Evidence map›Paper›PMID 42350656›Full record

ArticleCellular and molecular life sciences : CMLS2026

TRIM32-mediated ABI2 downregulation promotes anoikis resistance and metastasis by regulating EMT in lung adenocarcinoma.

Yongting Liu, Zhaohui Jiang, Yulong Zhao, Qiong Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 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
–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

4 authors.

Yongting LiuDepartment of Geriatrics, Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, 410008, China.
Zhaohui JiangDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Yulong ZhaoDepartment of Clinical Laboratory, Xiangya Hospital of Central South University, Changsha, 410008, China.
Qiong ChenDepartment of Geriatrics, Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, 410008, China. qiongch@csu.edu.cn.ORCID http://orcid.org/0009-0001-5577-8202

Funding

Fundamental Research Funds for the Central Universities of Central South University 2025ZZTS0238Hunan Provincial Innovation Foundation for Postgraduate CX20250358Key Technologies Research and Development Program 2020YFC2008600National Multidisciplinary Cooprative Diagnosis and Treatment Capacity Building Project for Major Diseases Lung Cancer, ID: z027002National Natural Science Foundation of China 82370055
6 · The paper itself

Abstract

Metastasis largely drives the high mortality of lung adenocarcinoma (LUAD), with anoikis resistance acting as a critical mediator in this process. This study aims to reveal the role and mechanism of ABI2 in anoikis resistance and LUAD metastasis. ABI2 expression levels and clinical value were analyzed using multiple databases. Functional studies were conducted in LUAD cells under attached or detached culture. The level of apoptosis was assessed by flow cytometry and Calcein-AM/EthD-1 staining. The metastasis ability was detected by transwell assay and lung metastasis model by tail vein injection. The ubiquitination effect of TRIM32 on ABI2 was analyzed by coimmunoprecipitation. This study revealed that ABI2 was significantly downregulated in LUAD tissues and anoikis-resistant LUAD cells. Functionally, ABI2 overexpression suppressed the anoikis resistance and LUAD metastasis, while ABI2 knockdown exerted the opposite effects. Mechanistically, ABI2 inhibited anoikis resistance by regulating epithelial-mesenchymal transition (EMT), thereby inhibiting tumor metastasis. EMT activation could rescue the effects of ABI2 on anoikis and metastasis. In addition, anoikis resistance modulated ABI2 ubiquitination by altering TRIM32 localization. Clinically, patients with low ABI2 and high TRIM32 experienced the worst prognosis in TCGA-LUAD. And a negative correlation between ABI2 and TRIM32 was further observed in both the public cohorts and the real-world cohort. In conclusion, ABI2 exerts tumor-suppressive effects in LUAD by inhibiting anoikis resistance and metastasis. The TRIM32‑ABI2‑EMT axis shows encouraging preclinical prospects, yet sufficient follow-up studies are indispensable to support its clinical therapeutic potential.

Indexed as

Adaptor Proteins, Signal TransducingAdenocarcinoma of LungAnoikisEpithelial-Mesenchymal TransitionLung NeoplasmsTripartite Motif ProteinsUbiquitin-Protein LigasesAnimalsCell Line, TumorDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CAdaptor Proteins, Signal TransducingTranscription FactorsTRIM32 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasesApoptosis regulationLung metastasis modelPrognostic biomarkerUbiquitination

Identifiers

PMID42350656
PMCPMC13572349

What Socratic holds

Textmetadata
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 Socratic graph.