT played a key role in the apoptosis of renal carcinoma cells. Silencing RELT could inhibit cell migration, and induce apoptosis.
CONCLUSION RELT can regulate the tumor immune microenvironment and promote the malignant progression of tumors. Its high expression indicates a poor prognosis. It holds promise as a prognostic biomarker for KIRC and as a novel therapeutic target, offering a new strategy to improve survival outcomes in KIRC patients.

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