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Cells
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STAT3: Role in Cancer and Stem Cells
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STAT3: Role in Cancer and Stem Cells

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

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 10920

Special Issue Editor

Dr. Saurabh Agarwal

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John’s University, New York, NY 11439, USA
Interests: pediatric cancers; neuroblastoma; cancer stem cells; metastasis; signaling pathways in cancer; immunotherapy; epigenetics; genetics; small molecule inhibitors; translational therapeutics; p53-myc interaction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Signal Transducer and Activator of Transcription 3 (STAT3) is a transcription factor that regulate many important cellular and biological functions in normal and transformed cells. The STAT3 signaling pathway regulation is highly diverse and is involved in normal development and oncogenesis. Recent advances in the field of cell biology highlighted the role of STAT3 pathway in regulating different hallmarks of cancer such as tumorigenesis, proliferation, metastasis, relapse, drug-resistance, invasion, and migration. Furthermore, STAT3 also regulate the normal stem cells and cancer stem cells development and functions. These findings highlight the need for developing better understanding of the role and functions of STAT3 in cancer and stem cells. Given the importance of STAT3 signaling pathway, development of anti-STAT3 pharmacological approaches and concerted translational research efforts are much needed. In this special issue of Cells, we invite authors to contribute original research and review articles focusing on different aspects of STAT3 signaling pathway, role in cancer onset and progression, role in stem cells and cancer stem cells. We also invite articles on anti-STAT3 pharmacological approaches, therapeutic strategies, and clinical studies. The collected articles in this special issue will further enhance our knowledge for the role of STAT3 signaling in cancer and stem cells and hopefully will drive the development of novel therapeutic strategies.

Dr. Saurabh Agarwal
Guest Editor

Manuscript Submission Information

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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

  • STAT3
  • JAK
  • Cell Signaling
  • Transcription factor
  • Cancer stem cell
  • Tumorigenesis
  • Phosphorylation
  • STAT3 inhibitor
  • Metastasis
  • Apoptosis

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Published Papers (3 papers)

