Plk1 promotes the migration of human lung adenocarcinoma epithelial cells via STAT3 signaling

Yan, Weijuan; Yu, Hui; Li, Wei; Li, Fengsheng; Wang, Sinian; Ye, Nan; Jiang, Qisheng

doi:10.3892/ol.2018.9437

Cited by 23 publications

(25 citation statements)

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“…In the present study, we found that RO3280 mediated the inactivation of Wnt/β-catenin signaling in prostate cancer cells, as well as reduced the rates of cell proliferation, migration and invasion. Mounting evidence indicates that PLK1 has therapeutic potential in several cancers, including prostate cancer [18][19][20]. In our previous study, we observed high PLK1 expression levels in prostate cancer tissues and prostate cancer cell lines, similar to the findings of previous studies.…”

Section: Discussionsupporting

confidence: 89%

PLK1 downregulation by RO3280 prevents cell proliferation, migration, and invasion via the Wnt/β-catenin pathway in prostate cancer

Ding

Zhang

2021

Arch Med Sci

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IntroductionHigher expression levels of serine/threonine-protein kinase 1 (PLK1) are significantly associated with tumorigenesis and poor clinical prognoses. Consequently, PLK1 is considered a latent target in cancer treatment. We aimed to determine the cytotoxic effects of RO3280 on prostate cancer cells.Material and methodsPLK1 expression was investigated using real-time PCR and western blotting in prostate cancer tissues and paired normal tissues. Real-time cell analysis, cell counting kit-8 assays, and 5-ethynyl-2¢-deoxyuridine cell proliferation assays were applied for the examination of cell proliferation ability. Wound healing assays and transwell assays were used to assess the migratory and invasive abilities of the prostate cancer cell lines with or without RO3280 treatment. Moreover, the target genes and pathways were detected by transcriptomics RNA sequencing in the cells cultured in RO3280 and through a series of bioinformatics analyses. Finally, the Wnt/β-catenin pathway was screened out and verified by western blotting.ResultsWe observed the mRNA and protein overexpression of PLK1 in the prostate cancer cells and tissues. The inhibition of PLK1 by RO3280 significantly reduced the migratory, invasive, and proliferative properties of the RO3280-treated cancer cell lines compared with their controls. RO3280 mediated the inactivation of the Wnt/β-catenin pathway, and reduced the rates of cell proliferation, migration, and invasion in prostate cancer cells.ConclusionsThis study’s findings are significant owing to the identification of the specific anticancer mechanism of RO3280, which may have therapeutic effects. This trial provides clarity on the feasibility of the use of RO3280 as a cancer therapeutic agent for prostate cancer.

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Section: Discussionsupporting

confidence: 89%

PLK1 downregulation by RO3280 prevents cell proliferation, migration, and invasion via the Wnt/β-catenin pathway in prostate cancer

Ding

Zhang

2021

Arch Med Sci

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“…JUN and MYC) and are also known to have important roles in proliferation in lung epithelial cells. PLK1 is another interesting gene on the list which has been previously linked to proliferation and migration in non small cell lung cancers, a tumor type arising from lung epithelial cells [39,40].…”

Section: Activity Of Top Ranked Genes In Underlying Health Conditionsmentioning

confidence: 99%

Reconstructed signaling and regulatory networks identify potential drugs for SARS-CoV-2 infection

Ding

Lugo-Martinez

Yuan

et al. 2020

Preprint

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Several molecular datasets have been recently compiled to characterize the activity of SARS-CoV-2 within human cells. Here we extend computational methods to integrate several different types of sequence, functional and interaction data to reconstruct networks and pathways activated by the virus in host cells. We identify the key proteins in these networks and further intersect them with genes differentially expressed at conditions that are known to impact viral activity. Several of the top ranked genes do not directly interact with virus proteins though some were shown to impact other coronaviruses highlighting the importance of large scale data integration for understanding virus and host activity.

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“…Other physiological roles of PLK1 have been recognized, involving telomere stabilization, extracellular matrix invasion and regulation of topoisomerase IIa in cell cycle progression (see Figure 1B). 18–21 For example, Cyclin B1, a key component of the prophase initiation, was identified as an important target structure of PLK1, promoting its (Cyclin B1) nuclear translocation after phosphorylation 22. Activation of PLK1 in turn is a complex process, requiring phosphorylation of a conserved threonine residue (Thr 210) within the PLK1 kinase domain.…”

Section: Biological Function and Structure Of Polo-like Kinases And Hmentioning

confidence: 99%

<p>Polo-like kinase 1 inhibition in NSCLC: mechanism of action and emerging predictive biomarkers</p>

Stratmann

Sebastian

2019

LCTT

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Non-small cell lung cancer (NSCLC) is the leading cause of cancer death worldwide. Due to often unspecific disease symptoms, locally advanced or metastatic disease is diagnosed in the majority of all cases. Palliative treatment options comprise of conventional cytotoxic agents, immunotherapy with checkpoint inhibitors and the use of specific small-molecule tyrosine kinase inhibitors (TKI). However, these TKIs are mainly restricted to a small proportion of patients with lung cancer that harbor activating driver mutations. Still, the effectiveness and favorable safety profile of these compounds have prompted a systematic search for specific driver mechanisms of tumorigenesis and moreover the development of corresponding kinase inhibitors. In recent years, the Polo-like kinase (PLK) family has emerged as a key regulator in mitotic regulation. Its role in cell proliferation and the frequently observed overexpression in various tumor entities have raised much interest in basic and clinical oncology aiming to attenuate tumor growth by targeting the PLK. In this review, we give a comprehensive summary on the (pre-) clinical development of the different types of PLK inhibitors in lung cancer and summarize their mechanisms of action, safety and efficacy data and give an overview on translational research aiming to identify predictive biomarkers for a rational use of PLK inhibitors.

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Plk1 promotes the migration of human lung adenocarcinoma epithelial cells via STAT3 signaling

Cited by 23 publications

References 50 publications

PLK1 downregulation by RO3280 prevents cell proliferation, migration, and invasion via the Wnt/β-catenin pathway in prostate cancer

PLK1 downregulation by RO3280 prevents cell proliferation, migration, and invasion via the Wnt/β-catenin pathway in prostate cancer

Reconstructed signaling and regulatory networks identify potential drugs for SARS-CoV-2 infection

<p>Polo-like kinase 1 inhibition in NSCLC: mechanism of action and emerging predictive biomarkers</p>

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