• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

PPP6C,一种丝氨酸-苏氨酸磷酸酶,通过调节 MITF 活性调节黑素细胞分化,并有助于黑色素瘤的肿瘤发生。

PPP6C, a serine-threonine phosphatase, regulates melanocyte differentiation and contributes to melanoma tumorigenesis through modulation of MITF activity.

机构信息

Department of Surgery, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY, USA.

Department of Medicine, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY, USA.

出版信息

Sci Rep. 2022 Apr 2;12(1):5573. doi: 10.1038/s41598-022-08936-0.

DOI:10.1038/s41598-022-08936-0
PMID:35368039
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8976846/
Abstract

It is critical to understand the molecular mechanisms governing the regulation of MITF, a lineage specific transcription factor in melanocytes and an oncogene in melanoma. We identified PPP6C, a serine/threonine phosphatase, as a key regulator of MITF in melanoma. PPP6C is the only recurrently mutated serine/threonine phosphatase across all human cancers identified in sequencing studies and the recurrent R264C mutation occurs exclusively in melanoma. Using a zebrafish developmental model system, we demonstrate that PPP6C expression disrupts melanocyte differentiation. Melanocyte disruption was rescued by engineering phosphomimetic mutations at serine residues on MITF. We developed an in vivo MITF promoter assay in zebrafish and studied the effects of PPP6C(R264C) on regulating MITF promoter activity. Expression of PPP6C(R264C) cooperated with oncogenic NRAS(Q61K) to accelerate melanoma initiation in zebrafish, consistent with a gain of function alteration. Using a human melanoma cell line, we examined the requirement for PPP6C in proliferation and MITF expression. We show that genetic inactivation of PPP6C increases MITF and target gene expression, decreases sensitivity to BRAF inhibition, and increases phosphorylated MITF in a BRAF(V600E) mutant melanoma cell line. Our data suggests that PPP6C may be a relevant drug target in melanoma and proposes a mechanism for its action.

摘要

了解调控 MITF 的分子机制至关重要,MITF 是黑素细胞中一种谱系特异性转录因子,也是黑色素瘤中的癌基因。我们鉴定出 PPP6C 是黑色素瘤中 MITF 的关键调节因子,它是丝氨酸/苏氨酸磷酸酶家族中唯一在所有人类癌症测序研究中反复突变的磷酸酶,而 R264C 突变则仅发生在黑色素瘤中。利用斑马鱼发育模型系统,我们证明 PPP6C 的表达会破坏黑素细胞分化。通过对 MITF 丝氨酸残基进行磷酸模拟突变的工程设计,可挽救黑素细胞的破坏。我们在斑马鱼中开发了一种体内 MITF 启动子检测,研究了 PPP6C(R264C)对调节 MITF 启动子活性的影响。PPP6C(R264C)的表达与致癌性 NRAS(Q61K)协同作用,加速了斑马鱼黑色素瘤的起始,这与功能获得性改变一致。我们利用人类黑色素瘤细胞系研究了 PPP6C 在增殖和 MITF 表达中的作用。我们发现 PPP6C 的遗传失活增加了 MITF 和靶基因的表达,降低了 BRAF 抑制剂的敏感性,并增加了 BRAF(V600E)突变黑色素瘤细胞系中磷酸化 MITF 的水平。我们的数据表明 PPP6C 可能是黑色素瘤中一个相关的药物靶点,并提出了其作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/598dac6ca0d6/41598_2022_8936_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/99381f741115/41598_2022_8936_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/47383d2b76ed/41598_2022_8936_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/ff38bf7115e3/41598_2022_8936_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/f4b2eac2524e/41598_2022_8936_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/c357984718af/41598_2022_8936_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/598dac6ca0d6/41598_2022_8936_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/99381f741115/41598_2022_8936_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/47383d2b76ed/41598_2022_8936_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/ff38bf7115e3/41598_2022_8936_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/f4b2eac2524e/41598_2022_8936_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/c357984718af/41598_2022_8936_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af11/8976846/598dac6ca0d6/41598_2022_8936_Fig6_HTML.jpg

