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Journal articles on the topic 'MicroRNA-200'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Liu, Xiaodong, Jianhua Zhang, Botao Xie, Hao Li, Jihong Shen, and Jianheng Chen. "MicroRNA-200 Family Profile." American Journal of Therapeutics 23, no. 2 (2016): e388-e397. http://dx.doi.org/10.1097/mjt.0000000000000361.

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2

Tian, Yin, Qiong Pan, Yangyang Shang, Rong Zhu, Jun Ye, Yun Liu, Xiaoli Zhong, et al. "MicroRNA-200 (miR-200) Cluster Regulation by Achaete Scute-like 2 (Ascl2)." Journal of Biological Chemistry 289, no. 52 (November 4, 2014): 36101–15. http://dx.doi.org/10.1074/jbc.m114.598383.

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3

Shi, Min, Yulan Mu, Hui Zhang, Ming Liu, Jipeng Wan, Xiaoyan Qin, and Changzhong Li. "MicroRNA-200 and microRNA-30 family as prognostic molecular signatures in ovarian cancer." Medicine 97, no. 32 (August 2018): e11505. http://dx.doi.org/10.1097/md.0000000000011505.

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4

Hsieh, Pei-Ling, Chun-Chung Huang, and Cheng-Chia Yu. "Emerging Role of MicroRNA-200 Family in Dentistry." Non-Coding RNA 7, no. 2 (June 11, 2021): 35. http://dx.doi.org/10.3390/ncrna7020035.

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MicroRNAs (miRNAs) are endogenous non-coding RNAs ~22 nucleotides in length, which have been shown to participate in various biological processes. As one of the most researched miRNAs, the miR-200 family has been found to regulate several factors that are associated with the epithelial to mesenchymal transition (EMT) and cancer stem cells (CSCs) behavior. In this review, we briefly summarize the background of the miR-200 family and their implication in various dental diseases. We focus on the expression changes, biological functions, and clinical significance of the miR-200 family in oral cancer; periodontitis; oral potentially malignant disorder; gingival overgrowth; and other periodontal diseases. Additionally, we discuss the use of the miR-200 family as molecular biomarkers for diagnosis, prognostic, and therapeutic application.

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5

Senfter, Daniel, Sibylle Madlener, Georg Krupitza, and Robert M. Mader. "The microRNA-200 family: still much to discover." Biomolecular Concepts 7, no. 5-6 (December 1, 2016): 311–19. http://dx.doi.org/10.1515/bmc-2016-0020.

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AbstractIn the last decade, microRNAs (miRs or miRNAs) became of great interest in cancer research due to their multifunctional and active regulation in a variety of vital cellular processes. In this review, we discuss the miR-200 family, which is composed of five members (miR-141, miR-200a/200b/200c and miR-429). Although being among the best investigated miRNAs in the field, there are still many open issues. Here, we describe the potential role of miR-200 as prognostic and/or predictive biomarker, its influence on motility and cell migration as well as its role in epithelial to mesenchymal transition (EMT) and metastasis formation in different tumour types. Recent studies also demonstrated the influence of miR-200 on drug resistance and described a correlation between miR-200 expression levels and overall survival of patients. Despite intense research in this field, the full role of the miR-200 family in cancer progression and metastasis is not completely understood and seems to differ between different tumour types and different cellular backgrounds. To elucidate these differences further, a finer characterisation of the role of the individual miRNA-200 family members is currently under investigation.

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6

Shinozaki, Aya, Takashi Sakatani, Tetsuo Ushiku, Rumi Hino, Maya Isogai, Shunpei Ishikawa, Hiroshi Uozaki, Kenzo Takada, and Masashi Fukayama. "Downregulation of MicroRNA-200 in EBV-Associated Gastric Carcinoma." Cancer Research 70, no. 11 (May 18, 2010): 4719–27. http://dx.doi.org/10.1158/0008-5472.can-09-4620.

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7

Snowdon, Jaime, Xiao Zhang, Tim Childs, Victor A. Tron, and Harriet Feilotter. "The MicroRNA-200 Family Is Upregulated in Endometrial Carcinoma." PLoS ONE 6, no. 8 (August 29, 2011): e22828. http://dx.doi.org/10.1371/journal.pone.0022828.

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8

Castilla, María Ángeles, Juan Díaz-Martín, David Sarrió, Laura Romero-Pérez, María Ángeles López-García, Begoña Vieites, Michele Biscuola, Susana Ramiro-Fuentes, Clare M. Isacke, and José Palacios. "MicroRNA-200 Family Modulation in Distinct Breast Cancer Phenotypes." PLoS ONE 7, no. 10 (October 24, 2012): e47709. http://dx.doi.org/10.1371/journal.pone.0047709.

