ORIGINAL RESEARCH article

Front. Immunol.

Sec. Cancer Immunity and Immunotherapy

Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1569641

FOXP1 is Associated with Oncogenesis and Clinical Outcomes in Hematologic Malignancies

Provisionally accepted
Xiang-mei WenXiang-mei WenZi-jun XuZi-jun XuHao-Xi NiHao-Xi NiSu-Wan LiuSu-Wan LiuYe JinYe JinWei ZhaoWei ZhaoShu- Yu LuoShu- Yu LuoYuan-Yuan FangYuan-Yuan FangZhenwei MaoZhenwei MaoJiang LinJiang LinJun QianJun Qian*
  • Jiangsu University Affiliated People's Hospital, Zhenjiang, China

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Depending on the cellular context and cancer type, FOXP1 functions as an oncogene or a tumor suppressor. However, the clinical role of FOXP1 in hematologic malignancies has not been studied comprehensively. This study systematically analyzed the association of FOXP1 expression with clinical outcomes, including prognosis and immunotherapeutic response, as well as biological functions across a range of hematological cancers. Our findings demonstrated that FOXP1 expression was dysregulated in several hematological malignancies and was associated with poor prognosis. FOXP1 was highly expressed in acute myeloid leukemia (AML). Methylation of the FOXP1 promoter was significantly reduced in patients with AML compared to the healthy control subjects and those with myelodysplastic syndromes. FOXP1 promoter methylation showed an inverse relationship with FOXP1 gene expression in AML. Moreover, FOXP1 expression was associated with the tumor infiltration of B cells, natural killer cells, and T cells, as well as the cytolytic score across various hematologic malignancies. Our data showed that FOXP1 expression was a promising biomarker for predicting responses to immunotherapy in AML patients. Functionally, the knockdown of FOXP1 demonstrated antileukemic effects, including reduced AML cell proliferation and cell cycle arrest in the G1-S phase. In conclusion, this study systematically investigated the role of FOXP1 across a

Keywords: FoxP1, hematological malignancies, prognosis, Tumor Microenvironment, Methylation, Immunotherapy

Received: 01 Feb 2025; Accepted: 17 Jun 2025.

Copyright: © 2025 Wen, Xu, Ni, Liu, Jin, Zhao, Luo, Fang, Mao, Lin and Qian. 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: Jun Qian, Jiangsu University Affiliated People's Hospital, Zhenjiang, 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.

Supplementary Material