Zinc finger protein 263 promotes colorectal cancer cell progression by activating STAT3 and enhancing chemoradiotherapy resistance.

Du, Yadan; Chen, Yawen; Yan, Zaihua; Yang, Jian; Da, Mingxu

Du, Yadan; Chen, Yawen; Yan, Zaihua; Yang, Jian; Da, Mingxu.

Afiliación

Du Y; The First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, China.
Chen Y; Department of Surgical Oncology, Gansu Provincial Hospital, Lanzhou, 730000, China.
Yan Z; The First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, China.
Yang J; Department of Surgical Oncology, Gansu Provincial Hospital, Lanzhou, 730000, China.
Da M; The Second Department of Gastrointestinal Surgery, The Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, China.

Sci Rep ; 14(1): 21827, 2024 09 18.

Article en En | MEDLINE | ID: mdl-39294234

ABSTRACT

ABSTRACT

Zinc finger protein 263 (ZNF263) is frequently upregulated in various tumor types; however, its function and regulatory mechanism in colorectal cancer (CRC) have not yet been elucidated. In this study, the expression of ZNF263 was systematically examined using data from The Cancer Genome Atlas database and samples from patients with CRC. The results indicated that high expression of ZNF263 in CRC tissues is significantly associated with tumor grade, lymph node metastasis and disant metastasis. Additionally, overexpression of ZNF263 significantly promoted the proliferation, invasion, migration, and epithelial-mesenchymal transition of CRC cells, while also increasing signal transducer and activator of transcription 3 (STAT3) expression and mRNA stability. Conversely, knockdown of ZNF263 inhibited the malignant behavior of CRC cells and decreased STAT3 expression and mRNA stability. Further mechanism studies using chromatin immunoprecipitation (CHIP) and luciferase assays verified that ZNF263 directly binds to the STAT3 promoter. Rescue experiments demonstrated that the knockdown or overexpression of STAT3 could significantly reverse the effects of ZNF263 on CRC cells. Additionally, our study found that overexpression of ZNF263 enhanced the resistance of CRC cells to the chemoradiotherapy. In summary, this study not only elucidated the significant role of ZNF263 in CRC but also proposed novel approaches and methodologies for the diagnosis and treatment of this malignancy.

Asunto(s)

Proliferación Celular; Neoplasias Colorrectales; Proteínas de Unión al ADN; Regulación Neoplásica de la Expresión Génica; Factor de Transcripción STAT3; Femenino; Humanos; Masculino; Persona de Mediana Edad; Línea Celular Tumoral; Movimiento Celular; Quimioradioterapia/métodos; Neoplasias Colorrectales/patología; Neoplasias Colorrectales/genética; Neoplasias Colorrectales/metabolismo; Progresión de la Enfermedad; Resistencia a Antineoplásicos/genética; Transición Epitelial-Mesenquimal/genética; Factor de Transcripción STAT3/metabolismo; Proteínas de Unión al ADN/genética; Proteínas de Unión al ADN/metabolismo

Palabras clave

Chemotherapy; Colorectal cancer; Epithelial-mesenchymal transition; Radiotherapy; Signal transducer and activator of transcription 3; Zinc finger protein 263

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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Colorrectales / Regulación Neoplásica de la Expresión Génica / Proliferación Celular / Proteínas de Unión al ADN / Factor de Transcripción STAT3 Límite: Female / Humans / Male / Middle aged Idioma: En Revista: Sci Rep Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido

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