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  1. Article ; Online: Dynamic Alterations to Hepatic MicroRNA-29a in Response to Long-Term High-Fat Diet and EtOH Feeding.

    Liang, Tiebing / Kota, Janaiah / Williams, Kent E / Saxena, Romil / Gawrieh, Samer / Zhong, Xiaoling / Zimmers, Teresa A / Chalasani, Naga

    International journal of molecular sciences

    2023  Volume 24, Issue 19

    Abstract: MicroRNA-29a (miR-29a) is a well characterized fibro-inflammatory molecule and its aberrant expression is linked to a variety of pathological liver conditions. The long-term effects of a high-fat diet (HFD) in combination with different levels of EtOH ... ...

    Abstract MicroRNA-29a (miR-29a) is a well characterized fibro-inflammatory molecule and its aberrant expression is linked to a variety of pathological liver conditions. The long-term effects of a high-fat diet (HFD) in combination with different levels of EtOH consumption on miR-29a expression and liver pathobiology are unknown. Mice at 8 weeks of age were divided into five groups (calorie-matched diet plus water (CMD) as a control group, HFD plus water (HFD) as a liver disease group, HFD plus 2% EtOH (HFD + 2% E), HFD + 10% E, and HFD + 20% E as intervention groups) and fed for 4, 13, 26, or 39 weeks. At each time point, analyses were performed for liver weight/body weight (BW) ratio, AST/ALT ratio, as well as liver histology assessments, which included inflammation, estimated fat deposition, lipid area, and fibrosis. Hepatic miR-29a was measured and correlations with phenotypic traits were determined. Four-week feeding produced no differences between the groups on all collected phenotypic traits or miR-29a expression, while significant effects were observed after 13 weeks, with EtOH concentration-specific induction of miR-29a. A turning point for most of the collected traits was apparent at 26 weeks, and miR-29a was significantly down-regulated with increasing liver injury. Overall, miR-29a up-regulation was associated with a lower liver/BW ratio, fat deposition, inflammation, and fibrosis, suggesting a protective role of miR-29a against liver disease progression. A HFD plus increasing concentrations of EtOH produces progressive adverse effects on the liver, with no evidence of beneficial effects of low-dose EtOH consumption. Moreover, miR-29a up-regulation is associated with less severe liver injury.
    MeSH term(s) Mice ; Animals ; Diet, High-Fat/adverse effects ; Liver/metabolism ; Ethanol/toxicity ; Ethanol/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Liver Cirrhosis/metabolism ; Inflammation/metabolism ; MicroRNAs/metabolism ; Water/metabolism ; Mice, Inbred C57BL
    Chemical Substances Ethanol (3K9958V90M) ; MicroRNAs ; Water (059QF0KO0R)
    Language English
    Publishing date 2023-09-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241914564
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  2. Article ; Online: Pancreatic cancer: Stroma and its current and emerging targeted therapies.

    Kota, Janaiah / Hancock, Julie / Kwon, Jason / Korc, Murray

    Cancer letters

    2017  Volume 391, Page(s) 38–49

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human malignancies with a 5-year survival rate of 8%. Dense, fibrotic stroma associated with pancreatic tumors is a major obstacle for drug delivery to the tumor bed and plays a crucial ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human malignancies with a 5-year survival rate of 8%. Dense, fibrotic stroma associated with pancreatic tumors is a major obstacle for drug delivery to the tumor bed and plays a crucial role in pancreatic cancer progression. Targeting stroma is considered as a potential therapeutic strategy to improve anti-cancer drug efficacy and patient survival. Although numerous stromal depletion therapies have reached the clinic, they add little to overall survival and are often associated with toxicity. Furthermore, increasing evidence suggests the anti-tumor properties of stroma. Its complete ablation enhanced tumor progression and reduced survival. Consequently, efforts are now focused on developing stromal-targeted therapies that normalize the reactive stroma and avoid the extremes: stromal abundance vs. complete depletion. In this review, we summarized the state of current and emerging anti-stromal targeted therapies, with major emphasis on the role of miRNAs in PDAC stroma and their potential use as novel therapeutic agents to modulate PDAC tumor-stromal interactions.
    MeSH term(s) Adenocarcinoma/pathology ; Adenocarcinoma/therapy ; Carcinoma, Pancreatic Ductal/pathology ; Carcinoma, Pancreatic Ductal/therapy ; Humans ; MicroRNAs/metabolism ; Stromal Cells/pathology ; Tumor Microenvironment
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2017--10
    Publishing country Ireland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2016.12.035
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  3. Article: A Systematic Review of miR-29 in Cancer.

    Kwon, Jason J / Factora, Tricia D / Dey, Shatovisha / Kota, Janaiah

    Molecular therapy oncolytics

    2018  Volume 12, Page(s) 173–194

    Abstract: MicroRNAs (miRNA) are small non-coding RNAs (∼22 nt in length) that are known as potent master regulators of eukaryotic gene expression. miRNAs have been shown to play a critical role in cancer pathogenesis, and the misregulation of miRNAs is a well- ... ...

