ArticleMolecular and cellular biochemistry2026
Keratin 15 promotes tumor growth, invasion, epithelial-mesenchymal transition and radioresistance but represses ferroptosis via a Wnt/β-catenin signaling-related way in breast cancer.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Keratin 15 (KRT15) promotes tumor progression in several cancers, but its engagement in breast cancer is seldom uncovered. This study aimed to explore the impact of KRT15 modification on breast cancer growth, mobility, radiosensitivity, ferroptosis, and Wnt/β-catenin signaling pathway. A lentiviral vector containing short hairpin RNA or complementary DNA targeting KRT15 was transfected into MDA-MB-231 and MCF-7 cells in vitro. The transfected MCF-7 cells were further proposed to irradiation treatment. In vivo, female BALB/c nude mice were used to establish xenograft model with KRT15-overexpressed MDA-MB-231 cells and treated by irradiation. KRT15 overexpression promoted cell proliferation, migration, invasion, colony number, epithelial-mesenchymal transition (EMT, reflected by E-Cadherin, N-Cadherin, and Vimentin expressions), and S-stage cell cycle arrest in MDA-MB-231 and MCF-7 cells, but repressed cell apoptosis and ferroptosis (reflected by DMT1, SLC7A11, FTH1, and GPX4 expressions); while KRT15 knockdown exhibited the opposite effects. Importantly, KRT15 overexpression enhanced irradiation resistance in MCF-7 cells reflected by cell proliferation, migration, invasion, colony number, cell cycle, and cell apoptosis detections. Besides, KRT15 overexpression increased EMT and activated Wnt/β-catenin signaling pathway (reflected by β-catenin, TCF-1, c-Myc, CCND1, MMP7 expressions) in MCF-7 cells with or without irradiation. In vivo experiments further validated that KRT15 overexpression promoted tumor growth, EMT, Wnt/β-catenin signaling pathway, and irradiation resistance, but repressed the ferroptosis. Collectively, KRT15 may facilitate tumor growth, invasion, EMT, and radioresistance but represses ferroptosis in a Wnt/β-catenin signaling-related way, suggesting its potency as a treatment target for breast cancer management.
Indexed as
Identifiers
40900415What OpenQuestion holds
Registered trials
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.