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9

Paterson, Emily L., Natasha Kolesnikoff, Philip A. Gregory, Andrew G. Bert, Yeesim Khew-Goodall, and Gregory J. Goodall. "The microRNA-200 Family Regulates Epithelial to Mesenchymal Transition." Scientific World JOURNAL 8 (2008): 901–4. http://dx.doi.org/10.1100/tsw.2008.115.

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10

Škrha, Pavel, Aleš Hořínek, Eva Pazourková, Jan Hajer, Přemysl Frič, Jan Škrha, and Michal Anděl. "Serum microRNA-196 and microRNA-200 in pancreatic ductal adenocarcinoma of patients with diabetes mellitus." Pancreatology 16, no. 5 (September 2016): 839–43. http://dx.doi.org/10.1016/j.pan.2016.05.005.

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11

Zhang, Zhen-Zhen, Heng-Chang Cao, Dong-Li Huang, Qi Wu, Xiao-Fan Chen, Jun Wan, and Wei Zhang. "MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN." Tumor Biology 39, no. 5 (May 2017): 101042831770365. http://dx.doi.org/10.1177/1010428317703655.

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Recent studies suggested that microRNA-200 family microRNAs play critical roles in cancer initiation and metastasis. The underlying mechanism remained elusive. In this study, we show that microRNA-200c is upregulated in nasopharyngeal carcinoma cells. Manipulation of microRNA-200c levels affected cell growth, migration, and invasion in nasopharyngeal carcinoma cell lines. Furthermore, PTEN was identified as a direct target of microRNA-200c. Overexpression of PTEN resulted in similar effects to those of anti-microRNA-200c transfection. In vivo suppression of microRNA-200c level reduced tumor growth in mice. Overall, our data suggest that microRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN.

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12

Dhayat, Sameer A., Anna Hüsing, Norbert Senninger, Hartmut H. Schmidt, Jörg Haier, Heiner Wolters, and Iyad Kabar. "Circulating microRNA-200 Family as Diagnostic Marker in Hepatocellular Carcinoma." PLOS ONE 10, no. 10 (October 8, 2015): e0140066. http://dx.doi.org/10.1371/journal.pone.0140066.

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13

Ohsaka, Fumina, Yugo Karatsu, Yoshihiro Kadota, Takumi Tochio, Naoki Takemura, and Kei Sonoyama. "Gut commensals suppress interleukin-2 production through microRNA-200/BCL11B and microRNA-200/ETS-1 axes in lamina propria leukocytes of murine large intestine." Biochemical and Biophysical Research Communications 534 (January 2021): 808–14. http://dx.doi.org/10.1016/j.bbrc.2020.10.103.

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14

Dhayat, Sameer, Max Traeger, Jan Rehkaemper, Anda Stroese, Konrad Steinestel, Eva Wardelmann, Iyad Kabar, and Norbert Senninger. "Clinical Impact of Epithelial-to-Mesenchymal Transition Regulating MicroRNAs in Pancreatic Ductal Adenocarcinoma." Cancers 10, no. 9 (September 13, 2018): 328. http://dx.doi.org/10.3390/cancers10090328.

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive carcinoma entities worldwide with early and rapid dissemination. Recently, we discussed the role of microRNAs as epigenetic regulators of Epithelial-to-Mesenchymal Transition (EMT) in PDAC. In this study, we investigated their value as diagnostic and prognostic markers in tissue and blood samples of 185 patients including PDAC, non-malignant pancreatic disorders, and age-matched healthy controls. Expression of the microRNA-200-family (microRNAs -141, -200a, -200b, -200c, -429) and microRNA-148a was significantly downregulated in tissue of PDAC Union internationale contre le cancer (UICC) Stage II. Correspondingly, stromal PDAC tissue showed strong expression of Fibronectin, Vimentin, and ZEB-1 (Zinc finger E-box-binding homeobox) versus low expression of E-cadherin. Transient transfection of microRNA-200b and microRNA-200c mimics resulted in the downregulation of their key target ZEB-1. Inversely, blood serum analyses of patients with PDAC UICC Stages II, III, and IV showed a significant over-expression of microRNA-200-family members, microRNA-148a, microRNA-10b, and microRNA-34a. Correspondingly, Enzyme-linked Immunosorbent Assay (ELISA) analyses revealed a significant over-expression of soluble E-cadherin in serum samples of PDAC patients versus healthy controls. The best diagnostic accuracy to distinguish between PDAC and non-PDAC in this patient collective could be achieved in tissue by microRNA-148a with an area under the receiver-operating-characteristic (ROC) curve (AUC) of 0.885 and in blood serum by a panel of microRNA-141, -200b, -200c, and CA.19-9 with an AUC of 0.890. Both diagnostic tools outreach the diagnostic performance of the currently most common diagnostic biomarker CA.19-9 (AUC of 0.834). Kaplan Meier survival analysis of this patient collective revealed an improved overall survival in PDAC patients with high expression of tissue-related microRNA-34a, -141, -200b, -200c, and -429. In conclusion, EMT-regulating microRNAs have great potential as liquid and solid biopsy markers in PDAC patients. Their prognostic and therapeutic benefits remain important tasks for future studies.

