ArticleBioengineered2022
Sex-determining Region Y-box transcription factor 13 promotes breast cancer cell proliferation and glycolysis by activating the tripartite motif containing 11-mediated Wnt/β-catenin signaling pathway.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- POU3F2 regulates canonical Wnt signalling via SOX13 and ADNP to expand the neural progenitor population.Brain : a journal of neurology · 2025Article
- Canonical WNT/β-catenin signaling upregulates aerobic glycolysis in diverse cancer types.Molecular biology reports · 2024Review
- SOX13 as a potential prognostic biomarker linked to immune infiltration and ferroptosis inhibits the proliferation, migration, and metastasis of thyroid cancer cells.Frontiers in immunology · 2024Article
- Upregulation of FAM83F by c-Myc promotes cervical cancer growth and aerobic glycolysis via Wnt/β-catenin signaling activation.Cell death & disease · 2023Article
- Sox13 and M2-like leukemia-associated macrophages contribute to endogenous IL-34 caused accelerated progression of acute myeloid leukemia.Cell death & disease · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is the most frequent cancer among women and the second highest mortality in female across the world. Recent studies have illustrated that sex-determining region Y (SRY)-box protein (SOX) family plays essential roles in regulating various cancers. Nevertheless, the detailed effects of SOX13 on breast cancer are still uncovered. In our present study, SOX13 protein level was measured by using western blot assay in tissues and cells, and the results showed that SOX13 was upregulated in breast cancer tissues and cells compared with normal samples. Moreover, silencing SOX13 inhibited breast cancer cell viability, arrested cell cycle at G1/S phase and suppressed glycolysis, while overexpression of SOX13 reversed these events. Additionally, SOX13 knockdown reduced the level of proteins related to Wnt/β-catenin signaling pathway, whereas overexpression of tripartite motif containing 11 (TRM11) efficiently attenuated the effects, indicating that SOX13 controlled Wnt/β-catenin pathway depending on TRIM11. Furthermore, the data gained from xenograft tumor model illustrated that silencing SOX13 suppressed the tumor growth in nude mice and the glycolysis of tissues. In conclusion, our investigation illustrated that SOX13 facilitated breast cancer cell proliferation and glycolysis by modulating Wnt/β-catenin signaling pathway affected via TRIM11.
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Registered trials
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