Evidence map›Paper›PMID 41136360›Full record

ArticleCell death discovery2025

FHL2 enhances ITGB1-mediated ECM remodeling and cellular stiffness to promote radioresistance in non-small cell lung cancer.

Xiaoyu Pu, Kexin Chen, Lihua Dong, Junxuan Yi, Mingwei Wang, Xinfeng Wei, Mingqi Zhao, Mengdie Zhao, Xinyan Wang, Lijuan Ding and 1 more

Abstract read
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Xiaoyu PuJilin Provincial Key Laboratory of Radiation Oncology & Therapy, Department of Radiation Oncology & Therapy, The First Hospital of Jilin University, Changchun, China.
Kexin ChenInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.ORCID http://orcid.org/0000-0002-1503-6044
Lihua DongJilin Provincial Key Laboratory of Radiation Oncology & Therapy, Department of Radiation Oncology & Therapy, The First Hospital of Jilin University, Changchun, China.
Junxuan YiNational Health Commission Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, China.
Mingwei WangNational Health Commission Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, China.
Xinfeng WeiNational Health Commission Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, China.
Mingqi ZhaoNational Health Commission Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, China.
Mengdie ZhaoNational Health Commission Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, China.
Xinyan WangNational Health Commission Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, China.
Lijuan DingJilin Provincial Key Laboratory of Radiation Oncology & Therapy, Department of Radiation Oncology & Therapy, The First Hospital of Jilin University, Changchun, China. dinglijuan@jlu.edu.cn.ORCID http://orcid.org/0000-0002-1692-5089
Shunzi JinNational Health Commission Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, China. jinsz@jlu.edu.cn.ORCID http://orcid.org/0000-0001-7856-2634

Funding

Department of Science and Technology of Jilin Province (Jilin Province Science and Technology Department) No. YDZJ202401659ZYTSNational Natural Science Foundation of China (National Science Foundation of China) No. 82173454National Natural Science Foundation of China (National Science Foundation of China) No. 82273565
6 · The paper itself

Abstract

Radiotherapy is a cornerstone treatment for non-small cell lung cancer (NSCLC), but its efficacy is frequently limited by tumor-intrinsic radioresistance. Cellular stiffness and extracellular matrix (ECM) interactions are critical mechanisms underlying this resistance. The adaptor protein four-and-a-half LIM domains 2 (FHL2) has emerged as a key regulator of tumor radioresistance. This study elucidates the role of FHL2 in enhancing radioresistance in NSCLC through ECM remodeling and cellular stiffness. FHL2 was found to promote cell survival, DNA damage repair, and ECM remodeling in response to irradiation, with its interaction with integrin β1 (ITGB1) playing a pivotal role. Depletion of FHL2 significantly reduced cell survival and radioresistance in radioresistant NSCLC cell lines, while FHL2 overexpression upregulated ITGB1 expression. Notably, FHL2 depletion elicited effects comparable to ITGB1 knockdown, suggesting ITGB1 acts as a downstream effector of FHL2. Mechanistically, FHL2 enhances ITGB1-mediated ECM remodeling and cellular stiffness via FAK/MAPK signaling pathways, thereby promoting radioresistance. These findings position FHL2 as a potential biomarker and therapeutic target for overcoming radioresistance in NSCLC, offering a foundation for developing strategies to improve radiotherapy outcomes. This study underscores the critical role of FHL2/ITGB1 axis in tumor resistance mechanisms and highlights its therapeutic potential in NSCLC treatment.

Identifiers

PMID41136360
PMCPMC12552696

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.