Dual PLK1 and STAT3 inhibition promotes glioblastoma cells apoptosis through MYC

Wang, Hao; Tao, Zhennan; Feng, Mei; Li, Xuetao; Deng, Zhitong; Zhao, Guozheng; Yin, Hao; Pan, Tingzheng; Chen, Guangliang; Feng, Zibin; Li, Yanyan; Zhou, Youxin

doi:10.1016/j.bbrc.2020.09.008

Cited by 19 publications

(13 citation statements)

References 26 publications

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“…He et al reported that PLK1 was highly expressed and predicted a poor prognosis in hepatocellular carcinoma patients [52]. Similarly, Wang et al demonstrated that PLK1 levels were elevated in glioma compared with those in normal brain tissues, and high expression of PLK1 was associated with poor prognosis [53]. Overall, our analysis showed that PLK1 was highly expressed and a potential prognostic biomarker in various cancers, especially in glioma.…”

Section: Discusionsupporting

confidence: 68%

Polo-like kinase 1 plays an oncogenic role in pan-cancer based on bioinformatics and biological assays

Luo

Zhang

Zhen

et al. 2022

Preprint

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Polo-like kinases (PLKs) are crucial regulatory factors of the cell cycle process and their dysregulations often cause various diseases including tumorigenesis. Although the PLKs, including PLK1, have been extensively studied and reported, few pan-cancer analyses are attainable. The potential oncogenic roles of PLK1 were thus explored among different cancers according to various online websites and datasets. PLK1 is always overexpressed in many cancers, and there is a significant relationship between its expression and the prognosis of cancer patients. In addition, the enrichment analysis suggested that PLK1 might related to “cell cycle”, “DNA replication”, “mismatch repair”, and “immune response” in pan-cancer, especially in glioma. Therefore, the analyses about genetic alterations and immune in pan-cancer were conducted. Furthermore, flow cytometry, CCK8 and EdU assays can further verify the above results of enrichment analysis. Moreover, DNA methylation and ceRNA network were analyzed to explore the potential mechanisms of aberrant expression of PLK1. In conclusion, our research about the oncogenic roles of PLK1 in pan-cancer further supplemented the oncogenic mechanisms of PLK1 and developed new potential therapeutic directions.

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Section: Discusionsupporting

confidence: 68%

Polo-like kinase 1 plays an oncogenic role in pan-cancer based on bioinformatics and biological assays

Luo

Zhang

Zhen

et al. 2022

Preprint

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“…PLK1 plays a role in regulating the cell cycle and cell division [ 36 ]. In addition, PLK1 can suppress the apoptosis of glioblastoma cells [ 37 ]. PLK1 also participates in the DNA damage repair in different cells [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of PLK1 relieved the myocardial ischemia-reperfusion injury of rats through inducing the mitophagy and regulating the p-AMPK/FUNDC1 axis

et al. 2021

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Myocardial cell injury caused by myocardial ischemia and reperfusion is one of the main causes of the occurrence and development of heart disease. Recent study has shown that inducing mitophagy of cardiomyocytes is a crucial method to alleviate ischemia-reperfusion injury. While, Polo-like kinase 1 (PLK1) can induce the mitophagy of breast cancer cells. Moreover, PLK1 was able to promote the expression of p-AMPK and FUNDC1, which are the protective factors for myocardium. Therefore, the mouse model of ischemia/reperfusion was established and the effect of PLK1 on ischemia reperfusion induced myocardial damage was investigated. The PLK1 was overexpressed in H9c2 cells and rat model of ischemia/reperfusion. Ischemia reperfusion inhibited the expression of PLK1. While overexpression of PLK1 relieved the myocardial infarction and myocardium apoptosis through inducing mitophagy in rats model of ischemia reperfusion. In vitro, the H9c2 cells overexpressing the PLK1 were treated with the hypoxia and reoxygenation and the apoptosis, survival rate and expression of mitophagy-related proteins of H9c2 cells were detected using the flow cytometry, CCK-8 assay and western blotting. The results reveled that overexpression of PLK1 alleviated the hypoxia and reoxygenation induced apoptosis of H9c2 cells and promoted the expression of mitophagy-related proteins. In addition, enhanced PLK1 expression promoted the expression of p-AMPK and FUNDC1 in H9c2 cells. However, the inhibition of FUNDC1 abolished the positive effect of PLK1 on H9c2 cells mentioned above. In conclusion, PLK1 alleviated the ischemia reperfusion induced myocardial damage by inducing the mitophagy in a p-AMPK/FUNDC1 signaling dependent pathway.

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“…STAT3 induces EMT and promotes cancer invasion. Overexpression of STAT3 is associated with poor prognosis and triggers chemoresistance [154][155][156][157][158]. Exosomes alter the polarization of macrophages and transform them into cancer-associated macrophages.…”

Section: Exosomes and Tumor Growthmentioning

confidence: 99%

Emerging role of exosomes in cancer progression and tumor microenvironment remodeling

et al. 2022

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Cancer is one of the leading causes of death worldwide, and the factors responsible for its progression need to be elucidated. Exosomes are structures with an average size of 100 nm that can transport proteins, lipids, and nucleic acids. This review focuses on the role of exosomes in cancer progression and therapy. We discuss how exosomes are able to modulate components of the tumor microenvironment and influence proliferation and migration rates of cancer cells. We also highlight that, depending on their cargo, exosomes can suppress or promote tumor cell progression and can enhance or reduce cancer cell response to radio- and chemo-therapies. In addition, we describe how exosomes can trigger chronic inflammation and lead to immune evasion and tumor progression by focusing on their ability to transfer non-coding RNAs between cells and modulate other molecular signaling pathways such as PTEN and PI3K/Akt in cancer. Subsequently, we discuss the use of exosomes as carriers of anti-tumor agents and genetic tools to control cancer progression. We then discuss the role of tumor-derived exosomes in carcinogenesis. Finally, we devote a section to the study of exosomes as diagnostic and prognostic tools in clinical courses that is important for the treatment of cancer patients. This review provides a comprehensive understanding of the role of exosomes in cancer therapy, focusing on their therapeutic value in cancer progression and remodeling of the tumor microenvironment. Graphical Abstract

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Dual PLK1 and STAT3 inhibition promotes glioblastoma cells apoptosis through MYC

Cited by 19 publications

References 26 publications

Polo-like kinase 1 plays an oncogenic role in pan-cancer based on bioinformatics and biological assays

Polo-like kinase 1 plays an oncogenic role in pan-cancer based on bioinformatics and biological assays

Overexpression of PLK1 relieved the myocardial ischemia-reperfusion injury of rats through inducing the mitophagy and regulating the p-AMPK/FUNDC1 axis

Emerging role of exosomes in cancer progression and tumor microenvironment remodeling

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