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15

Ren, Hongyan, Cong Tao, Kui Li, Yanzhen Bi, and Xinmin Zheng. "Generation of a Floxed Allele of the Mouse MicroRNA-200 Clusters." Applied Biochemistry and Biotechnology 182, no. 3 (January 11, 2017): 1218–28. http://dx.doi.org/10.1007/s12010-016-2394-z.

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16

Dhayat, Sameer A., Wolf A. Mardin, Gabriele Köhler, Ralf Bahde, Thorsten Vowinkel, Heiner Wolters, Norbert Senninger, Jörg Haier, and Soeren T. Mees. "The microRNA-200 family-A potential diagnostic marker in hepatocellular carcinoma?" Journal of Surgical Oncology 110, no. 4 (June 4, 2014): 430–38. http://dx.doi.org/10.1002/jso.23668.

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17

Bodulev, Oleg L., Ivan I. Galkin, Shulin Zhao, Olga Y. Pletyushkina, and Ivan Y. Sakharov. "Quantitation of MicroRNA-155 in Human Cells by Heterogeneous Enzyme-Linked Oligonucleotide Assay Coupled with Mismatched Catalytic Hairpin Assembly Reaction." Biosensors 12, no. 8 (July 26, 2022): 570. http://dx.doi.org/10.3390/bios12080570.

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In the present work, we describe the development of a chemiluminescent enzyme-linked oligonucleotide assay coupled with mismatched catalytic hairpin assembly (mCHA) amplification for the quantitative determination of microRNA-155. To improve its sensitivity, a polymerase-free mCHA reaction was applied as an isothermal amplification method. The detection limit of the proposed assay was 400 fM. In addition, the high specificity of the assay was demonstrated. The proposed assay allowed assessment of the content of microRNA-155 in human cancer lines such as HepG2, Caco2, MCF7, and HeLa. The quantitation of microRNA-155 was performed after purification of short RNAs (less than 200 nt) from cell lysates since a high matrix effect was observed without this pre-treatment. The results of the quantitative determination of the microRNA content in cells were normalized using nematode microRNA-39, the concentration of which was determined using a heterogeneous assay developed by us using a strategy identical to that of the microRNA-155 assay.

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18

Cristina, T., B. Mateescu, A. Mitroi, G. Cozaru, C. Brinzan, M. State, A. Dumitru, et al. "P037 MicroRNA-31 and microRNA-200 family reflect disease activity in Crohn’s disease: results from the BIOMIR study." Journal of Crohn's and Colitis 16, Supplement_1 (January 1, 2022): i155. http://dx.doi.org/10.1093/ecco-jcc/jjab232.166.

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Abstract Background Accurate assessment of disease activity in inflammatory bowel disease (IBD) is of paramount importance in decisions regarding treatment strategies. To apply a treat-to-target strategy, a tight assessment of activity is mandatory. MicroRNAs (miRNAs) are small, non-coding short (ribonucleic acid) RNAs that have a role in the regulation of genes and protein expression. MiRNAs have altered expression in multiple autoimmune disorders including IBD. The aim of the study was to assess the tissue and circulating miR-31, miR-200b, and miR-200c expression levels as potential biomarkers for intestinal disease activity in patients with Crohn’s disease (CD). Methods The study included 45 patients with histopathologically confirmed CD and active disease (defined as fecal calprotectin (fCal) > 50 ug/g and Short Endoscopic Score of Crohn’s Disease (SES-CD) > 3), and 21 subjects as controls for the validation cohort. Demographic and clinical data, biomarkers (fCal), endoscopy data, the expression levels of miR-31, miR-200b, and miR-200c in tissue and serum were assessed (by RT-PCR). Receiver operating characteristic (ROC) analysis was performed to assess the miR-31, miR-200b, and miR-200c expression levels as potential biomarkers for active CD. Results Mean fCal was 1540 +/- 890 ug/g. Mean SES-CD was 8.9 +/- 4.2. Tissue and circulating miR-31 was significantly correlated with fCal (r = 0.81, r = 0.83, p < 0.01) and with SES-CD (r = 0.82, r = 0.79, p < 0.01). The expression level of miR-31 was significantly upregulated in CD tissue cases compared to the control tissue samples (6.24 ± 1.57 vs. 3.70 ± 1.44; p < 0.01). Similarly, serum miR-31 expression levels in CD patients were significantly upregulated than in control serum samples (-2.07 ± 1.00 vs. 0.78 ± 0.42; p < 0.01). The expression levels of tissue miR-200b and miR-200c were significantly upregulated in CD tissue cases compared to the control tissue samples (-5.25 ± 0.93 vs. -4.69 ± 0.80, p = 0.03 for miR-200b, and -0.86 ± 0.96 vs. 0.39 ± 0.66, p < 0.01 for miR-200c). Similarly, serum miR-200b and miR-200c expression levels in CD patients were significantly upregulated than in the control serum samples (p < 0.05). ROC analysis revealed that the expression levels of the selected miRNAs could help to discriminate active CD patients from healthy controls with very good specificity and sensitivity. Conclusion Tissue and circulating miR-31, miR-200b, and miR-200c reflect disease activity in CD patients and can be used as biomarkers for active CD. Furthermore, circulating miR-31, miR-200b, and miR-200c may be used as non-invasive biomarkers for active CD patients.

