Upregulation of POC1A in lung adenocarcinoma promotes tumour progression and predicts poor prognosis

Author:

Li Zi‐Hao1,Li Jia‐Yi2,Wu Zuo‐Tao1,Zhu Yong‐Jie1,Zhuo Ting3,Nong Ju‐Sen4,Qian Jing1,Peng Hua‐Jian1,Dai Lei1,Wang Yong‐Yong1,Chen Ming‐Wu1,Zeng Xiao‐Chun1ORCID

Affiliation:

1. Department of Cardio‐Thoracic Surgery The First Affiliated Hospital of Guangxi Medical University Nanning Guangxi China

2. Geriatrics Department of Endocrinology and Metabolism The First Affiliated Hospital of Guangxi Medical University Nanning Guangxi China

3. Department of Respiratory Medicine The First Affiliated Hospital of Guangxi Medical University Nanning Guangxi China

4. Department of Pediatric Surgery The First Affiliated Hospital of Guangxi Medical University Nanning Guangxi China

Abstract

AbstractLung adenocarcinoma (LUAD) is characterized by a high incidence rate and mortality. Recently, POC1 centriolar protein A (POC1A) has emerged as a potential biomarker for various cancers, contributing to cancer onset and development. However, the association between POC1A and LUAD remains unexplored. We extracted The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) data sets to analyse the differential expression of POC1A and its relationship with clinical stage. Additionally, we performed diagnostic receiver operator characteristic (ROC) curve analysis and Kaplan–Meier (KM) survival analysis to assess the diagnostic and prognostic value of POC1A in LUAD. Furthermore, we investigated the correlation between POC1A expression and immune infiltration, tumour mutation burden (TMB), immune checkpoint expression and drug sensitivity. Finally, we verified POC1A expression using real‐time quantitative polymerase chain reaction (RT‐qPCR) and immunohistochemistry (IHC). Cell experiments were conducted to validate the effect of POC1A expression on the proliferation, migration and invasion of lung cancer cells. POC1A exhibited overexpression in most tumour tissues, and its overexpression in LUAD was significantly correlated with late‐stage presentation and poor prognosis. The high POC1A expression group showed lower levels of immune infiltration but higher levels of immune checkpoint expression and TMB. Moreover, the high POC1A expression group demonstrated sensitivity to multiple drugs. In vitro experiments confirmed that POC1A knockdown led to decreased proliferation, migration, and invasion of lung cancer cells. Our findings suggest that POC1A may contribute to tumour development by modulating the cell cycle and immune cell infiltration. It also represents a potential therapeutic target and marker for the diagnosis and prognosis of LUAD.

Publisher

Wiley

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