相似文献

1
PPP6C, a serine-threonine phosphatase, regulates melanocyte differentiation and contributes to melanoma tumorigenesis through modulation of MITF activity.PPP6C,一种丝氨酸-苏氨酸磷酸酶,通过调节 MITF 活性调节黑素细胞分化,并有助于黑色素瘤的肿瘤发生。
Sci Rep. 2022 Apr 2;12(1):5573. doi: 10.1038/s41598-022-08936-0.
2
A conditional zebrafish MITF mutation reveals MITF levels are critical for melanoma promotion vs. regression in vivo.条件性斑马鱼 MITF 突变揭示了 MITF 水平在体内黑色素瘤促进与消退中至关重要。
J Invest Dermatol. 2014 Jan;134(1):133-140. doi: 10.1038/jid.2013.293. Epub 2013 Jul 5.
3
Oncogenic BRAF regulates melanoma proliferation through the lineage specific factor MITF.致癌性BRAF通过谱系特异性因子MITF调节黑色素瘤增殖。
PLoS One. 2008 Jul 16;3(7):e2734. doi: 10.1371/journal.pone.0002734.
4
Ppp6c haploinsufficiency accelerates UV-induced BRAF(V600E)-initiated melanomagenesis.Ppp6c单倍体不足会加速紫外线诱导的BRAF(V600E)引发的黑色素瘤发生。
Cancer Sci. 2021 Jun;112(6):2233-2244. doi: 10.1111/cas.14895. Epub 2021 Apr 10.
5
TFAP2 paralogs regulate melanocyte differentiation in parallel with MITF.TFAP2 旁系同源物与 MITF 协同调节黑素细胞分化。
PLoS Genet. 2017 Mar 1;13(3):e1006636. doi: 10.1371/journal.pgen.1006636. eCollection 2017 Mar.
6
A role for ATF2 in regulating MITF and melanoma development.ATF2 在调节 MITF 和黑色素瘤发生中的作用。
PLoS Genet. 2010 Dec 23;6(12):e1001258. doi: 10.1371/journal.pgen.1001258.
7
Deciphering the Role of Oncogenic MITFE318K in Senescence Delay and Melanoma Progression.解析致癌性 MITFE318K 在衰老延迟和黑色素瘤进展中的作用。
J Natl Cancer Inst. 2017 Aug 1;109(8). doi: 10.1093/jnci/djw340.
8
Inhibition of oncogenic BRAF activity by indole-3-carbinol disrupts microphthalmia-associated transcription factor expression and arrests melanoma cell proliferation.吲哚 - 3 - 甲醇对致癌性BRAF活性的抑制作用会破坏小眼畸形相关转录因子的表达并阻止黑色素瘤细胞增殖。
Mol Carcinog. 2017 Jan;56(1):49-61. doi: 10.1002/mc.22472. Epub 2016 Feb 15.
9
Differentiated melanocyte cell division occurs in vivo and is promoted by mutations in Mitf.有丝分裂后黑素细胞在体内发生分裂,其由 Mitf 突变所促进。
Development. 2011 Aug;138(16):3579-89. doi: 10.1242/dev.064014. Epub 2011 Jul 19.
10
Simultaneous suppression of MITF and BRAF V600E enhanced inhibition of melanoma cell proliferation.同时抑制MITF和BRAF V600E可增强对黑色素瘤细胞增殖的抑制作用。
Cancer Sci. 2009 Oct;100(10):1863-9. doi: 10.1111/j.1349-7006.2009.01266.x. Epub 2009 Jun 29.

引用本文的文献

1
Functional Role of Protein Phosphatase-6 (): Regulation of Expression and Modulation of Activity.蛋白磷酸酶6的功能作用( ):表达调控与活性调节
Curr Med Chem. 2025;32(22):4481-4498. doi: 10.2174/0109298673310356240630103257.
2
Loss of Fbxo45 in AT2 cells leads to insufficient histone supply and initiates lung adenocarcinoma.AT2细胞中Fbxo45的缺失导致组蛋白供应不足并引发肺腺癌。
Cell Death Differ. 2024 Dec 13. doi: 10.1038/s41418-024-01433-z.
3
Melanoma genomics - will we go beyond BRAF in clinics?黑色素瘤基因组学——我们在临床治疗上会超越 BRAF 吗?

