Evidence map›Paper›PMID 42143069›Full record

ArticleSignal transduction and targeted therapy2026

Disrupting SOX2 self-association and condensate formation to overcome chemotherapeutic drug resistance in lung squamous cell carcinoma.

Juehan Wang, Yulin Wen, Sainan Huang, Yanjiang Liu, Xiaotao Dong, Hongmo Liu, Zhihua Guo, Jin Li, Chengzhi Zhou, Hua Wang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Signal transduction and targeted therapy, 2026. 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
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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

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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

14 authors.

Juehan WangState Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.
Yulin WenState Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0001-5703-1068
Sainan HuangState Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.
Yanjiang LiuState Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.
Xiaotao DongSchool of Basic Medical Sciences, Henan University, Kaifeng, China.
Hongmo LiuDepartment of Pulmonary and Critical Care Medicine, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.
Zhihua GuoDepartment of Thoracic Surgery and Oncology, the First Affiliated Hospital of Guangzhou Medical University, State Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease, Guangzhou, China.
Jin LiState Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China.
Chengzhi ZhouThe First Affiliated Hospital of Guangzhou Medical University, National Center for Respiratory Medicine, National Clinical Research Center for Respiratory Disease, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou, China.ORCID http://orcid.org/0000-0003-0029-6879
Hua WangInstitute of Clinical Pharmacology, Anhui Medical University, Hefei, China.ORCID http://orcid.org/0000-0002-2605-5697
Lingling ZhangInstitute of Clinical Pharmacology, Anhui Medical University, Hefei, China.
Zhoufeng WangDepartment of Pulmonary and Critical Care Medicine, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.
Weimin LiDepartment of Pulmonary and Critical Care Medicine, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.ORCID http://orcid.org/0000-0003-0985-0311
Hongjie YaoState Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China. yao_hongjie@gzlab.ac.cn.ORCID http://orcid.org/0000-0003-2144-0147

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31925009 and U21A20195State Key Laboratory of Respiratory Disease (SKLRD) SKLRD-Z-202310
6 · The paper itself

Abstract

Chemotherapy remains a primary treatment for lung squamous cell carcinoma (LSCC), and its efficacy is limited due to drug resistance; however, the mechanisms involved in drug resistance are still unclear. In this study, we identify a significant correlation between SOX2 amplification and elevated mRNA expression in LSCC patients, establishing SOX2 as a key regulator of LSCC. Our data further demonstrate that SOX2 drives chemoresistance by forming biomolecular condensates via phase separation. SOX2 condensates function as protective compartments that physically sequester chemotherapeutic drugs, reducing availability to intracellular targets and cytotoxicity of these chemotherapeutic drugs. Exposure to chemotherapeutic stress further upregulates SOX2 expression and promotes its phase separation, thereby creating a vicious self-reinforcing cycle that amplifies chemoresistance. To overcome drug resistance induced by SOX2 condensation, we developed a cell-penetrating peptide, Hx1

Indexed as

Biomolecular CondensatesCarcinoma, Squamous CellDrug Resistance, NeoplasmLung NeoplasmsSOXB1 Transcription FactorsCell Line, TumorGene Expression Regulation, NeoplasticHumansPhase SeparationSOX2 protein, humanSOXB1 Transcription Factors

Identifiers

PMID42143069
PMCPMC13179957

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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.