{"paper_id":"b6d212a8-b7fb-4132-87ca-8b86349cd884","body_text":"Journal of \nNext Generation Sequencing & Applications Short Communication\nVol.06 Iss.2\nTropical diseases conference 2019 Differences in autophagy-associated mRNAs \nin peritoneal fluid of patients with endometriosis and gynecologic cancers\nSeung Geun Yeo1, Yuki Gen2, Hui ryeon Ju2, Sang Hoon Kim1, Sang Il Kim2,Dong Choon \nPark2\n1Medical Science Research Institute, Kyung Hee University Medical Center, Kyung Hee University, Seoul Korea \n2Department of Obstetrics and Gynecology, St. vincent’s Hospital, The Catholic University of Korea\nEndometriosis and gynecologic cancer show similar patterns of \ninvasion. Little is known about the roles of autophagy in endome-\ntriosis and, to date, the expression of autophagy-associated mR -\nNAs has not been compared in patients with endometriosis and \ngynecologic cancers. This study therefore compared the levels of \nexpression of autophagy-associated mRNAs in patients with en -\ndometriosis and gynecologic cancers. The levels of autophagy mR-\nNAs, including those encoding mTOR, P13KC3, Beclin-1, Bcl-2, \nLC3 II, FLIP, Rubicon, BIRC2 and BIRC5, were measured by \nreal time polymerase chain reaction in peritoneal fluid of 27 pa -\ntients with benign masses (control group), 42 patients with endo-\nmetriosis, and 43 patients with gynecologic (ovarian, uterine, and \ncervical) cancers. Findings in the three groups were compared.\nAutophagy mRNAs were present in all samples from patients with \nendometriosis and gynecologic cancers. The levels of PI3K, FLIP, \nand Rubicon mRNAs were significantly higher in the endometri-\nosis than in the control group (p<0.05 each). Compared with the \ngynecologic cancer group, the levels of LC3II and FLIP mRNAs \nwere significantly lower, and the levels of Beclin-1 and Rubicon \nmRNAs significantly higher, in the endometriosis group (p<0.05 \neach). Levels of PI3K and FLIP mRNA were significantly higher \nin the endometriosis and gynecologic cancer groups than in the \ncontrol group (p<0.05 each). PI3K, FLIP, and Rubicon mRNAs \nare closely associated with the pathogenesis of endometriosis. The \nsimilar increases in PI3K and FLIP mRNA expression observed \nin patients with endometriosis and gynecologic cancer suggest \nthat these conditions have similar autophagic characteristics. The \nlower levels of Beclin-1 mRNA in the gynecologic cancer than in \nother two groups suggest that lowerBeclin-1 mRNA levels increase \nthe likelihood of developing gynecologic cancer. Recent Publica -\ntions\nIntroduction:\nAutophagy is a manner of lysosomal self-degradation of cellular \ncomponents through forming autophagosomes which are con -\nserved in all eukaryotes (1, 2). This is a pivotal manner to main -\ntain mobile homeostasis (three). An autophagosome is a dou -\nble-membrane vesicle that incorporates sequestered cytoplasmic \ncargos and transports them to lysosomes (4). Autophagosome for-\nmation is an important step in autophagy and is first-rate-tuned \nby various autophagy-associated gene (ATG) products, inclusive \nof ATG5, ATG12, and ATG16. During autophagosome forma -\ntion, ATG5 is conjugated with ATG12 by means of ubiquitin-like \nconjugation structures and, similarly, forms a homodimer which \nincludes an ATG5-ATG12/ATG16 complicated (five, 6). The \ncomplex is localized to autophagy-associated membranes and me-\ndiates LC3 conversion (7–nine). LC3 conversion is widely used \nas a marker of autophagosome formation (10). It has been men -\ntioned that lack of ATG5, ATG12, or ATG16 outcomes in a lower \nof autophagosome formation, thereby impairing the autophagic \nsystem (11–thirteen).