致癌物质DDX46通过促进JMJD6/CDK4信号通路,促进胰腺癌的发展和吉西他滨耐药性的产生。

IF 2 4区 医学 Q3 ONCOLOGY
Neoplasma Pub Date : 2024-06-01 Epub Date: 2024-05-17 DOI:10.4149/neo_2024_230904N469
Guang Yang, Yun Wang, Kairui Wang, Xinjia Liu, Jing Yang
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引用次数: 0

摘要

胰腺癌(PAAD)是一种预后不良的致命恶性肿瘤。目前的治疗策略非常有限,而吉西他滨是一种典型的治疗药物,已被证实可以改善胰腺癌患者的预后。然而,吉西他滨的治疗效果远不能令人满意,仍有待进一步提高。DEAD-Box螺旋酶46(DDX46)是一种RNA螺旋酶,可促进多种癌症的发展。然而,它在PAAD中的作用却鲜为人知。本研究发现,DDX46在PAAD组织中高表达,并与不良预后相关。敲除DDX46可抑制PAAD细胞在体外和体内的生长,并使PAAD细胞对吉西他滨治疗敏感。在机制上,DDX46与JMJD6结合并促进JMJD6/CDK4信号通路。JMJD6的过表达逆转了DDX46敲除的抗肿瘤功能。我们的研究发现了PAAD进展的新病理机制,并为提高吉西他滨疗效提供了潜在的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oncogenic DDX46 promotes pancreatic cancer development and gemcitabine resistance by facilitating the JMJD6/CDK4 signaling pathway.

Pancreatic cancer (PAAD) is a fatal malignancy with a poor prognosis. The treatment strategies are quite limited and gemcitabine is the canonical one, which has been proven to improve the prognosis of PAAD patients. However, the treatment efficiency of gemcitabine is far from satisfactory and remains to be further improved. DEAD-Box Helicase 46 (DDX46) is a kind of RNA helicase, which promotes multiple cancers development. However, its role in PAAD is largely unknown. In the present study, we found DDX46 was highly expressed in PAAD tissues and correlated with poor prognosis. Knockdown of DDX46 repressed PAAD cell growth in vitro and in vivo and sensitized PAAD cells to gemcitabine treatment. Mechanically, DDX46 bound to JMJD6 and promoted JMJD6/CDK4 signaling pathway. Overexpression of JMJD6 reversed the anti-tumor function of DDX46 knockdown. Our study found a novel pathological mechanism of PAAD progression and provided a potential therapeutic target to improve gemcitabine efficiency.

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来源期刊
Neoplasma
Neoplasma 医学-肿瘤学
CiteScore
5.40
自引率
0.00%
发文量
238
审稿时长
3 months
期刊介绍: The journal Neoplasma publishes articles on experimental and clinical oncology and cancer epidemiology.
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