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抑制 microRNA-16 通过 NF-κB 信号通路靶向 IKBKB 促进肝癌对紫杉醇的耐药性。

Inhibition of microRNA-16 facilitates the paclitaxel resistance by targeting IKBKB via NF-κB signaling pathway in hepatocellular carcinoma.

机构信息

Organ Transplantation Center, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China.

Department of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, 510006, China.

出版信息

Biochem Biophys Res Commun. 2018 Sep 5;503(2):1035-1041. doi: 10.1016/j.bbrc.2018.06.113. Epub 2018 Aug 2.

DOI:10.1016/j.bbrc.2018.06.113
PMID:29935185
Abstract

Hepatocellular carcinoma (HCC) is a common malignant tumor usually resistant to chemotherapy. MicroRNAs play important roles in modulation of carcinogenesis and chemoresistance, which miR-16 has been reported to mediate chemoresistance in many types of cancers. However, the role of miR-16 in HCC remains unknown. The aim of this study was to investigate whether miR-16 is participated in chemoresistance in HCC and shed light on the underlying molecular mechanisms. The findings of the current study discover that miR-16 is down-regulated in HCC tissue and cell lines. The results demonstrate that the inhibition of miR-16 renders resistance to paclitaxel in vitro and in vivo by targeting IKBKB via NF-κB signaling pathway, suggesting that miR-16 may be a meaningful therapeutic potential to overcome drug resistance in HCC.

摘要

肝细胞癌(HCC)是一种常见的恶性肿瘤,通常对化疗有抵抗力。miRNA 在调节致癌作用和化疗耐药性方面发挥着重要作用,已有报道称 miR-16 可介导多种癌症的化疗耐药性。然而,miR-16 在 HCC 中的作用尚不清楚。本研究旨在探讨 miR-16 是否参与 HCC 的化疗耐药性,并阐明其潜在的分子机制。本研究发现 miR-16 在 HCC 组织和细胞系中下调。结果表明,通过 NF-κB 信号通路靶向 IKBKB,抑制 miR-16 可在体外和体内赋予紫杉醇耐药性,表明 miR-16 可能是克服 HCC 药物耐药性的有意义的治疗潜力。

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