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      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

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      Downregulation of PFTK1 Inhibits Migration and Invasion of Non-Small Cell Lung Cancer

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          Abstract

          Background

          PFTK1, a novel cyclin-dependent kinase, plays pivotal roles in tumorigenesis. Cell motility and invasiveness could be enhanced by PFTK1 in various tumors. However, the function of PFTK1 in NSCLC metastasis remains unclear. In this study, the potential role of PFTK1 in NSCLC metastasis was determined.

          Materials and Methods

          In this study, the potential function of PFTK1 in lung cancer patients was analyzed with the Kaplan–Meier plotter database. RNA interference-mediated knockdown of PFTK1 was established in two NSCLC cell lines (H1299 and 95C) to explore the role of PFTK1 in NSCLC. The efficacy of downregulation of PFTK1 was examined by Western blot and immunofluorescence. The role of PFTK1 in cell migration and invasion ability was detected by wound healing and transwell assays. The protein levels in lung cancer cells were determined by Western blot. Immunofluorescence analysis was used to evaluate the structure of filamentous actin.

          Results

          Overexpression of PFTK1 was associated with the poor survival prognosis in NSCLC patients. PFTK1 knockdown cells were constructed successfully. Suppression of PFTK1 significantly inhibited the cell migration and invasion in H1299 and 95C cells. Notably, after PFTK1 downregulation, the epithelial–mesenchymal transition (EMT) markers vimentin, ZEB1 and β-catenin were obviously decreased. Additionally, immunofluorescence analysis indicated that PFTK1 downregulation remarkably induced filamentous actin depolymerization.

          Conclusion

          In summary, PFTK1 could significantly promote lung cancer metastasis through changing EMT progress and modulating intracellular cytoskeleton F-actin expression. Taken together, our findings indicated that PFTK1 might serve as a novel therapeutic target for the inhibition of NSCLC progression.

          Most cited references17

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          Cancer metastasis - tricks of the trade.

          Rabia Zeeshan, Zeeshan Mutahir (2017)
          Decades of cancer research have unraveled genetic, epigenetic and molecular pathways leading to plausible therapeutic targets; many of which hold great promise in improving clinical outcomes. Metastatic tumors become evident early on and are one of the major causes of cancer-related fatalities worldwide. This review depicts the sequential events of cancer metastasis. Genetic and epigenetic heterogeneity influences local tumor cell invasion, intravasation, survival in circulation, extravasation and colonization to distant sites. Each sequential event is associated with heterogeneous tumor microenvironment, gain of competence, unique population of cancer stem cells (CSCs), circulatory pathway, compatible niche and immune system support. A tight regulation of metastasis-promoting mechanisms and, in parallel, evading inhibitory mechanisms contribute to the severity and site of metastasis. A comprehensive understanding of tumor cell fate as an individual entity, as well as in combination with different promoting factors and associated molecular mechanisms, is anticipated in the coming years. This will enable scientists to depict design strategies for targeted cancer therapies.
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            Lung cancer and metastasis: new opportunities and challenges.

            Xiangdong Wang, Alex Adjei (2015)
            Lung cancer continues to attract special attention since the real number of lung cancer mortality and incidence in 2014 was definitely higher than those estimated numbers according to the report from World Health Organization. The present special issue highly focuses on advanced discovery and development of lung cancer and metastasis and discusses about potential opportunities and challenges to be faced. The present issue explores clinical applications of cancer immunotherapies, gene therapies, radiotherapies, or target-oriented therapies. A new and novel methodology can be used to identify differential interactions of driver genes, cancer-predictive genes, subtype-specific genes, or disease-exclusive genes or gene pairs from imbalanced or heterogeneous datasets. We also demonstrate the importance of lung cancer-specific gene mutations, epigenetics, gene sequencing, heterogeneity, or biomarker discovery. Clinical bioinformatics is emphasized as a critical tool and merging science. Novel therapies are designed and expected on basis of oncogenic molecular aberrations in lung cancer.
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              A novel interplay between oncogenic PFTK1 protein kinase and tumor suppressor TAGLN2 in the control of liver cancer cell motility.

