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STAT5: Understanding the Biology of KRAS-Driven Pancreatic Cancer.

作者信息

Papavassiliou Kostas A, Adamopoulos Christos, Papavassiliou Athanasios G

机构信息

First University Department of Respiratory Medicine, 'Sotiria' Chest Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece.

Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Athens, Greece.

出版信息

J Cell Mol Med. 2024 Dec;28(24):e70303. doi: 10.1111/jcmm.70303.

DOI:10.1111/jcmm.70303
PMID:39698878
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11656218/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/417f/11656218/713ac382c161/JCMM-28-e70303-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/417f/11656218/713ac382c161/JCMM-28-e70303-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/417f/11656218/713ac382c161/JCMM-28-e70303-g001.jpg

相似文献

1
STAT5: Understanding the Biology of KRAS-Driven Pancreatic Cancer.信号转导及转录激活因子5:了解KRAS驱动的胰腺癌生物学特性
J Cell Mol Med. 2024 Dec;28(24):e70303. doi: 10.1111/jcmm.70303.
2
Pancreatic STAT5 activation promotes Kras-induced and inflammation-induced acinar-to-ductal metaplasia and pancreatic cancer.胰腺 STAT5 的激活促进 Kras 诱导的和炎症诱导的腺泡到导管化生和胰腺癌。
Gut. 2024 Oct 7;73(11):1831-1843. doi: 10.1136/gutjnl-2024-332225.
3
Identification of susceptibility loci in a mouse model of KRASG12D-driven pancreatic cancer.KRASG12D 驱动的胰腺癌小鼠模型中易感基因座的鉴定。
Cancer Res. 2010 Nov 1;70(21):8398-406. doi: 10.1158/0008-5472.CAN-09-3980. Epub 2010 Oct 19.
4
Krüppel-like Factor 5, Increased in Pancreatic Ductal Adenocarcinoma, Promotes Proliferation, Acinar-to-Ductal Metaplasia, Pancreatic Intraepithelial Neoplasia, and Tumor Growth in Mice.Krüppel 样因子 5 在胰腺导管腺癌中增加,促进增殖、腺泡到导管化生、胰腺上皮内瘤变和肿瘤生长在小鼠中。
Gastroenterology. 2018 Apr;154(5):1494-1508.e13. doi: 10.1053/j.gastro.2017.12.005. Epub 2017 Dec 15.
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Discovery of potent and noncovalent KRAS inhibitors: Structure-based virtual screening and biological evaluation.强效非共价KRAS抑制剂的发现:基于结构的虚拟筛选与生物学评价。
Front Pharmacol. 2022 Dec 22;13:1094887. doi: 10.3389/fphar.2022.1094887. eCollection 2022.
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Precise and efficient silencing of mutant Kras by CRISPR-CasRx controls pancreatic cancer progression.CRISPR-CasRx 精准高效沉默突变型 Kras 可控制胰腺癌进展。
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Kras induces changes in chromatin territories that differentially impact early nuclear reprogramming in pancreatic cells.Kras 诱导染色质领域发生变化,从而对胰腺细胞的早期核重编程产生不同影响。
Genome Biol. 2021 Oct 14;22(1):289. doi: 10.1186/s13059-021-02498-6.
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Identification of a novel IL-5 signaling pathway in chronic pancreatitis and crosstalk with pancreatic tumor cells.鉴定慢性胰腺炎中的新型 IL-5 信号通路及其与胰腺肿瘤细胞的串扰
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Cytokine CCL9 Mediates Oncogenic KRAS-Induced Pancreatic Acinar-to-Ductal Metaplasia by Promoting Reactive Oxygen Species and Metalloproteinases.细胞因子 CCL9 通过促进活性氧和金属蛋白酶介导致癌 KRAS 诱导的胰腺腺泡到导管化生。
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Metabolic reprogramming by mutant GNAS creates an actionable dependency in intraductal papillary mucinous neoplasms of the pancreas.突变型GNAS引起的代谢重编程在胰腺导管内乳头状黏液性肿瘤中产生了一个可靶向治疗的依赖关系。
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本文引用的文献

1
Distinct clinical outcomes and biological features of specific KRAS mutants in human pancreatic cancer.人类胰腺癌中特定 KRAS 突变体的不同临床结果和生物学特征。
Cancer Cell. 2024 Sep 9;42(9):1614-1629.e5. doi: 10.1016/j.ccell.2024.08.002. Epub 2024 Aug 29.
2
Pancreatic STAT5 activation promotes Kras-induced and inflammation-induced acinar-to-ductal metaplasia and pancreatic cancer.胰腺 STAT5 的激活促进 Kras 诱导的和炎症诱导的腺泡到导管化生和胰腺癌。
Gut. 2024 Oct 7;73(11):1831-1843. doi: 10.1136/gutjnl-2024-332225.
3
Strain-release alkylation of Asp12 enables mutant selective targeting of K-Ras-G12D.
Asp12 应变释放烷基化使 K-Ras-G12D 的突变体选择性靶向成为可能。
Nat Chem Biol. 2024 Sep;20(9):1114-1122. doi: 10.1038/s41589-024-01565-w. Epub 2024 Mar 5.
4
A selective small-molecule STAT5 PROTAC degrader capable of achieving tumor regression in vivo.一种选择性的小分子 STAT5 PROTAC 降解剂,能够在体内实现肿瘤消退。
Nat Chem Biol. 2023 Jun;19(6):703-711. doi: 10.1038/s41589-022-01248-4. Epub 2023 Feb 2.
5
Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenvironment.致癌性 KRAS 驱动的胰腺癌细胞代谢重编程利用肿瘤微环境中的细胞因子。
Cancer Discov. 2020 Apr;10(4):608-625. doi: 10.1158/2159-8290.CD-19-0297. Epub 2020 Feb 11.
6
mTOR direct crosstalk with STAT5 promotes de novo lipid synthesis and induces hepatocellular carcinoma.mTOR 与 STAT5 的直接串扰促进从头合成脂质并诱导肝细胞癌。
Cell Death Dis. 2019 Aug 14;10(8):619. doi: 10.1038/s41419-019-1828-2.
7
Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia.具有不同个性的双胞胎:STAT5B 而非 STAT5A 在 BCR/ABL 诱导的白血病中起着关键作用。
Leukemia. 2019 Jul;33(7):1583-1597. doi: 10.1038/s41375-018-0369-5. Epub 2019 Jan 24.
8
Suppression of STAT5b in pancreatic cancer cells leads to attenuated gemcitabine chemoresistance, adhesion and invasion.胰腺癌细胞中STAT5b的抑制导致吉西他滨化疗耐药性、黏附及侵袭能力减弱。
Oncol Rep. 2016 Jun;35(6):3216-26. doi: 10.3892/or.2016.4727. Epub 2016 Apr 1.
9
STAT5b as molecular target in pancreatic cancer--inhibition of tumor growth, angiogenesis, and metastases.STAT5b 作为胰腺癌的分子靶点——抑制肿瘤生长、血管生成和转移。
Neoplasia. 2012 Oct;14(10):915-25. doi: 10.1593/neo.12878.