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      STAT3 signaling in ovarian cancer: a potential therapeutic target

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          Abstract

          Accumulating evidence has shown that Signal Transducer and Activator of Transcription 3 (STAT3) is thought to be a promising target for cancer therapy as STAT3 is frequently overexpressed in a wide range of cancer cells as well as clinical specimens, promoting tumor progression. It is widely accepted that STAT3 regulates a variety of cellular processes, such as tumor cell growth, survival, invasion, cancer stem cell-like characteristic, angiogenesis and drug-resistance. In this review, we focus on the role of STAT3 in tumorigenesis in ovarian cancer and discuss the existing inhibitors of STAT3 signaling that can be promisingly developed as the strategies for ovarian cancer therapy.

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          Knocking down barriers: advances in siRNA delivery

          Kathryn Whitehead, Róbert Miklós Langer, Daniel Anderson (2009)
          Key Points RNA interference (RNAi) is a fundamental pathway in eukaryotic cells by which sequence-specific small interfering RNA (siRNA) is able to silence genes through the destruction of complementary mRNA. RNAi is an important therapeutic tool that can be used to silence aberrant endogenous genes or to knockdown genes essential to the proliferation of infectious organisms. Delivery remains the central challenge to the therapeutic application of RNAi technology. Before siRNA can take effect in the cytoplasm of a target cell, it must be transported through the body to the target site without undergoing clearance or degradation. Currently, the most effective synthetic, non-viral delivery agents of siRNA are lipids, lipid-like materials and polymers. Various cationic agents including stable nucleic acid–lipid particles, lipidoids, cyclodextrin polymers and polyethyleneimine polymers have been used to achieve the successful systemic delivery of siRNA in mammals without inducing significant toxicity. Direct conjugation of delivery agents to siRNA can facilitate delivery. For example, cholesterol-modified siRNA enables targeting to the liver. RNAi therapeutics have progressed to the clinic, where studies are being conducted to determine siRNA efficacy in treating several diseases, including age-related macular degeneration and respiratory syncytial virus. Moving forward, it will be important to pay close attention to the potential nonspecific immunostimulatory effects of siRNA. Modifications to siRNA can be used to minimize stimulation of the immune system, and an increased emphasis must be placed on performing proper controls to ensure that therapeutic effects are sequence-specific.
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            Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins.

            Shona Kerr, I Kerr, G Stark … (1994)
            Through the study of transcriptional activation in response to interferon alpha (IFN-alpha) and interferon gamma (IFN-gamma), a previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that then phosphorylate substrate proteins called STATs (signal transducers and activators of transcription). The phosphorylated STAT proteins move to the nucleus, bind specific DNA elements, and direct transcription. Recognition of the molecules involved in the IFN-alpha and IFN-gamma pathway has led to discoveries that a number of STAT family members exist and that other polypeptide ligands also use the Jak-STAT molecules in signal transduction.
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              Stattic: a small-molecule inhibitor of STAT3 activation and dimerization.

              Jochen Schust, Bianca Sperl, Angela Hollis … (2006)
              Signal transducers and activators of transcription (STATs) are a family of latent cytoplasmic transcription factors that transmit signals from the cell membrane to the nucleus. One family member, STAT3, is constitutively activated by aberrant upstream tyrosine kinase activities in a broad spectrum of cancer cell lines and human tumors. Screening of chemical libraries led to the identification of Stattic, a nonpeptidic small molecule shown to selectively inhibit the function of the STAT3 SH2 domain regardless of the STAT3 activation state in vitro. Stattic selectively inhibits activation, dimerization, and nuclear translocation of STAT3 and increases the apoptotic rate of STAT3-dependent breast cancer cell lines. We propose Stattic as a tool for the inhibition of STAT3 in cell lines or animal tumor models displaying constitutive STAT3 activation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cancer
                Journal ID (iso-abbrev): J Cancer
                Journal ID (publisher-id): jca
                Title: Journal of Cancer
                Publisher: Ivyspring International Publisher (Sydney )
                ISSN (Electronic): 1837-9664
                Publication date Collection: 2020
                Publication date (Electronic): 1 January 2020
                Volume: 11
                Issue: 4
                Pages: 837-848
                Affiliations
                Department of Radiation Oncology, Guangxi Medical University Cancer Hospital and Cancer Institute of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, P.R. China
                Author notes
                ✉ Corresponding author: Xiaodong Zhu, Address: Department of Radiation Oncology, Guangxi Medical University Cancer Hospital, No. 71 He Di Road, Nanning 530021, Guangxi, China. Tel.: +86-13978873616; E-mail: zhuxdonggxmu@ 123456126.com

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                Publisher ID: jcav11p0837
                DOI: 10.7150/jca.35011
                PMC ID: 6959025
                PubMed ID: 31949487
                SO-VID: ec15024c-05b5-4a62-a5c6-c4e161f47098
                Copyright © © The author(s)
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

                History
                Date received : 18 March 2019
                Date accepted : 8 September 2019
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: stat3,ovarian cancer,tumorigenesis,inhibitors
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: stat3, ovarian cancer, tumorigenesis, inhibitors

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