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Cells
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Role of STAT3 Signaling Pathway in Cancer
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Role of STAT3 Signaling Pathway in Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (31 May 2020) | Viewed by 35371

Special Issue Editors

Dr. Kyung-Soo Chun

E-Mail Website
Guest Editor
College of Pharmacy, Keimyung University, 1000 Sindang-dong, Dalseo-Gu, Daegu 704-701, Korea
Interests: reactive oxygen species; oxidative stress; skin cancer; carcinogenesis; cancer signlaing pathway; prostanoid receptor; apoptosis; cell proliferation
Special Issues, Collections and Topics in MDPI journals
Dr. Dae Joon Kim

E-Mail Website
Guest Editor
Department of Immunology and Microbiology, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX 78504, USA
Interests: skin carcinogenesis; UVB; PTP; PTK; chemoprevention

Special Issue Information

Dear Colleagues,

Signal transducers and activators of transcription (STATs) are a family of transcription factors that regulate cell proliferation, apoptosis, inflammation, and angiogenesis. The aberrant activation of STAT3 has long been strongly implicated in carcinogenesis. The activation of STAT3 involves the phosphorylation of its tyrosine-705 and serine-727 residues by various upstream kinases including Janus-activated kinases (JAKs), Src family kinases, and mitogen-activated protein (MAP) kinases. The phosphorylated STAT3 then dimerizes and translocates to the nucleus, where it binds to specific DNA response elements in the promoter regions of its target genes. The blockade of STAT3 activation inhibits cell proliferation and induces apoptosis. Thus, STAT3 is a prime target of many anticancer agents. Therefore, understanding the mechanisms that drive STAT3 signalling will be fundamental to our understanding of cancer, the development of novel therapeutic approaches, and ultimately to improved patient outcomes. In this Issue of Cells, “Role of STAT3 Signaling Pathway in Cancer”, experts are invited to contribute original research papers or review articles that will provide further insights on the functions of STAT3 in carcinogenesis.

Prof. Kyung-Soo Chun
Prof. Dae Joon Kim
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Cancer
  • STAT3
  • tumorigenesis
  • oncogenes
  • tumor suppressor gene
  • cell proliferation
  • apoptosis
  • small-molecule inhibitors
  • tyrosine kinases
  • growth factor receptors
  • cancer chemoprevention
  • phytochemical

Published Papers (5 papers)