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19

Hoefert, Jaimee E., Glen A. Bjerke, Dongmei Wang, and Rui Yi. "The microRNA-200 family coordinately regulates cell adhesion and proliferation in hair morphogenesis." Journal of Cell Biology 217, no. 6 (March 30, 2018): 2185–204. http://dx.doi.org/10.1083/jcb.201708173.

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The microRNA (miRNA)-200 (miR-200) family is highly expressed in epithelial cells and frequently lost in metastatic cancer. Despite intensive studies into their roles in cancer, their targets and functions in normal epithelial tissues remain unclear. Importantly, it remains unclear how the two subfamilies of the five-miRNA family, distinguished by a single nucleotide within the seed region, regulate their targets. By directly ligating miRNAs to their targeted mRNA regions, we identify numerous miR-200 targets involved in the regulation of focal adhesion, actin cytoskeleton, cell cycle, and Hippo/Yap signaling. The two subfamilies bind to largely distinct target sites, but many genes are coordinately regulated by both subfamilies. Using inducible and knockout mouse models, we show that the miR-200 family regulates cell adhesion and orientation in the hair germ, contributing to precise cell fate specification and hair morphogenesis. Our findings demonstrate that combinatorial targeting of many genes is critical for miRNA function and provide new insights into miR-200’s functions.

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20

Hilmarsdottir, Bylgja, Eirikur Briem, Jon Bergthorsson, Magnus Magnusson, and Thorarinn Gudjonsson. "Functional Role of the microRNA-200 Family in Breast Morphogenesis and Neoplasia." Genes 5, no. 3 (September 11, 2014): 804–20. http://dx.doi.org/10.3390/genes5030804.

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21

Chen, Ying, and Lei Zhang. "Members of the microRNA-200 family are promising therapeutic targets in cancer." Experimental and Therapeutic Medicine 14, no. 1 (May 22, 2017): 10–17. http://dx.doi.org/10.3892/etm.2017.4488.

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22

Chu, Chia-Hui, Wenchi Chou, Frank Wang, Chun-Nan Yeh, Tse-Ching Chen, and Ta-Sen Yeh. "Expression profile of microRNA-200 family in cholangiocarcinoma arising from choledochal cyst." Journal of Gastroenterology and Hepatology 31, no. 5 (April 28, 2016): 1052–59. http://dx.doi.org/10.1111/jgh.13204.

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23

Tang, Xin, Feng Wu, Jinshuo Fan, Yang Jin, Jianjun Wang, and Guanghai Yang. "Posttranscriptional Regulation of Interleukin-33 Expression by MicroRNA-200 in Bronchial Asthma." Molecular Therapy 26, no. 7 (July 2018): 1808–17. http://dx.doi.org/10.1016/j.ymthe.2018.04.016.

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24

Parwani, A. V. "A miR-200 microRNA cluster as prognostic marker in advanced ovarian cancer." Yearbook of Pathology and Laboratory Medicine 2010 (January 2010): 121–23. http://dx.doi.org/10.1016/s1077-9108(09)79412-5.

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25

Hu, Xiaoxia, Dusten M. Macdonald, Phyllis C. Huettner, Zhihui Feng, Issam M. El Naqa, Julie K. Schwarz, David G. Mutch, Perry W. Grigsby, Simon N. Powell, and Xiaowei Wang. "A miR-200 microRNA cluster as prognostic marker in advanced ovarian cancer." Gynecologic Oncology 114, no. 3 (September 2009): 457–64. http://dx.doi.org/10.1016/j.ygyno.2009.05.022.

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26

CHANG, LIANG, FENGJIE GUO, BINGJIE HUO, YALEI LV, YUDONG WANG, and WEI LIU. "Expression and clinical significance of the microRNA-200 family in gastric cancer." Oncology Letters 9, no. 5 (2015): 2317–24. http://dx.doi.org/10.3892/ol.2015.3028.

