Evidence map›Paper›PMID 42144424›Full record

ArticleScientific reports2026

ANO1 stabilizes partial EMT to drive colorectal cancer metastasis through PI3K/AKT/mTOR and ERK signaling pathways.

Fei Wu, Kun Zhang, Zhenwu Du, Xin Li, Longfei Yang, Linxian Zhao, Bo Cheng, Lili Nie, Qiwei Yang, Yujie Sui

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Fei WuDepartment of Obstetrics and Gynecology, The Second Hospital of Jilin University, 265 Ziqiang Street, Changchun, 130041, People's Republic of China.
Kun ZhangKey Laboratory for Molecular and Chemical Genetics of Critical Human Diseases of Jilin Province, The Second Hospital of Jilin University, 265 Ziqiang Street, Changchun, 130041, People's Republic of China.
Zhenwu DuDepartment of Orthopedics, The Second Hospital of Jilin University, 265 Ziqiang Street, Changchun, 130041, People's Republic of China.
Xin LiKey Laboratory for Molecular and Chemical Genetics of Critical Human Diseases of Jilin Province, The Second Hospital of Jilin University, 265 Ziqiang Street, Changchun, 130041, People's Republic of China.
Longfei YangKey Laboratory for Molecular and Chemical Genetics of Critical Human Diseases of Jilin Province, The Second Hospital of Jilin University, 265 Ziqiang Street, Changchun, 130041, People's Republic of China.
Linxian ZhaoDepartment of General Surgery, The Second Hospital of Jilin University, 265 Ziqiang Street, Changchun, 130041, People's Republic of China.
Bo ChengDepartment of Obstetrics and Gynecology, The Second Hospital of Jilin University, 265 Ziqiang Street, Changchun, 130041, People's Republic of China.
Lili NieDepartment of Ophthalmology, The Second Hospital of Jilin University, 265 Ziqiang Street, Changchun, 130041, People's Republic of China. niell@jlu.edu.cn.
Qiwei YangKey Laboratory for Molecular and Chemical Genetics of Critical Human Diseases of Jilin Province, The Second Hospital of Jilin University, 265 Ziqiang Street, Changchun, 130041, People's Republic of China. yangqw@jlu.edu.cn.
Yujie SuiKey Laboratory for Molecular and Chemical Genetics of Critical Human Diseases of Jilin Province, The Second Hospital of Jilin University, 265 Ziqiang Street, Changchun, 130041, People's Republic of China. suiyj@jlu.edu.cn.

Funding

Department of Science and Technology of Jilin Province, China No. YDZJ202201ZYTS026the Education Department of Jilin Province, China JJKH20231220KJ
6 · The paper itself

Abstract

Colorectal cancer (CRC) metastasis remains a clinically intractable challenge, where the partial epithelial-mesenchymal transition (partial EMT) state is a key driver of metastatic plasticity and treatment resistance. The calcium-activated chloride channel ANO1 (TMEM16A) is frequently overexpressed in epithelial tumors, yet its mechanism in regulating metastasis and partial EMT remains undefined. In this study, we identify ANO1 as a key stabilizer of the partial EMT state. ANO1 was upregulated in CRC tissues and correlated with poor patient survival. Functionally, ANO1 knockdown robustly suppressed CRC cell proliferation, migration, and invasion, and potently induced early apoptosis. Proteomic profiling linked ANO1 depletion to the downregulation of cytoskeletal and adhesion networks. Given the centrality of these processes to EMT, we specifically examined key EMT-associated molecules. Western blot results showed that ANO1 silencing reduced expression of mesenchymal markers (N-cadherin, vimentin, α-SMA) and EMT transcription factors (Zeb1, Snail, Twist), while also downregulating the epithelial marker E-cadherin. Immunofluorescence revealed that ANO1 depletion disrupted a spatially organized hybrid subcellular architecture, and flow cytometry demonstrated that ANO1 knockdown selectively depleted the E-cadherin

Indexed as

Anoctamin-1Colorectal NeoplasmsEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemNeoplasm ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansNeoplasm MetastasisSignal TransductionANO1 protein, humanAnoctamin-1MTOR protein, humanNeoplasm ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesANO1Colorectal cancerERK pathwayMetastasisPartial Epithelial-Mesenchymal TransitionPI3K/AKT/mTOR pathway

Identifiers

PMID42144424
PMCPMC13407880

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.