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Research

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16 pages, 4403 KiB  
Article
STAT3 Inhibitor ODZ10117 Suppresses Glioblastoma Malignancy and Prolongs Survival in a Glioblastoma Xenograft Model
by Byung-Hak Kim, Haeri Lee, Cheol Gyu Park, Ae Jin Jeong, Song-Hee Lee, Kum Hee Noh, Jong Bae Park, Chung-Gi Lee, Sun Ha Paek, Hyunggee Kim and Sang-Kyu Ye
Cells 2020, 9(3), 722; https://doi.org/10.3390/cells9030722 - 15 Mar 2020
Cited by 23 | Viewed by 5144
Abstract
Constitutively activated STAT3 plays an essential role in the initiation, progression, maintenance, malignancy, and drug resistance of cancer, including glioblastoma, suggesting that STAT3 is a potential therapeutic target for cancer therapy. We recently identified ODZ10117 as a small molecule inhibitor of STAT3 and [...] Read more.
Constitutively activated STAT3 plays an essential role in the initiation, progression, maintenance, malignancy, and drug resistance of cancer, including glioblastoma, suggesting that STAT3 is a potential therapeutic target for cancer therapy. We recently identified ODZ10117 as a small molecule inhibitor of STAT3 and suggested that it may have an effective therapeutic utility for the STAT3-targeted cancer therapy. Here, we demonstrated the therapeutic efficacy of ODZ10117 in glioblastoma by targeting STAT3. ODZ10117 inhibited migration and invasion and induced apoptotic cell death by targeting STAT3 in glioblastoma cells and patient-derived primary glioblastoma cells. In addition, ODZ10117 suppressed stem cell properties in glioma stem cells (GSCs). Finally, the administration of ODZ10117 showed significant therapeutic efficacy in mouse xenograft models of GSCs and glioblastoma cells. Collectively, ODZ10117 is a promising therapeutic candidate for glioblastoma by targeting STAT3. Full article
(This article belongs to the Special Issue Role of STAT3 Signaling Pathway in Cancer)
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16 pages, 3274 KiB  
Article
Administration of Steamed and Freeze-Dried Mature Silkworm Larval Powder Prevents Hepatic Fibrosis and Hepatocellular Carcinogenesis by Blocking TGF-β/STAT3 Signaling Cascades in Rats
by Da-Young Lee, Sun-Mi Yun, Moon-Young Song, Sang-Deok Ji, Jong-Gon Son and Eun-Hee Kim
Cells 2020, 9(3), 568; https://doi.org/10.3390/cells9030568 - 28 Feb 2020
Cited by 9 | Viewed by 3304
Abstract
Hepatocellular carcinoma (HCC) is the leading cause of cancer-related deaths worldwide and the majority of HCC patients occur with a background of hepatic fibrosis and cirrhosis. We have previously reported the hepatoprotective effects of steamed and freeze-dried mature silkworm larval powder (SMSP) in [...] Read more.
Hepatocellular carcinoma (HCC) is the leading cause of cancer-related deaths worldwide and the majority of HCC patients occur with a background of hepatic fibrosis and cirrhosis. We have previously reported the hepatoprotective effects of steamed and freeze-dried mature silkworm larval powder (SMSP) in a chronic ethanol-treated rat model. Here, we assessed the anti-fibrotic and anti-carcinogenic effects of SMSP on diethylnitrosamine (DEN)-treated rats. Wistar rats were intraperitoneally injected with DEN once a week for 12 or 16 weeks with or without SMSP administration (0.1 and 1 g/kg). SMSP administration significantly attenuated tumor foci formation and proliferation in the livers of the rats treated with DEN for 16 weeks. SMSP administration also inhibited hepatic fibrosis by decreasing the levels of collagen fiber and the expression of pro-collagen I and alpha-smooth muscle actin (α-SMA). Moreover, SMSP supplementation improved the major parameters of fibrosis such as transforming growth factor-β (TGF-β), connective tissue growth factor (CTGF), tumor necrosis factor-alpha (TNF-α), plasminogen activator inhibitor-1 (PAI-1), and collagen type I (Col1A1) in the livers from the rats treated with DEN for 16 weeks. As s possible mechanisms, we investigated the effects of SMSP on the TGF-β and signal transducer and activator of transcription 3 (STAT3)-mediated signaling cascades, which are known to promote hepatic fibrosis. We found that SMSP treatment inhibited the activation of TGF-β and the phosphorylation of STAT3 pathway in DEN-treated rats. Moreover, SMSP administration suppressed the expressions of the target genes of TGF-β and STAT3 induced by DEN treatment. Our findings provide experimental evidences that SMSP administration has inhibitory effects of hepatic fibrosis and HCC induced by DEN In Vivo and could be a promising strategy for the prevention or treatment of hepatic fibrosis and hepatocellular carcinogenesis. Full article
(This article belongs to the Special Issue Role of STAT3 Signaling Pathway in Cancer)
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Review

