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首页> 外文期刊>Journal of cellular physiology. >TRIM11 suppresses ferritinophagy and gemcitabine sensitivity through UBE2N/TAX1BP1 signaling in pancreatic ductal adenocarcinoma
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TRIM11 suppresses ferritinophagy and gemcitabine sensitivity through UBE2N/TAX1BP1 signaling in pancreatic ductal adenocarcinoma

机译：TRIM11抑制ferritinophagy和吉西他滨通过UBE2N / TAX1BP1信号灵敏度胰腺导管腺癌

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摘要

Gemcitabine is first-line chemotherapy for pancreatic cancer, however, the development of resistance limits its effectiveness. The tripartite motif-containing 11 (TRIM 11) protein plays crucial roles in tumor development and undergoes auto-polyubiquitination to promote interactions in selective autophagy. Therefore, Understanding whether TRIM11 is involved in ferritinophagy and gemcitabine resistance in pancreatic cancer is critical in developing pancreatic cancer therapeutics. TRIM11 expression was validated by Western blot analysis, real-time polymease chain reaction, and immunohistochemical staining. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Colony formation assays were performed to investigate pancreatic ductal adenocarcinomas (PDAC) cell viability. Mouse xenograft model of PDAC cells was established to verify the role of TRIM11 in vivo. Coim-munoprecipitation was used to identify the reciprocal regulation between TRIM11 and UBE2N. In this study, we found that TRIM11 expression were higher in PDAC cells and tissues. TRIM11 overexpression promotes PDAC cell proliferation in vitro and tumor growth in vivo. Decreased expression of TRIM 11 in PDAC patients is associated with decreased UBE2N and increased TAX1BP1 expression. Coimmu-noprecipitation established that TRIM 11 interacts and colocalizes with UBE2N. Mechanistically, TRIM11 promoted gemcitabine resistance and suppressed ferritinophagy through UBE2N-TAX1BP1 signaling. Our findings identify TRIM 11 as a key regulator of TAX1BP1 signaling with a crucial role in ferritinophagy and gemcitabine resistance in PDAC.
机译：吉西他滨是一线化疗然而,胰腺癌的发展电阻限制了其有效性。三方motif-containing 11(削减11)的蛋白质在肿瘤发展中扮演着至关重要的作用经历auto-polyubiquitination促进在选择性自噬的交互。理解TRIM11是否参与ferritinophagy和吉西他滨阻力胰腺癌在发展中是至关重要的胰腺癌的治疗。验证了免疫印迹分析,实时polymease连锁反应,免疫组织化学染色。

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