PCBP1 interacts with the HTLV-1 Tax oncoprotein to potentiate NF-&#954;B activation.

Su, Rui; Kang, Xue; Niu, Yifan; Zhao, Tiesuo; Wang, Hui

PCBP1 interacts with the HTLV-1 Tax oncoprotein to potentiate NF-κB activation.

Su, Rui; Kang, Xue; Niu, Yifan; Zhao, Tiesuo; Wang, Hui.

Afiliación

Su R; Department of Immunology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Kang X; Henan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Niu Y; Department of Immunology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Zhao T; Henan Key Laboratory of Immunology and Targeted Drug, Xinxiang Medical University, Xinxiang, China.
Wang H; Department of Immunology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.

Front Immunol ; 15: 1375168, 2024.

Article en En | MEDLINE | ID: mdl-38690287

ABSTRACT

ABSTRACT

Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma. The HTLV-1 Tax constitutively activates nuclear factor-κB (NF-κB) to promote the survival and transformation of HTLV-1-infected T cells. Despite extensive study of Tax, how Tax interacts with host factors to regulate NF-κB activation and HTLV-1-driven cell proliferation is not entirely clear. Here, we showed that overexpression of Poly (rC)-binding protein 1 (PCBP1) promoted Tax-mediated IκB kinase (IKK)-NF-κB signaling activation, whereas knockdown of PCBP1 attenuated Tax-dependent IKK-NF-κB activation. However, Tax activation of HTLV-1 long terminal repeat was unaffected by PCBP1. Furthermore, depletion of PCBP1 led to apoptosis and reduced proliferation of HTLV-1-transformed cells. Mechanistically, PCBP1 interacted and co-localized with Tax in the cytoplasm, and PCBP1 KH3 domain was indispensable for the interaction between PCBP1 and Tax. Moreover, PCBP1 facilitated the assembly of Tax/IKK complex. Collectively, our results demonstrated that PCBP1 may exert an essential effect in Tax/IKK complex combination and subsequent NF-κB activation, which provides a novel insight into the pathogenetic mechanisms of HTLV-1.

Asunto(s)

Proteínas de Unión al ADN; Productos del Gen tax; Ribonucleoproteínas Nucleares Heterogéneas; Virus Linfotrópico T Tipo 1 Humano; FN-kappa B; Proteínas de Unión al ARN; Humanos; Productos del Gen tax/metabolismo; FN-kappa B/metabolismo; Virus Linfotrópico T Tipo 1 Humano/fisiología; Proteínas de Unión al ARN/metabolismo; Proteínas de Unión al ARN/genética; Proteínas de Unión al ADN/metabolismo; Proteínas de Unión al ADN/genética; Ribonucleoproteínas Nucleares Heterogéneas/metabolismo; Ribonucleoproteínas Nucleares Heterogéneas/genética; Transducción de Señal; Células HEK293; Unión Proteica; Proliferación Celular; Infecciones por HTLV-I/metabolismo; Infecciones por HTLV-I/virología; Apoptosis; Quinasa I-kappa B/metabolismo; Interacciones Huésped-Patógeno

Palabras clave

HTLV-1 tax; IKK-NF-κB signaling; PCBP1; cell proliferation; interaction

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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Virus Linfotrópico T Tipo 1 Humano / Productos del Gen tax / FN-kappa B / Proteínas de Unión al ARN / Ribonucleoproteínas Nucleares Heterogéneas / Proteínas de Unión al ADN Límite: Humans Idioma: En Revista: Front Immunol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza

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