Evidence map›Paper›PMID 41261425›Full record

ArticleMolecular cancer2025

Long non-coding RNA AFAP1-AS1 promotes alternative splicing of AXIN2 by facilitating SRSFs phase separation to induce drug resistance in lung adenocarcinoma.

Jiawei Ouyang, Yijie Zhang, Xiangchan Hou, Fang Xiong, Lei Shi, Yu Zhong, Liting Yang, Can Guo, Zhaoyang Zeng, Qijia Yan and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
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

12 authors.

Jiawei Ouyang *NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, 410078, China.
Yijie Zhang *NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, 410078, China.
Xiangchan HouKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, School of Basic Medicine Sciences, Central South University, Changsha, Hunan, 410078, China.
Fang XiongKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, School of Basic Medicine Sciences, Central South University, Changsha, Hunan, 410078, China.
Lei ShiKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, School of Basic Medicine Sciences, Central South University, Changsha, Hunan, 410078, China.
Yu ZhongKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, School of Basic Medicine Sciences, Central South University, Changsha, Hunan, 410078, China.
Liting YangKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, School of Basic Medicine Sciences, Central South University, Changsha, Hunan, 410078, China.
Can GuoKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, School of Basic Medicine Sciences, Central South University, Changsha, Hunan, 410078, China.
Zhaoyang ZengNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, 410078, China.
Qijia YanDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China. yanqijia77@126.com.
Pan ChenNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, 410078, China. chenpan08@csu.edu.cn.
Wei XiongNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, 410078, China. xiongwei@csu.edu.cn.

Funding

FACTORS THAT MODIFY INSULIN ACTIONR01DK002001 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BUSE, MARIA G · 1986 to 2012
$3.1M
Factors that modify insulin actionR56DK002001 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BUSE, MARIA G · 2008 to 2008
$199k
Fundamental Research Funds for the Central South University 2023ZZTS0847Key Research and Development Program of Hunan Province of China 2023DK2001Key Research and Development Program of Hunan Province of China 2023SK2004National Natural Science Foundation of China 82073135National Natural Science Foundation of China 82472789NIDDK NIH HHS R01 DK002001NIDDK NIH HHS R56 DK002001
6 · The paper itself

Abstract

Lung cancer currently holds the highest global incidence and mortality rates among malignant tumors, with lung adenocarcinoma being the most prevalent and deadly subtype. Chemotherapy and targeted therapy remain the standard treatments for lung adenocarcinoma, but tumor resistance continues to be a significant clinical challenge. In this study, we identified that the long non-coding RNA actin filament associated protein 1 antisense RNA 1 (AFAP1-AS1), which is highly expressed in lung adenocarcinoma, regulates RNA alternative splicing by recruiting splicing factors such as serine and arginine rich splicing factor 1 and 3 (SRSF1 and SRSF3), promoting their liquid-liquid phase separation. Among the affected splicing events, the exon 7 skipping of the key regulatory gene AXIN2, involved in the Wnt/β-catenin signaling pathway, is most notably regulated by AFAP1-AS1, resulting in the translation of a truncated AXIN2 isoform (AXIN2-S). This isoform facilitates the accumulation of β-catenin in the nucleus and the persistent activation of Wnt/β-catenin signaling pathway, ultimately contributing to drug resistance in lung adenocarcinoma. Our work uncovers a novel function of AFAP1-AS1 in regulating RNA alternative splicing through the modulation of splicing factors phase separation. This mechanism highlights an unrecognized pathway by which AFAP1-AS1 promotes drug resistance in lung adenocarcinoma, suggesting that AFAP1-AS1 and its regulated splicing events may serve as potential biomarkers or therapeutic targets for the treatment of lung adenocarcinoma.

Indexed as

Adenocarcinoma of LungAlternative SplicingAxin ProteinDrug Resistance, NeoplasmLung NeoplasmsRNA, Long NoncodingSerine-Arginine Splicing FactorsAnimalsbeta CateninCell Line, TumorGene Expression Regulation, NeoplasticHumansMicePhase SeparationWnt Signaling PathwayAFAP1-AS1 long noncoding RNA, humanAXIN2 protein, humanAxin Proteinbeta CateninRNA, Long NoncodingSerine-Arginine Splicing FactorsAFAP1-AS1AXIN2 alternative splicingDrug resistanceLiquid-liquid phase separationLung adenocarcinoma

Identifiers

PMID41261425
PMCPMC12632050

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LicenceCC BY-NC-ND
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Registered trials

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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.