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黑素细胞系因子 miR-211 促进 BRAF 抑制剂耐药性。

The Melanocyte Lineage Factor miR-211 Promotes BRAF Inhibitor Resistance.

机构信息

Department of Dermatology, Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts, USA.

Department of Dermatology, Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts, USA.

出版信息

J Invest Dermatol. 2021 Feb;141(2):250-252. doi: 10.1016/j.jid.2020.07.010.

DOI:10.1016/j.jid.2020.07.010
PMID:33504438
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7850168/
Abstract

Resistance to targeted therapy and immunotherapy remains a major obstacle in improving care for patients with advanced melanoma. MicroRNAs play important roles in regulating gene networks involved in disease progression and resistance to therapy in cancers such as melanoma. MicroRNA miR-211 contributes to melanocyte and melanoma biology and has been implicated in targeted therapy resistance. Lee et al. (2020) report a novel mechanism by which miR-211 promotes resistance to BRAF inhibitor therapy via the upregulation of the extracellular signal-regulated kinase 5 signaling pathway.

摘要

靶向治疗和免疫治疗的耐药性仍然是改善晚期黑色素瘤患者治疗效果的主要障碍。microRNAs 在调节癌症(如黑色素瘤)中与疾病进展和治疗耐药性相关的基因网络中发挥重要作用。microRNA miR-211 参与黑素细胞和黑色素瘤的生物学过程,并与靶向治疗耐药性有关。Lee 等人(2020 年)报道了一种新的机制,即 miR-211 通过上调细胞外信号调节激酶 5 信号通路促进 BRAF 抑制剂治疗耐药性。

相似文献

1
The Melanocyte Lineage Factor miR-211 Promotes BRAF Inhibitor Resistance.黑素细胞系因子 miR-211 促进 BRAF 抑制剂耐药性。
J Invest Dermatol. 2021 Feb;141(2):250-252. doi: 10.1016/j.jid.2020.07.010.
2
MicroRNA-211 Modulates the DUSP6-ERK5 Signaling Axis to Promote BRAF-Driven Melanoma Growth In Vivo and BRAF/MEK Inhibitor Resistance.miRNA-211 调控 DUSP6-ERK5 信号轴促进 BRAF 驱动的黑色素瘤在体生长和 BRAF/MEK 抑制剂耐药性
J Invest Dermatol. 2021 Feb;141(2):385-394. doi: 10.1016/j.jid.2020.06.038. Epub 2020 Sep 2.
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miR-146a-5p impairs melanoma resistance to kinase inhibitors by targeting COX2 and regulating NFkB-mediated inflammatory mediators.miR-146a-5p 通过靶向 COX2 和调节 NFkB 介导的炎症介质来损害黑色素瘤对激酶抑制剂的耐药性。
Cell Commun Signal. 2020 Sep 23;18(1):156. doi: 10.1186/s12964-020-00601-1.
4
Elevated CRAF as a potential mechanism of acquired resistance to BRAF inhibition in melanoma.升高的CRAF作为黑色素瘤对BRAF抑制获得性耐药的潜在机制。
Cancer Res. 2008 Jun 15;68(12):4853-61. doi: 10.1158/0008-5472.CAN-07-6787.
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Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation.黑色素瘤通过 RTK 或 N-RAS 上调获得对 B-RAF(V600E)抑制的耐药性。
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Clin Cancer Res. 2017 Sep 15;23(18):5631-5638. doi: 10.1158/1078-0432.CCR-16-0758. Epub 2017 May 24.

引用本文的文献

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circRNA18_46222157_46248185 inhibits melanogenesis by targeting miR-211/EP300 pathway in goat melanocytes.环状RNA18_46222157_46248185通过靶向山羊黑素细胞中的miR-211/EP300途径抑制黑色素生成。
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本文引用的文献

1
MicroRNA-211 Modulates the DUSP6-ERK5 Signaling Axis to Promote BRAF-Driven Melanoma Growth In Vivo and BRAF/MEK Inhibitor Resistance.miRNA-211 调控 DUSP6-ERK5 信号轴促进 BRAF 驱动的黑色素瘤在体生长和 BRAF/MEK 抑制剂耐药性
J Invest Dermatol. 2021 Feb;141(2):385-394. doi: 10.1016/j.jid.2020.06.038. Epub 2020 Sep 2.
2
Efficient Suppression of NRAS-Driven Melanoma by Co-Inhibition of ERK1/2 and ERK5 MAPK Pathways.ERK1/2 和 ERK5 MAPK 通路的协同抑制可有效抑制NRAS 驱动的黑色素瘤。
J Invest Dermatol. 2020 Dec;140(12):2455-2465.e10. doi: 10.1016/j.jid.2020.03.972. Epub 2020 May 4.
3
Resistance to MAPK Inhibitors in Melanoma Involves Activation of the IGF1R-MEK5-Erk5 Pathway.黑色素瘤中对 MAPK 抑制剂的耐药性涉及 IGF1R-MEK5-Erk5 通路的激活。
Cancer Res. 2019 May 1;79(9):2244-2256. doi: 10.1158/0008-5472.CAN-18-2762. Epub 2019 Mar 4.
4
Cooperative targeting of melanoma heterogeneity with an AXL antibody-drug conjugate and BRAF/MEK inhibitors.联合使用 AXL 抗体药物偶联物和 BRAF/MEK 抑制剂靶向黑色素瘤异质性。
Nat Med. 2018 Feb;24(2):203-212. doi: 10.1038/nm.4472. Epub 2018 Jan 15.
5
miR-204-5p and miR-211-5p Contribute to BRAF Inhibitor Resistance in Melanoma.miR-204-5p 和 miR-211-5p 促进黑色素瘤对 BRAF 抑制剂的耐药性。
Cancer Res. 2018 Feb 15;78(4):1017-1030. doi: 10.1158/0008-5472.CAN-17-1318. Epub 2017 Dec 11.
6
BRAF inhibition alters the microRNA cargo in the vesicular secretome of malignant melanoma cells.BRAF 抑制改变了恶性黑素瘤细胞囊泡分泌组中的 microRNA 载量。
Proc Natl Acad Sci U S A. 2017 Jul 18;114(29):E5930-E5939. doi: 10.1073/pnas.1705206114. Epub 2017 Jul 6.
7
ERK5 and Cell Proliferation: Nuclear Localization Is What Matters.细胞外信号调节激酶5(ERK5)与细胞增殖:核定位至关重要。
Front Cell Dev Biol. 2016 Sep 22;4:105. doi: 10.3389/fcell.2016.00105. eCollection 2016.
8
MicroRNA 211 Functions as a Metabolic Switch in Human Melanoma Cells.微小RNA 211在人黑色素瘤细胞中作为一种代谢开关发挥作用。
Mol Cell Biol. 2016 Jan 19;36(7):1090-108. doi: 10.1128/MCB.00762-15.
9
Intronic miR-211 assumes the tumor suppressive function of its host gene in melanoma.内含子 miR-211 发挥其宿主基因在黑色素瘤中的肿瘤抑制功能。
Mol Cell. 2010 Dec 10;40(5):841-9. doi: 10.1016/j.molcel.2010.11.020. Epub 2010 Nov 25.
10
The regulation of miRNA-211 expression and its role in melanoma cell invasiveness.miRNA-211 表达的调控及其在黑色素瘤细胞侵袭中的作用。
PLoS One. 2010 Nov 1;5(11):e13779. doi: 10.1371/journal.pone.0013779.