本文引用的文献

1
Current status of intralesional agents in treatment of malignant melanoma.瘤内注射药物治疗恶性黑色素瘤的现状
Ann Transl Med. 2021 Jun;9(12):1038. doi: 10.21037/atm-21-491.
2
PPP6C negatively regulates oncogenic ERK signaling through dephosphorylation of MEK.PPP6C 通过去磷酸化 MEK 负调控致癌 ERK 信号。
Cell Rep. 2021 Mar 30;34(13):108928. doi: 10.1016/j.celrep.2021.108928.
3
The MEK/ERK Network as a Therapeutic Target in Human Cancer.MEK/ERK 网络作为人类癌症的治疗靶点。
J Cancer Res Clin Oncol. 2024 Sep 28;150(9):433. doi: 10.1007/s00432-024-05957-2.
4
The Impact of Mutational Hotspots on Cancer Survival.突变热点对癌症生存的影响。
Cancers (Basel). 2024 Mar 6;16(5):1072. doi: 10.3390/cancers16051072.
5
A Comprehensive Analysis of Cutaneous Melanoma Patients in Greece Based on Multi-Omic Data.基于多组学数据对希腊皮肤黑色素瘤患者的综合分析
Cancers (Basel). 2023 Jan 28;15(3):815. doi: 10.3390/cancers15030815.
6
Innate immune checkpoint inhibitor resistance is associated with melanoma sub-types exhibiting invasive and de-differentiated gene expression signatures.先天免疫检查点抑制剂耐药与表现出侵袭性和去分化基因表达特征的黑色素瘤亚型有关。
Front Immunol. 2022 Sep 28;13:955063. doi: 10.3389/fimmu.2022.955063. eCollection 2022.
Mol Cancer Res. 2021 Mar;19(3):361-374. doi: 10.1158/1541-7786.MCR-20-0687. Epub 2020 Nov 2.
4
Recent Advances of SHP2 Inhibitors in Cancer Therapy: Current Development and Clinical Application.SHP2 抑制剂在癌症治疗中的最新进展:当前的发展和临床应用。
J Med Chem. 2020 Oct 22;63(20):11368-11396. doi: 10.1021/acs.jmedchem.0c00249. Epub 2020 Jun 10.
5
Zebrafish MITF-Low Melanoma Subtype Models Reveal Transcriptional Subclusters and MITF-Independent Residual Disease.斑马鱼 MITF-Low 黑色素瘤亚型模型揭示了转录亚群和 MITF 非依赖性残留疾病。
Cancer Res. 2019 Nov 15;79(22):5769-5784. doi: 10.1158/0008-5472.CAN-19-0037. Epub 2019 Oct 3.
6
MITF controls the TCA cycle to modulate the melanoma hypoxia response.MITF 通过调控 TCA 循环来调节黑色素瘤的缺氧反应。
Pigment Cell Melanoma Res. 2019 Nov;32(6):792-808. doi: 10.1111/pcmr.12802. Epub 2019 Jul 8.
7
SHP2 Inhibition Overcomes RTK-Mediated Pathway Reactivation in KRAS-Mutant Tumors Treated with MEK Inhibitors.SHP2 抑制克服了 MEK 抑制剂治疗中 KRAS 突变肿瘤中 RTK 介导的通路再激活。
Mol Cancer Ther. 2019 Jul;18(7):1323-1334. doi: 10.1158/1535-7163.MCT-18-0852. Epub 2019 May 8.
8
BRAF Splice Variant Resistance to RAF Inhibitor Requires Enhanced MEK Association.BRAF 剪接变异体对 RAF 抑制剂的耐药性需要增强的 MEK 结合。
Cell Rep. 2018 Nov 6;25(6):1501-1510.e3. doi: 10.1016/j.celrep.2018.10.049.
9
Improved estimation of cancer dependencies from large-scale RNAi screens using model-based normalization and data integration.基于模型的归一化和数据集成提高了大规模 RNAi 筛选中癌症相关性的估计。
Nat Commun. 2018 Nov 2;9(1):4610. doi: 10.1038/s41467-018-06916-5.
10
BRAF/MAPK and GSK3 signaling converges to control MITF nuclear export.BRAF/MAPK 和 GSK3 信号传导汇聚以控制 MITF 的核输出。
Proc Natl Acad Sci U S A. 2018 Sep 11;115(37):E8668-E8677. doi: 10.1073/pnas.1810498115. Epub 2018 Aug 27.