              W Leung, A Ching, A Chan … (2011)
              The PFTK1 gene encodes a cdc2-related serine/threonine protein kinase that has been shown to confer cell migratory properties in hepatocellular carcinoma (HCC). However, the prognostic value and biological mechanism by which PFTK1 promotes HCC motility remain largely unknown. Here, we showed from tissue microarray that common upregulations of PFTK1 in primary HCC tumors (n=133/180) correlated significantly with early age onset (40 years), advance tumor grading and presence of microvascular invasion (P0.05). To understand downstream phosphorylated substrate(s) of PFTK1, phospho-proteins in PFTK1 expressing and knockdown Hep3B cells were profiled by two-dimensional-polyacrylamide gel electrophoresis mass spectrometric analysis. Protein identification of differential spots revealed β-actin (ACTB) and transgelin2 (TAGLN2) as the two most profound phosphorylated changes affected by PFTK1. We verified the presence of TAGLN2 serine phosphorylation and ACTB tyrosine phosphorylation. Moreover, reduced TAGLN2 and ACTB phosphorylations in PFTK1-suppressed Hep3B corresponded to distinct actin depolymerizations and marked inhibition on cell invasion and motility. Given that TAGLN2 is a tumor suppressor whose function has been ascribed in cancer metastasis, we examined if TAGLN2 is an intermediate substrate in the biological path of PFTK1. We showed in PFTK1-suppressed cells that knockdown of TAGLN2 over-rode the inhibitory effect on cell invasion and motility, and a recovery on actin polymerization was evident. Interestingly, we also found that unphosphorylated TAGLN2 in PFTK1-suppressed cells elicited strong actin-binding ability, a mechanism that possibly halts the actin cytoskeleton dynamics. Site-directed mutagenesis of TAGLN2 suggested that PFTK1 regulates the actin-binding affinity of TAGLN2 through the S83 and S163 residues, which if mutated can significantly affect HCC cell motility. Taken together, our data propose a novel, oncogene-tumor suppressor interplay, where oncogenic PFTK1 confers HCC cell motility through inactivating the actin-binding motile suppressing function of TAGLN2 via phosphorylation.
              Article 0 comments Cited 18 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Onco Targets Ther
                Journal ID (iso-abbrev): Onco Targets Ther
                Journal ID (publisher-id): ott
                Journal ID (pmc): ott
                Title: OncoTargets and therapy
                Publisher: Dove
                ISSN (Electronic): 1178-6930
                Publication date (Electronic): 22 September 2020
                Publication date Collection: 2020
                Volume: 13
                Pages: 9281-9289
                Affiliations
                [1 ]Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University , Beijing 100026, People’s Republic of China
                [2 ]Departments of Internal Medicine, Beijing Obstetrics and Gynecology Hospital, Capital Medical University , Beijing 100026, People’s Republic of China
                Author notes
                Correspondence: Wentao Yue Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University , No. 251, Yaojiayuan Road, Chaoyang District, Beijing100026, People’s Republic of China Email yuewt2000@yahoo.com
                Chenghong Yin Departments of Internal Medicine, Beijing Obstetrics and Gynecology Hospital, Capital Medical University , No. 251, Yaojiayuan Road, Chaoyang District, Beijing100026, People’s Republic of China Email modscn@126.com
                [*]

                These authors contributed equally to this work

                Author information
                http://orcid.org/0000-0001-7485-0428
                http://orcid.org/0000-0002-1838-4255
                http://orcid.org/0000-0002-5917-1125
                Article
                Publisher ID: 265540
                DOI: 10.2147/OTT.S265540
                PMC ID: 7519878
                SO-VID: d6910d82-10e2-46fc-9b16-780e39e081fc
                Copyright © © 2020 Jiang et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 02 June 2020
                Date accepted : 20 August 2020
                Page count
                Figures: 7, References: 21, Pages: 9
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: non-small cell lung cancer,pftk1,invasion
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: non-small cell lung cancer, pftk1, invasion

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