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

Zhili Wei, Yiming Zhao, Jing Cai, Yajun Xie

Abstract read

In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed

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1 · What the graph read from it

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Who cites it

1 citing paper in PubMed.

Single-cell-marker-based subtyping and multi-level analyses uncover the prognostic effects, dysregulations and therapeutic indicative potential of an eight-gene signature in lung adenocarcinoma.Cancer cell international · 2026
Article

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5 · Who and what money

Authors and funding

4 authors.

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

Yiming ZhaoCollege of Medical Informatics, Chongqing Medical University, Chongqing 400016, China.

Jing CaiNational Talent Introduction Demonstration Base, the College of Basic Medicine, Harbin Medical University, Harbin 150081, China.

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

Funding

the Basic Science and Frontier Technology Research Program of Chongqing Science and Tech-nology Commission cstc2021jcyj-msxmX0312the National Natural Science Funds of China 32270834the Top-notch Talents Program for Graduate Students of Chongqing Medical University BJRC202211

6 · The paper itself

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.

Indexed as

Adenocarcinoma of LungCell MovementCell ProliferationGene Expression Regulation, NeoplasticLung NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionA549 CellsApoptosisCell Line, TumorDisease ProgressionEpithelial-Mesenchymal TransitionHumansNuclear ProteinsTumor Suppressor Protein p53Nuclear ProteinsProto-Oncogene Proteins c-aktTumor Suppressor Protein p53C1orf131cell cyclelung cancernucleolar proteinproliferation

Identifiers

PMID38928092

DOI10.3390/ijms25126381

PMCPMC11203618

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.