ORIGINAL RESEARCH article
Front. Oncol.
Sec. Head and Neck Cancer
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1564601
This article is part of the Research TopicAdvances in the Treatment of Nasopharyngeal CancerView all 4 articles
tRF-1:28-Val-CAC-2 promotes the development of nasopharyngeal cancer by targeting EPHB2
Provisionally accepted
Hui Li1,2,3*
Xiaomin Wang2,3
Anchi Sun2,3Weiwei Liu2Rongrong Lv2,3Mingjie Zhang2Zhiwei Xing2Shiyin Ma2,3*
Yehai Liu1*Kai Zhang2*- 1Anhui Medical University, Hefei, Anhui Province, China
- 2Bengbu Medical University, Bengbu, China
- 3Anhui Engineering Technology Research Center of Biochemical Pharmaceutical, Bengbu, China
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Background: Nasopharyngeal carcinoma (NPC) is highly aggressive, with a particularly high incidence in South China. The cure rate of previous treatments is decreasing year by year, underscoring the need to devise new approaches to treating affected patients. This study was developed to examine the tRF-1:28-Val-CAC-2 expression in NPC and to elucidate its effects on proliferative, migratory, and apoptotic dynamics in NPC cells. Methods and Results: RT- qPCR was used to quantify tRF-1:28-Val-CAC-2 expression in NPC cells. Transfection was used to manipulate tRF-1:28-Val-CAC-2 expression levels, and proliferation, migration, and invasion were then evaluated through CCK-8, wound-healing, colony formation, and Transwell approaches. Apoptotic induction and cell cycle progression were assessed through flow cytometry, while EMT-related marker expression was assessed via qPCR and Western immunoblotting. The effects of tRF-1:28-Val-CAC-2 on the growth and distant metastasis of tumors were then tested in vivo using nude mice. NPC cells exhibited tRF-1:28-Val-CAC-2 upregulation that was associated with significantly increased proliferative, migratory, and invasive activity together with the suppression of apoptotic death. In vivo experiments further confirmed the ability of tRF-1:28-Val-CAC-2 to promote tumor growth and distant metastasis. At a mechanistic level, these effects were related to the control of EPHB2 gene expression by tRF-1:28 Val-CAC-2, thereby shaping the survival and malignancy of the cells. Conclusions: These results demonstrate that tRF-1:28-Val-CAC-2 promoted EPHB2 to enhance tumorigenic behavior in NPC cells, underscoring its key role as a novel target for therapeutic intervention.
Keywords: tRF-1:28-Val-CAC-2, EBPH2, NPC, tsRNA, EMT
Received: 21 Jan 2025; Accepted: 28 Apr 2025.
Copyright: © 2025 Li, Wang, Sun, Liu, Lv, Zhang, Xing, Ma, Liu and Zhang. 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:
Hui Li, Anhui Medical University, Hefei, 230032, Anhui Province, China
Shiyin Ma, Bengbu Medical University, Bengbu, China
Yehai Liu, Anhui Medical University, Hefei, 230032, Anhui Province, China
Kai Zhang, Bengbu Medical University, Bengbu, China
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