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Central Roles of STAT3-Mediated Signals in Onset and Development of Cancers : Tumorigenesis and Immunosurveillance

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Title: Central Roles of STAT3-Mediated Signals in Onset and Development of Cancers : Tumorigenesis and Immunosurveillance
Authors: Hashimoto, Shigeru Browse this author →KAKEN DB
Hashimoto, Ari Browse this author →KAKEN DB
Muromoto, Ryuta Browse this author →KAKEN DB
Kitai, Yuichi Browse this author →KAKEN DB
Oritani, Kenji Browse this author →KAKEN DB
Matsuda, Tadashi Browse this author →KAKEN DB
Keywords: STAT3
immune evasion
Issue Date: 22-Aug-2022
Publisher: MDPI
Journal Title: Cells
Volume: 11
Issue: 16
Start Page: 2618
Publisher DOI: 10.3390/cells11162618
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 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.
Type: article
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 松田 正

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