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      An Update on Pharmacological Potential of Boswellic Acids against Chronic Diseases

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          Abstract

          Natural compounds, in recent years, have attracted significant attention for their use in the prevention and treatment of diverse chronic diseases as they are devoid of major toxicities. Boswellic acid (BA), a series of pentacyclic triterpene molecules, is isolated from the gum resin of Boswellia serrata and Boswellia carteri. It proved to be one such agent that has exhibited efficacy against various chronic diseases like arthritis, diabetes, asthma, cancer, inflammatory bowel disease, Parkinson’s disease, Alzheimer’s, etc. The molecular targets attributed to its wide range of biological activities include transcription factors, kinases, enzymes, receptors, growth factors, etc. The present review is an attempt to demonstrate the diverse pharmacological uses of BA, along with its underlying molecular mechanism of action against different ailments. Further, this review also discusses the roadblocks associated with the pharmacokinetics and bioavailability of this promising compound and strategies to overcome those limitations for developing it as an effective drug for the clinical management of chronic diseases.

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          Targeting the STAT3 signaling pathway in cancer: role of synthetic and natural inhibitors.

          Kodappully Siveen, Sakshi Sikka, Rohit Surana … (2014)
          Signal transducers and activators of transcription (STATs) comprise a family of cytoplasmic transcription factors that mediate intracellular signaling that is usually generated at cell surface receptors and thereby transmit it to the nucleus. Numerous studies have demonstrated constitutive activation of STAT3 in a wide variety of human tumors, including hematological malignancies (leukemias, lymphomas, and multiple myeloma) as well as diverse solid tumors (such as head and neck, breast, lung, gastric, hepatocellular, colorectal and prostate cancers). There is strong evidence to suggest that aberrant STAT3 signaling promotes initiation and progression of human cancers by either inhibiting apoptosis or inducing cell proliferation, angiogenesis, invasion, and metastasis. Suppression of STAT3 activation results in the induction of apoptosis in tumor cells, and accordingly its pharmacological modulation by tyrosine kinase inhibitors, antisense oligonucleotides, decoy nucleotides, dominant negative proteins, RNA interference and chemopreventive agents have been employed to suppress the proliferation of various human cancer cells in culture and tumorigenicity in vivo. However, the identification and development of novel drugs that can target deregulated STAT3 activation effectively remains an important scientific and clinical challenge. This review presents the evidence for critical roles of STAT3 in oncogenesis and discusses the potential for development of novel cancer therapies based on mechanistic understanding of STAT3 signaling cascade. Copyright © 2013 Elsevier B.V. All rights reserved.
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            Targeting transcription factor NF-kappaB to overcome chemoresistance and radioresistance in cancer therapy.

            Feng Li, Gautam Sethi (2010)
            Activation of transcription factor NF-kappaB is frequently encountered in tumor cells and contributes to aggressive tumor growth and resistance to chemotherapy and ionizing radiation during cancer treatment. Accumulating evidence over the last few years indicate that most chemotherapeutic agents and radiation therapy activate NF-kappaB in vitro and in vivo. Moreover, induction of chemoresistance and radioresistance is mediated through several genes regulated by NF-kappaB and inhibition of this transcription factor increases sensitivity of cancer cells to the apoptotic action of chemotherapeutic agents and to radiation exposure. This review explores the role of NF-kappaB and its regulated genes in resistance of tumor cells to chemotherapeutic agents and radiation and evaluates the importance of targeting NF-kappaB as a potential therapeutic approach to overcome chemoresistance and radioresistance for cancer treatment.
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              Signal Transducer and Activator of Transcription (STATs) Proteins in Cancer and Inflammation: Functions and Therapeutic Implication

              Chin-Yap Loh, Aditya Arya, Ahmed Fadhil Naema … (2019)
              Signal Transducer and Activator of Transcription (STAT) pathway is connected upstream with Janus kinases (JAK) family protein and capable of integrating inputs from different signaling pathways. Each family member plays unique functions in signal transduction and crucial in mediating cellular responses to different kind of cytokines. STAT family members notably STAT3 and STAT5 have been involved in cancer progression whereas STAT1 plays opposite role by suppressing tumor growth. Persistent STAT3/5 activation is known to promote chronic inflammation, which increases susceptibility of healthy cells to carcinogenesis. Here, we review the role of STATs in cancers and inflammation while discussing current therapeutic implications in different cancers and test models, especially the delivery of STAT3/5 targeting siRNA using nanoparticulate delivery system.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 22 August 2019
                Publication date Collection: September 2019
                Volume: 20
                Issue: 17
                Electronic Location Identifier: 4101
                Affiliations
                [1 ]Cancer Biology Laboratory and DBT-AIST International Centre for Translational and Environmental Research(DAICENTER), Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Assam 781039, India
                [2 ]Musculoskeletal Research Group and Tumour Biology, Chair of Vegetative Anatomy, Institute of Anatomy, Ludwig-Maximilian-University, 80336 Munich, Germany
                [3 ]Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore
                Author notes
                [* ]Correspondence: phcgs@ 123456nus.edu.sg (G.S.); kunnumakkara@ 123456iitg.ernet.in or ajai78@ 123456gmail.com (A.B.K.); Tel.: +65-65163267 (G.S.); +91-361-258-2231 or +91-789-600-5326 (A.B.K.); Fax: +65-68737690 (G.S.); +91-361-258-2249 (A.B.K.)
                Article
                Publisher ID: ijms-20-04101
                DOI: 10.3390/ijms20174101
                PMC ID: 6747466
                PubMed ID: 31443458
                SO-VID: 03ffbd22-afcc-4369-b227-bb858f99fc12
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 24 July 2019
                Date accepted : 16 August 2019
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: boswellic acid,chronic diseases,molecular targets,pharmacokinetics,bioavailability
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: boswellic acid, chronic diseases, molecular targets, pharmacokinetics, bioavailability

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