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      Functions of Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) in Gynecologic Disorders

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          Abstract

          Peroxisome proliferator-activated receptor gamma (PPARγ) is a member of a class of nuclear hormone receptors intimately involved in the regulation of expression of myriad genes that regulate energy metabolism, cell differentiation, apoptosis, and inflammation. Although originally discovered as a pivotal regulator of adipocyte differentiation, the roles that PPARγ plays in gynecological disorders are still unknown. There are a number of studies on the functions of PPARγ and its agonists in gynecological disorders. In this mini-review, we provide a brief summary of the advances in recent years.

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          DNA double-strand breaks: signaling, repair and the cancer connection.

          K K Khanna, S P Jackson, Stefan Kubicek … (2001)
          To ensure the high-fidelity transmission of genetic information, cells have evolved mechanisms to monitor genome integrity. Cells respond to DNA damage by activating a complex DNA-damage-response pathway that includes cell-cycle arrest, the transcriptional and post-transcriptional activation of a subset of genes including those associated with DNA repair, and, under some circumstances, the triggering of programmed cell death. An inability to respond properly to, or to repair, DNA damage leads to genetic instability, which in turn may enhance the rate of cancer development. Indeed, it is becoming increasingly clear that deficiencies in DNA-damage signaling and repair pathways are fundamental to the etiology of most, if not all, human cancers. Here we describe recent progress in our understanding of how cells detect and signal the presence and repair of one particularly important form of DNA damage induced by ionizing radiation-the DNA double-strand break (DSB). Moreover, we discuss how tumor suppressor proteins such as p53, ATM, Brca1 and Brca2 have been linked to such pathways, and how accumulating evidence is connecting deficiencies in cellular responses to DNA DSBs with tumorigenesis.
          Article 0 comments Cited 550 times – based on 0 reviews     Review now
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            The role of autophagy in cancer development and response to therapy.

            Yasuko Kondo, Takao Kanzawa, Raymond Sawaya … (2005)
            Autophagy is a process in which subcellular membranes undergo dynamic morphological changes that lead to the degradation of cellular proteins and cytoplasmic organelles. This process is an important cellular response to stress or starvation. Many studies have shed light on the importance of autophagy in cancer, but it is still unclear whether autophagy suppresses tumorigenesis or provides cancer cells with a rescue mechanism under unfavourable conditions. What is the present state of our knowledge about the role of autophagy in cancer development, and in response to therapy? And how can the autophagic process be manipulated to improve anticancer therapeutics?
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              Lysosomes and autophagy in cell death control.

              Guido Kroemer, Marja Jäättelä (2005)
              Lysosomal hydrolases participate in the digestion of endocytosed and autophagocytosed material inside the lysosomal/autolysosomal compartment in acute cell death when released into the cytosol and in cancer progression following their release into the extracellular space. Lysosomal alterations are common in cancer cells. The increased expression and altered trafficking of lysosomal enzymes participates in tissue invasion, angiogenesis and sensitization to the lysosomal death pathway. But lysosomal heat-shock protein 70 locally prevents lysosomal-membrane permeabilization. Similarly, alterations in the autophagic compartment are linked to carcinogenesis and resistance to chemotherapy. Targeting these pathways might constitute a novel approach to cancer therapy.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Med Insights Oncol
                Journal ID (iso-abbrev): Clin Med Insights Oncol
                Journal ID (publisher-id): Clinical Medicine Insights: Oncology
                Title: Clinical Medicine Insights. Oncology
                Publisher: Libertas Academica
                ISSN (Electronic): 1179-5549
                Publication date Collection: 2015
                Publication date (Electronic): 27 April 2015
                Volume: 9
                Pages: 43-49
                Affiliations
                [1 ]Laboratory of Nuclear Receptors and Cancer Research, Basic Medical Research Center, Nantong University School of Medicine, Nantong, Jiangsu, China
                [2 ]Department of Obstetrics and Gynecology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China
                Author notes
                Article
                Publisher ID: cmo-9-2015-043
                DOI: 10.4137/CMO.s23527
                PMC ID: 4412418
                PubMed ID: 25987855
                SO-VID: 2be8d04f-3b14-499d-aa75-b04239179f3e
                Copyright © © 2015 the authors, publisher and licensee Libertas Academica Limited
                License:

                This is an open-access article distributed under the terms of the Creative Commons CC-BY-NC 3.0 License

                History
                Date received : 07 January 2015
                Date revision received : 25 February 2015
                Date accepted : 27 February 2015
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: pparγ,pparγ agonists,gynecologic disorders
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: pparγ, pparγ agonists, gynecologic disorders

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