The final, formatted version of the article will be published soon.
ORIGINAL RESEARCH article
Front. Oncol.
Sec. Neuro-Oncology and Neurosurgical Oncology
Volume 15 - 2025 |
doi: 10.3389/fonc.2025.1537687
ATP1B3 may promote glioma proliferation and migration through MAPK/NF-KB signaling pathway
Provisionally accepted- 1 Basic Medical College, Jiamusi University, Jiamusi, China
- 2 Shandong Provincial Qianfoshan Hospital, Jinan, Shandong Province, China
Objective: To investigate the function of ATPase Na+/K+ Transporting Subunit Beta 3 (ATP1B3) in gliomas and the molecular mechanisms associated with them in order to identify a novel target and approach for glioma clinical diagnosis and treatment.Results: Database analysis revealed a negative correlation between the patients' prognosis and the expression level of ATP1B3, and a positive correlation with the malignant degree of the glioma. The mRNA and protein expression levels of ATP1B3 were significantly decreased after knockout, and the proliferation, migration and invasion ability of cells in knockout group were significantly lower than those in control group, with statistical difference. The immunoprecipitation results were negative, and the knockdown group's PPP1CA expression was lower than the control group's. Following ATP1B3 knockdown, Cyclin D1 and VEGFA protein expression levels dropped, and the effects were statistically significant. There was a statistically significant drop in the expression levels of p-Raf1, p-MEK 1/2, p-ERK 1/2, p-IκBα, and p-P65 following ATP1B3 deletion.Conclusion: In gliomas, ATP1B3 is highly expressed. Glioma cell motility, invasion, and proliferation all decline when ATP1B3 expression is lowered. The downstream protein PPP1CA is indirectly regulated by ATP1B3. By controlling the MAPK and NF-κB signaling pathways, ATP1B3 may have a role in the invasion, migration, and proliferation of glioma cells. As a result, the ATP1B3 gene might be a biological target for treatment and a possible neurotumor diagnostic.Key words: glioma; ATP1B3; Proliferation; Migration; MAPK signaling pathway; NF-κB signaling pathways
Keywords: Glioma, ATP1B3, proliferation, Migration, MAPK signaling pathway, NF-κB signaling pathways
Received: 01 Dec 2024; Accepted: 22 Jan 2025.
Copyright: © 2025 Yan, Sun, Feng, Hu and Zhu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Quan Sun, Basic Medical College, Jiamusi University, Jiamusi, China
Yan Feng, Shandong Provincial Qianfoshan Hospital, Jinan, 250014, Shandong Province, China
Qingyun Hu, Basic Medical College, Jiamusi University, Jiamusi, China
Jinling Zhu, Basic Medical College, Jiamusi University, Jiamusi, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.