\nAutophagy is involved in various stress responses, and dysreg -\nulation of autophagy has been determined in many sicknesses, \nsuch as cardiac ischemia/reperfusion injury, Crohn’s sickness, \nneurodegeneration, myopathy, and diabetes, functioning because \nthe driving or exacerbating aspect inside the pathogenesis of the \ndiseases (3). In addition, autophagy is implicated in cancer de -\nvelopment, even though it continues to be debatable whether or \nnot autophagy promotes or suppresses the increase of cancer cells \n(14). Several reviews have proven that autophagy is a prosurviv -\nal process in established most cancers cells, and the inhibition \nof autophagy is one of the strategies for cancer remedy (14–17). \nTherefore, elucidation of the quality molecular mechanisms of \nautophagic procedures is important in expertise the position of \nautophagy in the pathogenesis of numerous diseases. Several vital \nregulators had been identified, and their expression mechanisms \nhave been elucidated in numerous models (reviewed in references \n4 and 18). Several microRNAs (miRNAs) were suggested to be \npivotal regulators of autophagy (19–21). In this have a look at, we \ninvestigated the regulatory mechanism of autophagosome forma -\ntion on the RNA degree.\nHuR (human antigen R) (also referred to as HuA or ELAVL1) is \na member of the Hu/ELAV (embryonic lethal strange vision)-like \nRNA binding protein (RBP) family containing three RNA recog -\nnition motifs (RRM) (22). HuR binds to AU-rich factors (ARE) \ninside the untranslated areas (UTRs) of goal mRNAs and regu -\nlates gene expression by affecting the stableness or translation \nof goal mRNAs (22, 23). HuR is ubiquitously expressed and has \nessential roles in immune reaction, angiogenesis, metastasis, and \ncancer improvement through regulating cell proliferation, migra -\ntion, survival, dying, and autophagy (24). HuR is thought to sell \ncellular increase and survival by using increasing most cancers-re -\n\nShort Communication\nVol.06 Iss.2\nVolume 06 • Issue 2\nlated genes, consisting of the Cox-2, hypoxia-inducible element \n1α (HIF-1α), and vascular endothelial growth component (VEGF) \ngenes, and augmented expression of HuR is related to cancer pro-\ngression in a few kinds of most cancers (23, 25–27). Several efforts \nhave been made to validate the capability of HuR as a molecular \ntarget for most cancers remedy (28–30).\nHere, we look at the role of HuR within the regulation of au -\ntophagosome formation and display that HuR silencing reduces \nautophagosome formation and the autophagic flux of human \nliver cells. Along with previous studies showing SQSTM1/p62 \nregulation through HuR (31, 32), we identify ATG5, ATG12, and \nATG16 mRNAs as novel objectives of HuR and reveal augmented \nexpression of ATG5, ATG12, ATG16, and HuR in hepatocellu -\nlar carcinoma (HCC). Our outcomes provide a molecular mech -\nanism of autophagosome formation regulated by HuR and the \ncapacity of HuR concentrated on in cancer development.\nBiography :\nSpecialist in Robot-assisted surgery, single port laparoscopic sur -\ngery, gynecologic oncology(cancer), laparoscopic surgery for gyne-\ncologic cancer, and general gynecology. Department of Obstetrics \nand Gynecology, St. vincent’s Hospital, The Catholic University \nof Korea\nReferences:\n• Yang HL, Mei J, Chang KK, Zhou WJ, Huang LQ, Li \nMQ. Autophagy in endometriosis. Am J Transl Res. 2017; \n9(11):4707-4725\n• Zhan L, Li J, Wei B. Autophagy in endometriosis: Friend or \nfoe? Biochem Biophys Res Commun. 2018; 495(1): 60-63. \n• Tsukada M, Ohsumi Y. Isolation and characterization of au -\ntophagy-defective mutants of Saccharomyces cerevisiae. FEBS \nLett. 1993; 333: 169–174.\n• Mizushima N, Yoshimori T, Ohsumi Y. The role of Atg pro-\nteins in autophagosome formation. Annu. Rev. Cell Dev. \nBiol. 2011; 27: 107–132.\n• Levine B, Kroemer G. Autophagy in the pathogenesis of dis-\nease. Cell. 2008; 132: 27–42.\n• Mizushima N, Komatsu M. Autophagy: renovation of cells \nand tissues. Cell. 2011; 147: 728–741.\n• Choi AM, Ryter SW, Levine B. Autophagy in human health \nand disease. N. Engl. J. Med. 2013; 368: 651–662.\n• Hirsch M, Duffy J, Davis CJ, Nieves Plana M, Khan KS. In -\nternational Collaboration to Harmonise Outcomes and Mea-\nsures for Endometriosis. BJOG. 2016 Oct; 123(11): 1761-8. \n• Tae Gyu Choi, Sung Soo Kim. Autophagy in Redox Signal -\nling. Hanyang Med Rev. 2013; 33: 83-89\n• Cuervo AM. Autophagy: in sickness and in health. Trends \nNote: This work is partly presented at 6th International  Conference on Tropical Medicine and Infectious Diseases (January 28-29, 2019 Barcelona, Spain).\nCell Biol. 2004; 14: 70-77.\n• Gozuacik D, Kimchi A. Autophagy as a cell death and tumor \nsuppression mechanism Oncogene. 2004; 23: 2891-2906","source_license":"CC0","license_restricted":false}