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17 pages, 1156 KiB  
Review
Perspectives Regarding the Intersections between STAT3 and Oxidative Metabolism in Cancer
by Kyung-Soo Chun, Jeong-Hoon Jang and Do-Hee Kim
Cells 2020, 9(10), 2202; https://doi.org/10.3390/cells9102202 - 29 Sep 2020
Cited by 28 | Viewed by 5474
Abstract
Signal transducer and activator of transcription 3 (STAT3) functions as a major molecular switch that plays an important role in the communication between cytokines and kinases. In this role, it regulates the transcription of genes involved in various biochemical processes, such as proliferation, [...] Read more.
Signal transducer and activator of transcription 3 (STAT3) functions as a major molecular switch that plays an important role in the communication between cytokines and kinases. In this role, it regulates the transcription of genes involved in various biochemical processes, such as proliferation, migration, and metabolism of cancer cells. STAT3 undergoes diverse post-translational modifications, such as the oxidation of cysteine by oxidative stress, the acetylation of lysine, or the phosphorylation of serine/threonine. In particular, the redox modulation of critical cysteine residues present in the DNA-binding domain of STAT3 inhibits its DNA-binding activity, resulting in the inactivation of STAT3-mediated gene expression. Accumulating evidence supports that STAT3 is a key protein that acts as a mediator of metabolism and mitochondrial activity. In this review, we focus on the post-translational modifications of STAT3 by oxidative stress and how the modification of STAT3 regulates cell metabolism, particularly in the metabolic pathways in cancer cells. Full article
(This article belongs to the Special Issue Role of STAT3 Signaling Pathway in Cancer)
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24 pages, 5051 KiB  
Review
A STAT3 of Addiction: Adipose Tissue, Adipocytokine Signalling and STAT3 as Mediators of Metabolic Remodelling in the Tumour Microenvironment
by Rose Kadye, Mihlali Stoffels, Sidne Fanucci, Siso Mbanxa and Earl Prinsloo
Cells 2020, 9(4), 1043; https://doi.org/10.3390/cells9041043 - 22 Apr 2020
Cited by 11 | Viewed by 4608
Abstract
Metabolic remodelling of the tumour microenvironment is a major mechanism by which cancer cells survive and resist treatment. The pro-oncogenic inflammatory cascade released by adipose tissue promotes oncogenic transformation, proliferation, angiogenesis, metastasis and evasion of apoptosis. STAT3 has emerged as an important mediator [...] Read more.
Metabolic remodelling of the tumour microenvironment is a major mechanism by which cancer cells survive and resist treatment. The pro-oncogenic inflammatory cascade released by adipose tissue promotes oncogenic transformation, proliferation, angiogenesis, metastasis and evasion of apoptosis. STAT3 has emerged as an important mediator of metabolic remodelling. As a downstream effector of adipocytokines and cytokines, its canonical and non-canonical activities affect mitochondrial functioning and cancer metabolism. In this review, we examine the central role played by the crosstalk between the transcriptional and mitochondrial roles of STAT3 to promote survival and further oncogenesis within the tumour microenvironment with a particular focus on adipose-breast cancer interactions. Full article
(This article belongs to the Special Issue Role of STAT3 Signaling Pathway in Cancer)
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23 pages, 2781 KiB  
Review
Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition
by Wook Jin
Cells 2020, 9(1), 217; https://doi.org/10.3390/cells9010217 - 15 Jan 2020
Cited by 261 | Viewed by 16296
Abstract
The JAK/STAT3 signaling pathway plays an essential role in various types of cancers. Activation of this pathway leads to increased tumorigenic and metastatic ability, the transition of cancer stem cells (CSCs), and chemoresistance in cancer via enhancing the epithelial–mesenchymal transition (EMT). EMT acts [...] Read more.
The JAK/STAT3 signaling pathway plays an essential role in various types of cancers. Activation of this pathway leads to increased tumorigenic and metastatic ability, the transition of cancer stem cells (CSCs), and chemoresistance in cancer via enhancing the epithelial–mesenchymal transition (EMT). EMT acts as a critical regulator in the progression of cancer and is involved in regulating invasion, spread, and survival. Furthermore, accumulating evidence indicates the failure of conventional therapies due to the acquisition of CSC properties. In this review, we summarize the effects of JAK/STAT3 activation on EMT and the generation of CSCs. Moreover, we discuss cutting-edge data on the link between EMT and CSCs in the tumor microenvironment that involves a previously unknown function of miRNAs, and also discuss new regulators of the JAK/STAT3 signaling pathway. Full article
(This article belongs to the Special Issue Role of STAT3 Signaling Pathway in Cancer)
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