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27

Guo, Lixia, Jingyu Wang, Ping Yang, Qiang Lu, Ting Zhang, and Yanan Yang. "MicroRNA-200 promotes lung cancer cell growth through FOG2-independent AKT activation." IUBMB Life 67, no. 9 (August 27, 2015): 720–25. http://dx.doi.org/10.1002/iub.1412.

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28

Sun, Lingjun, Taowei Chen, Tao Li, and Jianda Yu. "LncRNA IUR downregulates ZEB1 by upregulating miR-200 to inhibit prostate carcinoma." Physiological Genomics 51, no. 11 (November 1, 2019): 607–11. http://dx.doi.org/10.1152/physiolgenomics.00062.2019.

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We in this study investigated the role of imatinib-upregulated lncRNA (IUR) in prostate carcinoma (PC). We observed that IUR was downregulated in PC, and its expression levels decreased with the increase of clinical stages. In PC tissues, microRNA (miR)-200 was positively, while ZEB1 was inversely correlated with IUR. In PC cells, IUR and miR-200 overexpression mediated the downregulated ZEB1. IUR overexpression mediated the upregulation of miR-200, while IUR expression was not significantly affected by miR-200 overexpression. Cell invasion and migration analysis showed that IUR and miR-200 overexpression resulted in decreased invasion and migration rates. ZEB1 overexpression played an opposite role and attenuated the effects of IUR and miR-200 overexpression. Therefore, IUR can downregulate ZEB1 by upregulating miR-200 to inhibit PC cell invasion and migration.

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29

Uhan, Sara, and Nina Hauptman. "Metastatic EMT Phenotype Is Governed by MicroRNA-200-Mediated Competing Endogenous RNA Networks." Cells 11, no. 1 (December 28, 2021): 73. http://dx.doi.org/10.3390/cells11010073.

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Epithelial–mesenchymal transition (EMT) is a fundamental physiologically relevant process that occurs during morphogenesis and organ development. In a pathological setting, the transition from epithelial toward mesenchymal cell phenotype is hijacked by cancer cells, allowing uncontrolled metastatic dissemination. The competing endogenous RNA (ceRNA) hypothesis proposes a competitive environment resembling a large-scale regulatory network of gene expression circuits where alterations in the expression of both protein-coding and non-coding genes can make relevant contributions to EMT progression in cancer. The complex regulatory diversity is exerted through an array of diverse epigenetic factors, reaching beyond the transcriptional control that was previously thought to single-handedly govern metastatic dissemination. The present review aims to unravel the competitive relationships between naturally occurring ceRNA transcripts for the shared pool of the miRNA-200 family, which play a pivotal role in EMT related to cancer dissemination. Upon acquiring more knowledge and clinical evidence on non-genetic factors affecting neoplasia, modulation of the expression levels of diverse ceRNAs may allow for the development of novel prognostic/diagnostic markers and reveal potential targets for the disruption of cancer-related EMT.

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30

Belgardt, Bengt-Frederik, Kashan Ahmed, Martina Spranger, Mathieu Latreille, Remy Denzler, Nadiia Kondratiuk, Ferdinand von Meyenn, et al. "The microRNA-200 family regulates pancreatic beta cell survival in type 2 diabetes." Nature Medicine 21, no. 6 (May 18, 2015): 619–27. http://dx.doi.org/10.1038/nm.3862.

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31

Bojmar, Linda, Elin Karlsson, Sander Ellegård, Hans Olsson, Bergthor Björnsson, Olof Hallböök, Marie Larsson, Olle Stål, and Per Sandström. "The Role of MicroRNA-200 in Progression of Human Colorectal and Breast Cancer." PLoS ONE 8, no. 12 (December 20, 2013): e84815. http://dx.doi.org/10.1371/journal.pone.0084815.

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32

Cai, Chunxiao, Hassan Ashktorab, Xiaowu Pang, Yuan Zhao, Wei Sha, Yulan Liu, and Xinbin Gu. "Abstract A13: The microRNA-200 family overcomes cisplatin resistance by targeting ceramide glycosylation." Cancer Research 72, no. 2 Supplement (January 8, 2012): A13. http://dx.doi.org/10.1158/1538-7445.nonrna12-a13.

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Gilyazova, Irina R., Elizaveta A. Klimentova, Kirill V. Bulygin, Adel A. Izmailov, Marina A. Bermisheva, Elmira F. Galimova, Ruslan I. Safiullin, Shamil N. Galimov, Valentin N. Pavlov, and Elsa K. Khusnutdinova. "MicroRNA-200 family expression analysis in metastatic clear cell renal cell carcinoma patients." Cancer Gene Therapy 27, no. 10-11 (November 4, 2019): 768–72. http://dx.doi.org/10.1038/s41417-019-0149-z.

