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KIF2C as a potential therapeutic target: insights from lung adenocarcinoma subtype classification and functional experiments

KIF2C as a potential therapeutic target: insights from lung adenocarcinoma subtype classification and functional experiments

Zhi Xu ^1,2, Rui Miao ^1,2, Tao Han ^1,2, Yafeng Liu ^1,2, Jiawei Zhou ^1,2, Jianqiang Guo ^1,2, Yingru Xing ^1,3, Ying Bai ^1,2, Jing Wu ^1,2, Dong Hu ^1,2,4

Zhi Xu ^1,2, Rui Miao ^1,2, Tao Han ^1,2

¹School of Medicine, Anhui University of Science and Technology, Chongren Building, No 168, Taifeng St, Huainan, 232001, P. R. China.
²Anhui Province Engineering Laboratory of Occupational Health and Safety, Anhui University of Science and Technology, Huainan, 232001, P. R. China.
³Department of Clinical Laboratory, Anhui Zhongke Gengjiu Hospital, Hefei, 230041, P. R. China.
⁴Key Laboratory of Industrial Dust Prevention and Control & Occupational Safety and Health of the Ministry of Education, Anhui University of Science and Technology, Huainan, 232001, P. R. China.

⁰School of Medicine, Anhui University of Science and Technology, Chongren Building, No 168, Taifeng St, Huainan, 232001, P. R. China.

Molecular Omics +

|

June 28, 2024

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View abstract on PubMed

Summary

This summary is machine-generated.

This study identifies two lung adenocarcinoma (LUAD) subtypes and a key gene, KIF2C. High KIF2C expression indicates poor prognosis and suggests KIF2C as a potential therapeutic target for LUAD.

Area Of Science

Oncology
Molecular Biology
Genomics

Background

Lung adenocarcinoma (LUAD) is a major cause of cancer mortality.
Identifying prognostic markers and therapeutic targets is crucial for improving LUAD patient outcomes.

Purpose Of The Study

To evaluate the prognostic significance of gene subtypes in LUAD.
To investigate the role of kinesin family member 2C (KIF2C) in LUAD progression.

Main Methods

Utilized TCGA-LUAD dataset to identify high-expression genes associated with overall survival (OS) and progression-free interval (PFI).
Applied consensus clustering to classify LUAD patients into two subtypes (C1 and C2).
Employed random forest algorithm to identify KIF2C as a prognostic hub gene; functional impact assessed via in vitro and in vivo experiments.

Main Results

Identified 163 key genes and two distinct LUAD subtypes with differential OS, PFI, pathological stages, drug sensitivity, and immunotherapy response.
KIF2C was highly expressed in the C2 subtype, correlating with poor prognosis.
KIF2C promoted LUAD cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT); KIF2C knockdown inhibited tumor growth in vivo.

Conclusions

Delineated distinct LUAD subtypes with significant clinical implications.
Highlighted KIF2C as a potential therapeutic target for personalized LUAD treatment.

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