C17orf75（Njmu-R1）促进肝细胞癌的进展：一项全癌分析和实验验证
C17orf75 (Njmu-R1) promotes hepatocellular carcinoma progression: a pan-cancer analysis and experimental validation.
摘要(中文译文)
染色体17开放阅读框75（C17orf75）编码蛋白Njmu-R1（Protein Njmu-R1），该蛋白参与细胞内囊泡运输；然而，其在肿瘤进展中的作用仍很大程度上尚不清楚。本研究分析了来自癌症基因组图谱（TCGA）、基因表达综合数据库（GEO）和人类蛋白质图谱（HPA）的公共数据集，以评估C17orf75的表达谱、突变景观及其诊断和预后价值。随后进行生物信息学分析以探讨其与免疫浸润的关联。此外，在Hep3B和MHCC-97H细胞上进行了功能实验，并对临床肝细胞癌（LIHC）样本进行了免疫组织化学（IHC）检测。C17orf75在多种癌症类型中显著上调，尤其是在LIHC中。C17orf75表达升高与LIHC的不良预后及晚期临床病理特征相关。功能富集分析表明，C17orf75相关基因参与细胞周期调控、DNA复制和上皮-间质转化（EMT）。此外，C17orf75表达与免疫浸润、铁死亡相关基因及m6A调控因子密切相关。敲低C17orf75可抑制LIHC细胞的增殖、迁移和侵袭。敲低C17orf75诱导G2期阻滞，但对凋亡无显著影响。此外，敲低C17orf75可抑制EMT。C17orf75通过调控细胞周期进程和EMT在LIHC进展中发挥重要作用，并可能作为LIHC的潜在治疗靶点。
Abstract
Chromosome 17 Open Reading Frame 75 (C17orf75) encodes the protein Njmu-R1 (Protein Njmu-R1),, which is involved in intracellular vesicle trafficking; however, its role in tumor progression remains largely unclear. Public datasets from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and the Human Protein Atlas (HPA) were analyzed to evaluate the expression profile, mutation landscape, and diagnostic and prognostic value of C17orf75. Bioinformatics analyses were subsequently performed to explore its associations with immune infiltration. In addition, functional assays were conducted on Hep3B and MHCC-97H cells, and immunohistochemistry (IHC) was performed on clinical liver hepatocellular carcinoma (LIHC) samples. C17orf75 was significantly upregulated in multiple cancer types, particularly in LIHC. Elevated C17orf75 expression was associated with unfavorable prognosis and advanced clinicopathological features in LIHC. Functional enrichment analyses indicated that C17orf75-related genes were involved in cell cycle regulation, DNA replication, and epithelial-mesenchymal transition (EMT). Furthermore, C17orf75 expression was closely correlated with immune infiltration, ferroptosis-related genes, and m6A regulators. Knockdown of C17orf75 inhibited the proliferation, migration, and invasion of LIHC cells. C17orf75 knockdown induced G2-phase arrest without significantly affecting apoptosis. Moreover, knockdown of C17orf75 suppressed EMT. C17orf75 plays an important role in LIHC progression by regulating cell cycle progression and EMT, and it may serve as a potential therapeutic target for LIHC.
如何引用
AMA
Hao Liang, Nanbin Liu, Yibing Melody Zhai, Shiyan Guo, Ke Du, Kun Li, et al. C17orf75 (Njmu-R1) promotes hepatocellular carcinoma progression: a pan-cancer analysis and experimental validation.. Frontiers in immunology. 2026; doi:10.3389/fimmu.2026.1828437.
APA
Hao Liang, Nanbin Liu, Yibing Melody Zhai, Shiyan Guo, Ke Du, Kun Li, et al (2026). C17orf75 (Njmu-R1) promotes hepatocellular carcinoma progression: a pan-cancer analysis and experimental validation.. Frontiers in immunology. https://doi.org/10.3389/fimmu.2026.1828437
GB/T 7714
Hao Liang, Nanbin Liu, Yibing Melody Zhai, Shiyan Guo, Ke Du, Kun Li, et al. C17orf75 (Njmu-R1) promotes hepatocellular carcinoma progression: a pan-cancer analysis and experimental validation.[J]. Frontiers in immunology, 2026 doi:10.3389/fimmu.2026.1828437.
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