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Cai, Jiping, Xiaoyu Liu, Jinwei Cheng, You Li, Xiao Huang, Yuzhen Li, Xiaoye Ma, Hongyu Yu, Huimin Liu, and Ruili Wei. "MicroRNA-200 is commonly repressed in conjunctival MALT lymphoma, and targets cyclin E2." Graefe's Archive for Clinical and Experimental Ophthalmology 250, no. 4 (December 20, 2011): 523–31. http://dx.doi.org/10.1007/s00417-011-1885-4.

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Ohlsson Teague, E. M. C., V. Nisenblat, S. A. Robertson, and M. L. Hull. "506. MENSTRUAL CYCLE VARIATIONS IN PLASMA microRNA EXPRESSION PROFILES." Reproduction, Fertility and Development 21, no. 9 (2009): 106. http://dx.doi.org/10.1071/srb09abs506.

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microRNAs are short, single-stranded RNAs that regulate gene expression at the post-transcriptional level. Plasma and serum microRNAs correlate closely with microRNA profiles of diseased tissue and have been explored as blood-based biomarkers for human diseases, including steroid-driven malignancies. However, reproductive steroid signalling regulates the expression of specific microRNAs and this could impact the utility of microRNA biomarkers in reproductive aged women. We hypothesised that microRNA expression profiles are altered by steroid hormone fluctuations associated with the menstrual cycle. To test this hypothesis, plasma microRNA expression was measured in healthy women at 3 stages of a 28 day menstrual cycle; ie menstrual (day 3-5), follicular (day 9–13) and implantation window/secretory phase (day 18–22). Total RNA was extracted from plasma, multiplex reverse transcription was performed, and the cDNA pre-amplified prior to expression analysis of 667 microRNAs on Taqman low density PCR arrays (n=6 women). Preliminary data shows that up to 200 microRNAs may be detected with this methodology, and that at least 14 of these are differentially expressed (fold change ≥±1.5) at follicular and secretory phase, as compared to menstrual phase. We plan to confirm these findings with standard Taqman microRNA assays (n=10 women). Our findings suggest that plasma miRNA expression profiles change over the menstrual cycle, and that this could confound microRNA-based diagnostic tests. We hope to demonstrate the most appropriate cycle phase for blood-based miRNA profiling, facilitating the development of plasma microRNA-based diagnostic tests and providing valuable information to researchers studying circulating microRNA profiles in reproductive aged women.

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36

Lin, Zhen, Xia Wang, Claire Fewell, Jennifer Cameron, Qinyan Yin, and Erik K. Flemington. "Differential Expression of the miR-200 Family MicroRNAs in Epithelial and B Cells and Regulation of Epstein-Barr Virus Reactivation by the miR-200 Family Member miR-429." Journal of Virology 84, no. 15 (May 19, 2010): 7892–97. http://dx.doi.org/10.1128/jvi.00379-10.

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ABSTRACT The miR-200 microRNA family is important for maintaining the epithelial phenotype, partially through suppressing ZEB1 and ZEB2. Since ZEB1 inhibits Epstein-Barr virus (EBV) reactivation, we hypothesized that expression of miR-200 family members in epithelial cells may partly account for higher levels of EBV reactivation in this tissue (relative to nonplasma B cells). Here we show that, whereas miR-200 family members are expressed in epithelial cells, their expression is low in latently infected B cells. Furthermore, the miR-200 family member miR-429 shows elevated expression in plasma cell lines and is induced by B-cell-receptor activation in Akata cells. Lastly, expression of miR-429 can break latency.

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37

Moimas, Silvia, Francesco Salton, Beata Kosmider, Nadja Ring, Maria C. Volpe, Karim Bahmed, Luca Braga, et al. "miR-200 family members reduce senescence and restore idiopathic pulmonary fibrosis type II alveolar epithelial cell transdifferentiation." ERJ Open Research 5, no. 4 (October 2019): 00138–2019. http://dx.doi.org/10.1183/23120541.00138-2019.

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RationaleAlveolar type II (ATII) cells act as adult stem cells contributing to alveolar type I (ATI) cell renewal and play a major role in idiopathic pulmonary fibrosis (IPF), as supported by familial cases harbouring mutations in genes specifically expressed by these cells. During IPF, ATII cells lose their regenerative potential and aberrantly express pathways contributing to epithelial–mesenchymal transition (EMT). The microRNA miR-200 family is downregulated in IPF, but its effect on human IPF ATII cells remains unproven. We wanted to 1) evaluate the characteristics and transdifferentiating ability of IPF ATII cells, and 2) test whether miR-200 family members can rescue the regenerative potential of fibrotic ATII cells.MethodsATII cells were isolated from control or IPF lungs and cultured in conditions promoting their transdifferentiation into ATI cells. Cells were either phenotypically monitored over time or transfected with miR-200 family members to evaluate the microRNA effect on the expression of transdifferentiation, senescence and EMT markers.ResultsIPF ATII cells show a senescent phenotype (p16 and p21), overexpression of EMT (ZEB1/2) and impaired expression of ATI cell markers (AQP5 and HOPX) after 6 days of culture in differentiating medium. Transfection with certain miR-200 family members (particularly miR-200b-3p and miR-200c-3p) reduced senescence marker expression and restored the ability to transdifferentiate into ATI cells.ConclusionsWe demonstrated that ATII cells from IPF patients express senescence and EMT markers, and display a reduced ability to transdifferentiate into ATI cells. Transfection with certain miR-200 family members rescues this phenotype, reducing senescence and restoring transdifferentiation marker expression.

