ORIGINAL RESEARCH article
Front. Oncol.
Sec. Hematologic Malignancies
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1665309
B7-H7 knockdown suppresses the proliferation, metastasis, and drug resistance of B-cell non-Hodgkin lymphoma cells by inhibiting the PI3K/Akt pathway
Provisionally accepted
- Linyi People's Hospital, Linyi, China
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Background: The activation of key immune regulatory factors is an important driving factor in the progression of therapeutic resistance in patients with B-NHL. As a novel immune regulatory factor of the B7 family, surface B7-H7 interacts with receptors on active T cells to promote tumor immune escape. However, investigations of B7-H7 on B-NHL are still lacking. Methods: In vitro assays were performed to examine the proliferation, migration, invasion, and starvation tolerance abilities of B7-H7 knockdown cells. A xenograft mouse model of B-NHL was established to investigate the in vivo functions of B7-H7. The impact of B7-H7 on patient prognosis was analyzed using the GEPIA and GEO datasets. We also examined whether B7-H7 knockdown affects resistance to rituximab (RTX) and verified this by establishing a rituximab-resistant cell line (RRC). Finally, RNA sequencing was performed on B7-H7 knockdown cells, rituximab-treated cells, and rituximab-resistant cells. Results: B7-H7 knockdown inhibited tumor growth in vivo and suppressed cell proliferation, migration, invasion, and starvation-bearing ability in vitro. Patients with diffuse large B-cell lymphoma (DLBCL) with high expression of B7-H7 showed an increased death rate. B7-H7 knockdown increased sensitivity to rituximab, and the strong resistance of RRC was weakened to some extent when B7-H7 expression in RRC was inhibited. RNA sequencing revealed that the PI3K/Akt pathway may play an important role in B7-H7 knockdown in cells and drug-resistant strains. This was confirmed by western blotting and agonist/inhibitor treatment. Conclusions: Suppression of B7-H7 inhibited tumor progression and induced RTX sensitivity by suppressing the PI3K/Akt pathway.
Keywords: B7-H7, B-NHL, rituximab, Resistance, Cancer Progression, PI3K/AKT
Received: 14 Jul 2025; Accepted: 29 Sep 2025.
Copyright: © 2025 Zhai, Zou, Yin, Ge, Xiong, Yan, Xie and Wang. 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:
Xiaoli Xie, xiexiaoli1992@163.com
Lijuan Wang, wanglj730@163.com
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