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综述:3-磷酸肌醇依赖性蛋白激酶-1(PDPK1)——一种新兴的癌症干细胞靶点

Mini-Review: PDPK1 (3-phosphoinositide dependent protein kinase-1), An Emerging Cancer Stem Cell Target.

作者信息

Domrachev Bogdan, Singh Sitanshu, Li Dandan, Rudloff Udo

机构信息

Rare Tumor Initiative, Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.

Thoracic & GI Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.

出版信息

J Cancer Treatment Diagn. 2021 Apr 30;5(1):30-35. doi: 10.29245/2578-2967/2021/1.1194.

DOI:10.29245/2578-2967/2021/1.1194
PMID:34079928
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8168947/
Abstract

Cancer stem cells (CSCs) are subpopulations of tumor cells that possess abilities for self-renewal, differentiation, and tumor initiation. These rare but therapy-recalcitrant cells are assumed to repopulate tumors following administration of systemic chemotherapy driving therapy failure, tumor recurrence, and disease progression. In early clinical trials, anti-CSC therapies have found limited success to-date possibly due to the inherent heterogeneity and plasticity of CSCs and the incomplete characterization of essential CSC targets. Here, we review the role of 3-phosphoinositide dependent protein kinase-1 (PDPK1) as an emerging CSC target. While most previous studies have relied on CSC models which are based on lineage and tissue-specific marker profiles to define the relationships between putative target and CSC traits, this review discusses PDPK1 and its role in CSC biology with an emphasis on CSC systems which are based on proposed function like label-retaining cancer cells (LRCCs).

摘要

癌症干细胞(CSCs)是肿瘤细胞的亚群,具有自我更新、分化和启动肿瘤的能力。这些罕见但对治疗具有抗性的细胞被认为在全身化疗后会重新填充肿瘤,从而导致治疗失败、肿瘤复发和疾病进展。在早期临床试验中,抗CSC疗法迄今取得的成功有限,这可能是由于CSCs固有的异质性和可塑性以及关键CSC靶点的表征不完整。在此,我们综述了3-磷酸肌醇依赖性蛋白激酶-1(PDPK1)作为新兴CSC靶点的作用。虽然大多数先前的研究依赖于基于谱系和组织特异性标记谱的CSC模型来定义假定靶点与CSC特征之间的关系,但本综述讨论了PDPK1及其在CSC生物学中的作用,重点是基于如标记保留癌细胞(LRCCs)等拟议功能的CSC系统。

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本文引用的文献

1
Plasticity of Cancer Stem Cell: Origin and Role in Disease Progression and Therapy Resistance.癌症干细胞可塑性:起源及其在疾病进展和治疗耐药中的作用。
Stem Cell Rev Rep. 2020 Apr;16(2):397-412. doi: 10.1007/s12015-019-09942-y.
2
Tumor Dormancy and Slow-Cycling Cancer Cells.肿瘤休眠和慢周期癌细胞。
Adv Exp Med Biol. 2019;1164:199-206. doi: 10.1007/978-3-030-22254-3_15.
3
A Pan-ALDH1A Inhibitor Induces Necroptosis in Ovarian Cancer Stem-like Cells.一种泛 ALDH1A 抑制剂诱导卵巢癌类干细胞发生细胞坏死。
MALAT1-miRNAs network regulate thymidylate synthase and affect 5FU-based chemotherapy.
MALAT1-miRNAs 网络调节胸苷酸合成酶并影响基于 5FU 的化疗。
Mol Med. 2022 Aug 3;28(1):89. doi: 10.1186/s10020-022-00516-2.
4
Network controllability solutions for computational drug repurposing using genetic algorithms.利用遗传算法解决计算药物再利用的网络可控性问题。
Sci Rep. 2022 Jan 26;12(1):1437. doi: 10.1038/s41598-022-05335-3.
Cell Rep. 2019 Mar 12;26(11):3061-3075.e6. doi: 10.1016/j.celrep.2019.02.032.
4
Cancer Stem Cells: The Architects of the Tumor Ecosystem.肿瘤干细胞:肿瘤生态系统的建筑师。
Cell Stem Cell. 2019 Jan 3;24(1):41-53. doi: 10.1016/j.stem.2018.12.009.
5
Targeting Cancer Stemness in the Clinic: From Hype to Hope.靶向肿瘤干细胞:从炒作到希望。
Cell Stem Cell. 2019 Jan 3;24(1):25-40. doi: 10.1016/j.stem.2018.11.017. Epub 2018 Dec 27.
6
Loss of PDPK1 abrogates resistance to gemcitabine in label-retaining pancreatic cancer cells.PDPK1 的缺失消除了标签保留胰腺癌细胞对吉西他滨的耐药性。
BMC Cancer. 2018 Jul 31;18(1):772. doi: 10.1186/s12885-018-4690-1.
7
Reciprocal Signaling between Glioblastoma Stem Cells and Differentiated Tumor Cells Promotes Malignant Progression.胶质母细胞瘤干细胞与分化肿瘤细胞之间的相互信号传递促进恶性进展。
Cell Stem Cell. 2018 Apr 5;22(4):514-528.e5. doi: 10.1016/j.stem.2018.03.011.
8
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