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Gibbons, D. L., W. Lin, C. Creighton, S. Zhang, G. Lozano, and J. Kurie. "Use of a murine model of NSCLC to evaluate the role of the microRNA-200 family in regulating EMT and metastasis." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 11006. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.11006.

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11006 Background: Non-small cell lung cancer (NSCLC) is the leading cause of cancer death worldwide, primarily due to metastatic disease. Unfortunately, we lack a clear understanding of the molecular and cellular basis for lung cancer metastasis, partly because the experimental study is hampered by lack of good models. Methods/Results: To address this deficiency we have developed an experimental murine model of metastatic NSCLC using cell lines derived from a genetic mouse model of human lung adenocarcinoma that develops metastatic disease owing to the expression of K-rasG12D and p53R172H. An expression signature derived from the spontaneous metastatic tumors in these animals is prognostic when applied to a large series of early-stage patient tumors, illustrating that the model recapitulates features of the human disease. Combined mRNA and microRNA profiling of highly metastatic subcutaneous tumors versus non-metastatic tumors revealed a signature for the epithelial-to-mesenchymal transition (including increases in known EMT-inducing transcription factors and down-regulation of genes responsible for maintenance of epithelial polarity) and associated loss of the microRNA-200 family (miR-141, 200a, 200b, 200c & 429) expression. Forced expression of the miR-200 family produced a more epithelial cell phenotype and associated changes in the ability of the cancer cells to respond to EMT-inducing stimuli such as TGFβ. We believe this to be a mechanism whereby changes in the tumor microenvironment influence tumor cell state and ability to undergo metastasis. Conclusions: New therapeutic targets to address the problem of metastatic NSCLC will only emerge from a better understanding of the tumor biology. Using this experimental animal model has revealed a role for EMT in the pathogenesis of the disease and the microRNA-200 family as regulators of the cellular switch. We are currently working to understand the microenvironment regulation of the miR-200 members. This work should provide new insights into the cell biology of tumor progression and metastasis, while generating new potential targets for therapy of metastatic disease. [Table: see text]

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Jimenez, Patricia T., Monica A. Mainigi, R. Ann Word, W. Lee Kraus, and Carole R. Mendelson. "miR-200 Regulates Endometrial Development During Early Pregnancy." Molecular Endocrinology 30, no. 9 (August 17, 2016): 977–87. http://dx.doi.org/10.1210/me.2016-1050.

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Abstract For successful embryo implantation, endometrial stromal cells must undergo functional and morphological changes, referred to as decidualization. However, the molecular mechanisms that regulate implantation and decidualization are not well defined. Here we demonstrate that the estradiol- and progesterone-regulated microRNA (miR)-200 family was markedly down-regulated in mouse endometrial stromal cells prior to implantation, whereas zinc finger E-box binding homeobox-1 and -2 and other known and predicted targets were up-regulated. Conversely, miR-200 was up-regulated during in vitro decidualization of human endometrial stromal cells. Knockdown of miR-200 negatively affected decidualization and prevented the mesenchymal-epithelial transition-like changes that accompanied decidual differentiation. Notably, superovulation of mice and humans altered miR-200 expression. Our findings suggest that hormonal alterations that accompany superovulation may negatively impact endometrial development and decidualization by causing aberrant miR-200 expression.

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Lee, Jung Soo, Young-Ho Ahn, Hye Sung Won, Der Sheng Sun, Yeo Hyung Kim, and Yoon Ho Ko. "Prognostic Role of the MicroRNA-200 Family in Various Carcinomas: A Systematic Review and Meta-Analysis." BioMed Research International 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/1928021.

