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核仁蛋白 C1orf131 是一种新型基因，通过 AKT 信号通路参与肺腺癌细胞的进展。

The Nucleolar Protein C1orf131 Is a Novel Gene Involved in the Progression of Lung Adenocarcinoma Cells through the AKT Signalling Pathway.

机构信息

The Ministry of Education Key Laboratory of Laboratory Medical Diagnostics, the College of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China.

College of Medical Informatics, Chongqing Medical University, Chongqing 400016, China.

出版信息

Int J Mol Sci. 2024 Jun 9;25(12):6381. doi: 10.3390/ijms25126381.

DOI:10.3390/ijms25126381
PMID:38928092
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11203618/
Abstract

Lung adenocarcinoma (LUAD) is the most widespread cancer in the world, and its development is associated with complex biological mechanisms that are poorly understood. Here, we revealed a marked upregulation in the mRNA level of C1orf131 in LUAD samples compared to non-tumor tissue samples in The Cancer Genome Atlas (TCGA). Depletion of C1orf131 suppressed cell proliferation and growth, whereas it stimulated apoptosis in LUAD cells. Mechanistic investigations revealed that C1orf131 knockdown induced cell cycle dysregulation via the AKT and p53/p21 signalling pathways. Additionally, C1orf131 knockdown blocked cell migration through the modulation of epithelial-mesenchymal transition (EMT) in lung adenocarcinoma. Notably, we identified the C1orf131 protein nucleolar localization sequence, which included amino acid residues 137-142 (KKRKLT) and 240-245 (KKKRKG). Collectively, C1orf131 has potential as a novel therapeutic marker for patients in the future, as it plays a vital role in the progression of lung adenocarcinoma.

摘要

肺腺癌（LUAD）是世界上最广泛的癌症，其发展与复杂的生物学机制有关，这些机制尚不清楚。在这里，我们在癌症基因组图谱（TCGA）中发现 LUAD 样本中的 C1orf131mRNA 水平明显上调，与非肿瘤组织样本相比。C1orf131 的缺失抑制了 LUAD 细胞的增殖和生长，而刺激了细胞凋亡。机制研究表明，C1orf131 敲低通过 AKT 和 p53/p21 信号通路诱导细胞周期失调。此外，C1orf131 敲低通过调节肺腺癌细胞中的上皮-间充质转化（EMT）来阻断细胞迁移。值得注意的是，我们鉴定了 C1orf131 蛋白核仁定位序列，其包含氨基酸残基 137-142（KKRKLT）和 240-245（KKKRKG）。总之，C1orf131 作为一种新型治疗标志物，有望用于未来的患者，因为它在肺腺癌的进展中发挥着重要作用。

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