Evidence map›Paper›PMID 40496172›Full record

ArticleBreast cancer (Dove Medical Press)2025

ALKBH5 Promotes Breast Cancer Stemness Through Regulating Wnt/β-Catenin Signaling.

Kailin Wang, Kaiting Wang

Abstract read
In one paragraph

Article in Breast cancer (Dove Medical Press), 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

2 authors.

Kailin WangInstitute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, 518112, People's Republic of China.
Kaiting WangInstitute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, 518112, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Breast cancer is the most prevalent disease and the fourth cause of cancer death among female globally. The N6-methyladenylate methylation (m Methods: ALKBH5-silenced breast cancer cell-line MCF-7 was constructed to investigate its functional impact. Cell proliferation, migration and invasion ability were evaluated by CCK8 and transwell assays under ALKBH5 inhibition. Spheroid formation and in vitro extreme limiting dilution analysis (ELDA) were performed to elucidate the effect of ALKBH5 deficiency on stemness of MCF-7 cells. The m Results: Silencing ALKBH5 significantly suppressed MCF-7 cell proliferation, migration, and invasion abilities. Moreover, ALKBH5 depletion also diminished the stemness of breast cancer cells in vitro. Further investigation illustrated that ALKBH5 may regulate Wnt/β-catenin signaling via an m Conclusion: This study establishes a link between ALKBH5 and cancer stemness in breast cancer, providing insights into the functional role of demethylase ALKBH5 in breast cancer progression.

Indexed as

ALKBH5breast cancerCTNNB1(m6A)N6-methyladenosinestemness

Identifiers

PMID40496172
PMCPMC12151075

What Socratic holds

Textmetadata
LicenceCC BY-NC
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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.