ORIGINAL RESEARCH article
Front. Oncol.
Sec. Cancer Genetics
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1645671
Role of Meox1 in Promoting Lung Tumor Vascularization and Impairing CD8 + T Cell Mediated Immunity
Provisionally accepted
- 1Guangzhou National Laboratory, Guangzhou, China
- 2Guangzhou Medical University, Guangzhou, China
- 3Qingyuan People's Hospital, Qingyuan, China
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Endothelial cells play a critical role in tumor-associated vasculature formation and immune modulation, and dysregulation of transcription factors (TFs) such as Meox1 has been associated with various cancers, including non-small cell lung cancer (NSCLC). Meox1 has been implicated in promoting both tumor-promoting and immune-suppressing functions. In this study, we investigated the functional role of Meox1 in NSCLC by employing a siRNA-based knockdown approach to selectively reduce its expression. Our preliminary findings reveal that siRNA-mediated Meox1 knockdown significantly impairs the capacity of tube formation at the cellular level. Furthermore, we observed a marked reduction in tumor cell proliferation and an increase in CD8 expression, a marker of T-cell activity in an animal model system, indicating that Meox1 may also play a regulatory role in immune-mediated tumor suppression. Our findings not only deepen our understanding of the molecular mechanisms underlying lung cancer progression but also open new avenues for the development of targeted therapies aimed at restoring tumor-associated endothelial cell function and enhancing immune responses against cancer.
Keywords: Tumor-associated vasculature formation, Transcription Factors, MEOX1, CD8 expression, NSCLC
Received: 12 Jun 2025; Accepted: 04 Aug 2025.
Copyright: © 2025 Zhang, Yang, Li and Chen. 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: Wei Zhang, Guangzhou National Laboratory, Guangzhou, China
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