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Polo样激酶1抑制剂在奥希替尼耐药的非小细胞肺癌细胞中的作用 The effect of PLK1 inhibitor in osimertinib resistant non-small cell lung carcinoma cells

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PROVIDER: S-EPMC10630054 | biostudies-literature | 2023 Oct

REPOSITORIES: biostudies-literature

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去泛素化酶JOSD2通过调控DNA损伤修复影响非小细胞肺癌细胞对抗肿瘤药物的敏感性 Deubiquitinating enzyme JOSD2 affects susceptibility of non-small cell lung carcinoma cells to anti-cancer drugs through DNA damage repair

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Reduced expression of semaphorin 3A in osteoclasts causes lymphatic expansion in a Gorham-Stout disease (GSD) mouse model 破骨细胞中信号素3A表达的减少导致小鼠GSD模型中淋巴管扩张

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人源化靶向CD19 CAR-T细胞治疗复发/难治急性B淋巴细胞白血病的有效性及安全性 Safety and efficacy of humanized CD19-targeted CAR-T cells in patients with relapsed/refractory acute B cell lymphoblastic leukemia

Project description:目的观察人源化靶向CD19嵌合抗原受体T细胞（CAR-T）治疗复发/难治急性B淋巴细胞白血病（R/R B-ALL）患者的有效性及安全性。方法分析2020年2月至2021年7月于浙江大学医学院附属第一医院接受人源化靶向CD19 CAR-T细胞治疗的41例R/R B-ALL患者的有效性和安全性。结果中位第15（9～47）天，41例患者的完全缓解率为95.1％（39/41），其中38例患者骨髓经流式细胞术检测微小残留病灶阴性。39例完全缓解的患者中17例未接受进一步治疗，70.6％（12/17）的患者在随访结束时仍处于缓解状态，输注最早的两例患者无进展生存期达12.6个月；另外17例患者缓解后行巩固性造血干细胞移植（10例）或CD22 CAR-T细胞序贯治疗（7例），76.5％（13/17）的患者在随访结束时仍处于缓解状态；其余5例患者未接受巩固性治疗，在CAR-T细胞治疗后中位第72（55～115）天复发。1年总生存率为73.6％（95％CI 55.2％～92.3％），1年无进展生存率为56.2％（95％CI 38.1％～75.2％）。所有患者均发生了细胞因子释放综合征，63.4％（26/41）为1～2级。3例患者发生免疫效应细胞相关神经毒性综合征。结论人源化靶向CD19 CAR-T细胞能有效诱导R/R B-ALL患者获得完全缓解，且不良反应可耐受。

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Inhibition of PLK1 Destabilizes EGFR and Sensitizes EGFR-Mutated Lung Cancer Cells to Small Molecule Inhibitor Osimertinib.

Project description:Tyrosine kinase inhibitors (TKI) targeting the epidermal growth factor receptor (EGFR) have significantly prolonged survival in EGFR-mutant non-small cell lung cancer patients. However, the development of resistance mechanisms prohibits the curative potential of EGFR TKIs. Combination therapies emerge as a valuable approach to preventing or delaying disease progression. Here, we investigated the combined inhibition of polo-like kinase 1 (PLK1) and EGFR in TKI-sensitive EGFR-mutant NSCLC cells. The pharmacological inhibition of PLK1 destabilized EGFR levels and sensitized NSCLC cells to Osimertinib through induction of apoptosis. In addition, we found that c-Cbl, a ubiquitin ligase of EGFR, is a direct phosphorylation target of PLK1 and PLK1 impacts the stability of c-Cbl in a kinase-dependent manner. In conclusion, we describe a novel interaction between mutant EGFR and PLK1 that may be exploited in the clinic. Co-targeting PLK1 and EGFR may improve and prolong the clinical response to EGFR TKI in patients with an EGFR-mutated NSCLC.

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Project description: Not available

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Nonpeptidic, Polo-Box Domain-Targeted Inhibitors of PLK1 Block Kinase Activity, Induce Its Degradation and Target-Resistant Cells.

Project description:PLK1, polo-like kinase 1, is a central player regulating mitosis. Inhibition of the subcellular localization and kinase activity of PLK1 through the PBD, polo-box domain, is a viable alternative to ATP-competitive inhibitors, for which the development of resistance and inhibition of related PLK family members are concerns. We describe novel nonpeptidic PBD-binding inhibitors, termed abbapolins, identified through successful application of the REPLACE strategy and demonstrate their potent antiproliferative activity in prostate tumors and other cell lines. Furthermore, abbapolins show PLK1-specific binding and inhibitory activity, as measured by a cellular thermal shift assay and an ability to block phosphorylation of TCTP, a validated target of PLK1-mediated kinase activity. Additional evidence for engagement of PLK1 was obtained through the unique observation that abbapolins induce PLK1 degradation in a manner that closely matches antiproliferative activity. Moreover, abbapolins demonstrate antiproliferative activity in cells that are dramatically resistant to ATP-competitive PLK1 inhibitors.

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p53-dependent repression of polo-like kinase-1 (PLK1).

Project description:PLK1 is a critical mediator of G₂/M cell cycle transition that is inactivated and depleted as part of the DNA damage-induced G₂/M checkpoint. Here we show that downregulation of PLK1 expression occurs through a transcriptional repression mechanism and that p53 is both necessary and sufficient to mediate this effect. Repression of PLK1 by p53 occurs independently of p21 and of arrest at G₁/S where PLK1 levels are normally repressed in a cell cycle-dependent manner through a CDE/CHR element. Chromatin immunoprecipitation analysis indicates that p53 is present on the PLK1 promoter at two distinct sites termed p53RE1 and p53RE2. Recruitment of p53 to p53RE2, but not to p53RE1, is stimulated in response to DNA damage and/or p53 activation and is coincident with repression-associated changes in the chromatin. Downregulation of PLK1 expression by p53 is relieved by the histone deacetylase inhibitor, trichostatin A, and involves recruitment of histone deacetylase to the vicinity of p53RE2, further supporting a transcriptional repression mechanism. Additionally, wild type, but not mutant, p53 represses expression of the PLK1 promoter when fused upstream of a reporter gene. Silencing of PLK1 expression by RNAi interferes with cell cycle progression consistent with a role in the p53-mediated checkpoint. These data establish PLK1 as a direct transcriptional target of p53, independently of p21, that is required for efficient G₂/M arrest.

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Regulating a key mitotic regulator, polo-like kinase 1 (PLK1).

Project description:During cell division, duplicated genetic material is separated into two distinct daughter cells. This process is essential for initial tissue formation during development and to maintain tissue integrity throughout an organism's lifetime. To ensure the efficacy and efficiency of this process, the cell employs a variety of regulatory and signaling proteins that function as mitotic regulators and checkpoint proteins. One vital mitotic regulator is polo-like kinase 1 (PLK1), a highly conserved member of the polo-like kinase family. Unique from its paralogues, it functions specifically during mitosis as a regulator of cell division. PLK1 is spatially and temporally enriched at three distinct subcellular locales; the mitotic centrosomes, kinetochores, and the cytokinetic midbody. These localization patterns allow PLK1 to phosphorylate specific downstream targets to regulate mitosis. In this review, we will explore how polo-like kinases were originally discovered and diverged into the five paralogues (PLK1-5) in mammals. We will then focus specifically on the most conserved, PLK1, where we will discuss what is known about how its activity is modulated, its role during the cell cycle, and new, innovative tools that have been developed to examine its function and interactions in cells.

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