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Background/Aims.The miRNA-200 (miR-200) family may act as key inhibitors of epithelial-to-mesenchymal transition. However, the potential prognostic value of miR-200s in various human malignancies remains controversial. This meta-analysis analyzed the associations between miR-200 levels and survival outcomes in a variety of tumors.Methods.Eligible published studies were identified by searching the Embase, PubMed, CINAHL, and Google scholar databases. Patient clinical data were pooled, and pooled hazard ratios (HRs) with 95% confidence intervals (95% CI) were used to calculate the strength of this association.Results.The pooled HRs suggested that high tissue expression of miR-200 family members was associated with better survival (overall survival [OS]: HR = 0.70, 95% CI 0.54–0.91; progression-free survival [PFS]: HR = 0.63, 95% CI 0.52–0.76) in thirty-four eligible articles. In contrast, higher expression of circulating miR-200 members was significantly associated with poor clinical outcome (OS, HR = 1.68, 95% CI 1.15–2.46; PFS, HR = 2.62, 95% CI 1.68–4.07).Conclusion.The results from this meta-analysis suggest that miR-200 family members are potential prognostic biomarkers in patients with various carcinomas. To apply these findings in the clinic, large prospective studies are needed to validate the prognostic values of miR-200s in individual cancer types.

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MINN, YANG-KI, DA HYE LEE, WOO JIN HYUNG, JI EUN KIM, JUNJEONG CHOI, SEUNG-HO YANG, HOTAEK SONG, BEOM JIN LIM, and SE HOON KIM. "MicroRNA-200 family members and ZEB2 are associated with brain metastasis in gastric adenocarcinoma." International Journal of Oncology 45, no. 6 (September 26, 2014): 2403–10. http://dx.doi.org/10.3892/ijo.2014.2680.

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Sánchez-Cid, Lourdes, Mònica Pons, Juan José Lozano, Nuria Rubio, Marta Guerra-Rebollo, Aroa Soriano, Laia Paris-Coderch, et al. "MicroRNA-200, associated with metastatic breast cancer, promotes traits of mammary luminal progenitor cells." Oncotarget 8, no. 48 (September 7, 2017): 83384–406. http://dx.doi.org/10.18632/oncotarget.20698.

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Epstein, David M. "Special delivery: microRNA-200–containing extracellular vesicles provide metastatic message to distal tumor cells." Journal of Clinical Investigation 124, no. 12 (November 17, 2014): 5107–8. http://dx.doi.org/10.1172/jci79191.

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Peng, Zongyu, Wenru Zhu, Jinzhao Dai, and Fang Ju. "MicroRNA-200 as potential diagnostic markers for colorectal cancer: meta-analysis and experimental validation." Cellular and Molecular Biology 64, no. 6 (May 15, 2018): 77. http://dx.doi.org/10.14715/cmb/2018.64.6.14.

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Yeh, Ta-Sen, Frank Wang, Tse-Ching Chen, Chun-Nan Yeh, Ming-Chin Yu, Yi-Yin Jan, and Miin-Fu Chen. "Expression Profile of MicroRNA-200 Family in Hepatocellular Carcinoma With Bile Duct Tumor Thrombus." Annals of Surgery 259, no. 2 (February 2014): 346–54. http://dx.doi.org/10.1097/sla.0000000000000223.

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Choi, Pui-Wah, Wai Wing So, Junzheng Yang, Shubai Liu, Ka Kui Tong, Kin Ming Kwan, Jamie S. L. Kwok, et al. "MicroRNA-200 family governs ovarian inclusion cyst formation and mode of ovarian cancer spread." Oncogene 39, no. 20 (March 25, 2020): 4045–60. http://dx.doi.org/10.1038/s41388-020-1264-x.

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Reddy, Marpadga A., Wen Jin, Louisa Villeneuve, Mei Wang, Linda Lanting, Ivan Todorov, Mitsuo Kato, and Rama Natarajan. "Pro-Inflammatory Role of MicroRNA-200 in Vascular Smooth Muscle Cells From Diabetic Mice." Arteriosclerosis, Thrombosis, and Vascular Biology 32, no. 3 (March 2012): 721–29. http://dx.doi.org/10.1161/atvbaha.111.241109.

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Elson-Schwab, Ilan, Anna Lorentzen, and Christopher J. Marshall. "MicroRNA-200 Family Members Differentially Regulate Morphological Plasticity and Mode of Melanoma Cell Invasion." PLoS ONE 5, no. 10 (October 4, 2010): e13176. http://dx.doi.org/10.1371/journal.pone.0013176.

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Han, Yuyan, Heather L. Francis, Shannon Glaser, Jennifer McCarra, Gianfranco Alpini, Jay Sharma, Giuseppina Dusio, Chang-Gong Liu, Christopher Johnson, and Fanyin Meng. "740 Epigenetic Regulation of MicroRNA-200 Family in Human Gall Bladder Cancer Stem Cells." Gastroenterology 142, no. 5 (May 2012): S—926—S—927. http://dx.doi.org/10.1016/s0016-5085(12)63594-x.

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Howe, Erin N., Dawn R. Cochrane, and Jennifer K. Richer. "The miR-200 and miR-221/222 microRNA Families: Opposing Effects on Epithelial Identity." Journal of Mammary Gland Biology and Neoplasia 17, no. 1 (February 17, 2012): 65–77. http://dx.doi.org/10.1007/s10911-012-9244-6.

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