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Review

25 pages, 1641 KiB  
Review
Central Roles of STAT3-Mediated Signals in Onset and Development of Cancers: Tumorigenesis and Immunosurveillance
by Shigeru Hashimoto, Ari Hashimoto, Ryuta Muromoto, Yuichi Kitai, Kenji Oritani and Tadashi Matsuda
Cells 2022, 11(16), 2618; https://doi.org/10.3390/cells11162618 - 22 Aug 2022
Cited by 17 | Viewed by 4014
Abstract
Since the time of Rudolf Virchow in the 19th century, it has been well-known that cancer-associated inflammation contributes to tumor initiation and progression. However, it remains unclear whether a collapse of the balance between the antitumor immune response via the immunological surveillance system [...] Read more.
Since the time of Rudolf Virchow in the 19th century, it has been well-known that cancer-associated inflammation contributes to tumor initiation and progression. However, it remains unclear whether a collapse of the balance between the antitumor immune response via the immunological surveillance system and protumor immunity due to cancer-related inflammation is responsible for cancer malignancy. The majority of inflammatory signals affect tumorigenesis by activating signal transducer and activation of transcription 3 (STAT3) and nuclear factor-κB. Persistent STAT3 activation in malignant cancer cells mediates extremely widespread functions, including cell growth, survival, angiogenesis, and invasion and contributes to an increase in inflammation-associated tumorigenesis. In addition, intracellular STAT3 activation in immune cells causes suppressive effects on antitumor immunity and leads to the differentiation and mobilization of immature myeloid-derived cells and tumor-associated macrophages. In many cancer types, STAT3 does not directly rely on its activation by oncogenic mutations but has important oncogenic and malignant transformation-associated functions in both cancer and stromal cells in the tumor microenvironment (TME). We have reported a series of studies aiming towards understanding the molecular mechanisms underlying the proliferation of various types of tumors involving signal-transducing adaptor protein-2 as an adaptor molecule that modulates STAT3 activity, and we recently found that AT-rich interactive domain-containing protein 5a functions as an mRNA stabilizer that orchestrates an immunosuppressive TME in malignant mesenchymal tumors. In this review, we summarize recent advances in our understanding of the functional role of STAT3 in tumor progression and introduce novel molecular mechanisms of cancer development and malignant transformation involving STAT3 activation that we have identified to date. Finally, we discuss potential therapeutic strategies for cancer that target the signaling pathway to augment STAT3 activity. Full article
(This article belongs to the Special Issue STAT3: Role in Cancer and Stem Cells)
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14 pages, 816 KiB  
Review
Roads to Stat3 Paved with Cadherins
by Hanad Adan, Juliet Daniel and Leda Raptis
Cells 2022, 11(16), 2537; https://doi.org/10.3390/cells11162537 - 16 Aug 2022
Cited by 3 | Viewed by 2382
Abstract
The engagement of cadherins, cell-to-cell adhesion proteins, triggers a dramatic increase in the levels and activity of the Rac/Cdc42 GTPases, through the inhibition of proteasomal degradation. This leads to an increase in transcription and secretion of IL6 family cytokines, activation of their common [...] Read more.
The engagement of cadherins, cell-to-cell adhesion proteins, triggers a dramatic increase in the levels and activity of the Rac/Cdc42 GTPases, through the inhibition of proteasomal degradation. This leads to an increase in transcription and secretion of IL6 family cytokines, activation of their common receptor, gp130, in an autocrine manner and phosphorylation of the signal transducer and activator of transcription-3 (Stat3) on tyrosine-705 by the Jak kinases. Stat3 subsequently dimerizes, migrates to the nucleus and activates the transcription of genes involved in cell division and survival. The Src oncogene also increases Rac levels, leading to secretion of IL6 family cytokines and gp130 activation, which triggers a Stat3-ptyr705 increase. Interestingly, at the same time, Src downregulates cadherins in a quantitative manner, while cadherins are required to preserve gp130 levels for IL6 family signalling. Therefore, a fine balance between Src527F/Rac/IL6 and Src527F/cadherin/gp130 levels is in existence, which is required for Stat3 activation. This further demonstrates the important role of cadherins in the activation of Stat3, through preservation of gp130 function. Conversely, the absence of cadherin engagement correlates with low Stat3 activity: In sparsely growing cells, both gp130 and Stat3-ptyr705 levels are very low, despite the fact that cSrc is active in the FAK (focal adhesion kinase)/cSrc complex, which further indicates that the engagement of cadherins is important for Stat3 activation, not just their presence. Furthermore, the caveolin-1 protein downregulates Stat3 through binding and sequestration of cadherins to the scaffolding domain of caveolin-1. We hypothesize that the cadherins/Rac/gp130 axis may be a conserved pathway to Stat3 activation in a number of systems. This fact could have significant implications in Stat3 biology, as well as in drug testing and development. Full article
(This article belongs to the Special Issue STAT3: Role in Cancer and Stem Cells)
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Figure 1

10 pages, 612 KiB  
Review
Biological Hallmarks and Emerging Strategies to Target STAT3 Signaling in Multiple Myeloma
by Jianbiao Zhou and Wee-Joo Chng
Cells 2022, 11(6), 941; https://doi.org/10.3390/cells11060941 - 10 Mar 2022
Cited by 9 | Viewed by 3047
Abstract
Multiple myeloma (MM) is the second most common hematological malignancy, characterized by an abnormal accumulation of plasma cells in the bone marrow. Signal transducer and activator of transcription 3 (STAT3) is a cytoplasmic transcription factor that modulates the transcription of multiple genes to [...] Read more.
Multiple myeloma (MM) is the second most common hematological malignancy, characterized by an abnormal accumulation of plasma cells in the bone marrow. Signal transducer and activator of transcription 3 (STAT3) is a cytoplasmic transcription factor that modulates the transcription of multiple genes to regulate various principal biological functions, for example, cell proliferation and survival, stemness, inflammation and immune responses. Aberrant STAT3 activation has been identified as a key driver of tumorigenesis in many types of cancers, including MM. Herein, we summarize the current evidence for the role of STAT3 in affecting cancer hallmark traits by: (1) sustaining MM cell survival and proliferation, (2) regulating tumor microenvironment, (3) inducing immunosuppression. We also provide an update of different strategies for targeting STAT3 in MM with special emphasis on JAK inhibitors that are currently undergoing clinical trials. Finally, we discuss the challenges and future direction of understanding STAT3 signaling in MM biology and the clinical development of STAT3 inhibitors. Full article
(This article belongs to the Special Issue STAT3: Role in Cancer and Stem Cells)
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