Zinc finger protein 263 upregulates interleukin 33 and suppresses autophagy to accelerate the malignant progression of non-small cell lung cancer

• Jiao Xu ^[2] ; Yanjuan Zhou ^[2] ; Qiang Wang ^[3] ; Yuxin Liu ^[1] ; Jianlei Tang ^[4]
  1. [1] Jiangsu University

     Jiangsu University

     China

     
  2. [2] Department of Respiratory and Critical Care Medicine, WuJin Hospital Affiliated With Jiangsu University, WuJin Clinical College of Xuzhou Medical University, Changzhou, Jiangsu, People’s Republic of China
  3. [3] Department of Cardiothoracic Surgery, WuJin Hospital Affiliated to Jiangsu University, WuJin Clinical College of Xuzhou Medical University, Changzhou, Jiangsu, People’s Republic of China
  4. [4] Department of Intensive Care Unit, WuJin Hospital Affiliated With Jiangsu University, WuJin Clinical College of Xuzhou Medical University, 2 Yongning North Road, Changzhou, Jiangsu, People’s Republic of China

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• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 26, Nº. 4, 2024, págs. 924-935
• Idioma: inglés
• Texto completo no disponible (Saber más ...)
• Resumen

  • Purpose Non-small cell lung cancer (NSCLC) is a complex disease that remains a major public health concern worldwide. One promising avenue for NSCLC treatment is the targeting of transcription factors that regulate key pathways involved in cancer progression. In this study, we investigated the role of the transcription factor ZNF263 in NSCLC and its impact on the regulation of IL33, apoptosis, and autophagy.

    Methods Levels of ZNF263 in tissues and cell lines were identified, after which the effects of its knockdown on cellular malignant behaviors, apoptosis and autophagy were assessed. Based on bioinformatics analysis, ZNF263 was found to bind to IL33 promoter, their mutual relationship was confirmed, as well as the role of IL33 in the regulation of ZNF263. The involvement of ZNF263 in the growth of xenograft tumors was assessed using tumor-bearing nude mouse models.

    Results Experimental results revealed that ZNF263 was upregulated in NSCLC tissue samples and cell lines. Its expression level is positively correlated with cellular malignant behaviors. We further demonstrated that ZNF263 upregulated IL33 expression, which, in turn, promoted the proliferation and migration, inhibited apoptosis and autophagy in NSCLC cells. Furthermore, ZNF263 knockdown reduced the growth of xenograft tumors in nude mice.

    Conclusion This finding suggests that the inhibition of ZNF263 or IL33 may represent a novel therapeutic strategy for NSCLC. Importantly, our results highlight the crucial role of transcription factors in NSCLC and their potential as therapeutic targets.