    Abstract MicroRNAs (miRNA) are small non-coding RNAs (∼22 nt in length) that are known as potent master regulators of eukaryotic gene expression. miRNAs have been shown to play a critical role in cancer pathogenesis, and the misregulation of miRNAs is a well-known feature of cancer. In recent years, miR-29 has emerged as a critical miRNA in various cancers, and it has been shown to regulate multiple oncogenic processes, including epigenetics, proteostasis, metabolism, proliferation, apoptosis, metastasis, fibrosis, angiogenesis, and immunomodulation. Although miR-29 has been thoroughly documented as a tumor suppressor in the majority of studies, some controversy remains with conflicting reports of miR-29 as an oncogene. In this review, we provide a systematic overview of miR-29's functional role in various mechanisms of cancer and introspection on the contradictory roles of miR-29.
    Language English
    Publishing date 2018-12-31
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2372-7705
    ISSN 2372-7705
    DOI 10.1016/j.omto.2018.12.011
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  4. Article ; Online: Global targetome analysis reveals critical role of miR-29a in pancreatic stellate cell mediated regulation of PDAC tumor microenvironment.

    Dey, Shatovisha / Liu, Sheng / Factora, Tricia D / Taleb, Solaema / Riverahernandez, Primavera / Udari, Lata / Zhong, Xiaoling / Wan, Jun / Kota, Janaiah

    BMC cancer

    2020  Volume 20, Issue 1, Page(s) 651

    Abstract: Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive forms of malignancies with a nearly equal incidence and mortality rates in patients. Pancreatic stellate cells (PSCs) are critical players in PDAC microenvironment to ... ...

    Abstract Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive forms of malignancies with a nearly equal incidence and mortality rates in patients. Pancreatic stellate cells (PSCs) are critical players in PDAC microenvironment to promote the aggressiveness and pathogenesis of the disease. Dysregulation of microRNAs (miRNAs) have been shown to play a significant role in progression of PDAC. Earlier, we observed a PSC-specific downregulation of miR-29a in PDAC pancreas, however, the mechanism of action of the molecule in PSCs is still to be elucidated. The current study aims to clarify the regulation of miR-29a in PSCs and identifies functionally important downstream targets that contribute to tumorigenic activities during PDAC progression.
    Methods: In this study, using RNAseq approach, we performed transcriptome analysis of paired miR-29a overexpressing and control human PSCs (hPSCs). Enrichment analysis was performed with the identified differentially expressed genes (DEGs). miR-29a targets in the dataset were identified, which were utilized to create network interactions. Western blots were performed with the top miR-29a candidate targets in hPSCs transfected with miR-29a mimic or scramble control.
    Results: RNAseq analysis identified 202 differentially expressed genes, which included 19 downregulated direct miR-29a targets. Translational repression of eight key pro-tumorigenic and -fibrotic targets namely IGF-1, COL5A3, CLDN1, E2F7, MYBL2, ITGA6 and ADAMTS2 by miR-29a was observed in PSCs. Using pathway analysis, we find that miR-29a modulates effectors of IGF-1-p53 signaling in PSCs that may hinder carcinogenesis. We further observe a regulatory role of the molecule in pathways associated with PDAC ECM remodeling and tumor-stromal crosstalk, such as INS/IGF-1, RAS/MAPK, laminin interactions and collagen biosynthesis.
    Conclusions: Together, our study presents a comprehensive understanding of miR-29a regulation of PSCs, and identifies essential pathways associated with PSC-mediated PDAC pathogenesis. The findings suggest an anti-tumorigenic role of miR-29a in the context of PSC-cancer cell crosstalk and advocates for the potential of the molecule in PDAC targeted therapies.
    MeSH term(s) Apoptosis ; Biomarkers, Tumor/genetics ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/immunology ; Carcinoma, Pancreatic Ductal/pathology ; Cell Movement ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/genetics ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/pathology ; Pancreatic Stellate Cells/immunology ; Pancreatic Stellate Cells/metabolism ; Pancreatic Stellate Cells/pathology ; Transcriptome ; Tumor Cells, Cultured ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology
    Chemical Substances Biomarkers, Tumor ; MicroRNAs
    Language English
    Publishing date 2020-07-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 2041352-X
    ISSN 1471-2407 ; 1471-2407
    ISSN (online) 1471-2407
    ISSN 1471-2407
    DOI 10.1186/s12885-020-07135-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Loss of miR-29a/b1 promotes inflammation and fibrosis in acute pancreatitis.

    Dey, Shatovisha / Udari, Lata M / RiveraHernandez, Primavera / Kwon, Jason J / Willis, Brandon / Easler, Jeffrey J / Fogel, Evan L / Pandol, Stephen / Kota, Janaiah

    JCI insight

    2021  Volume 6, Issue 19

    Abstract: MicroRNA-29 (miR-29) is a critical regulator of fibroinflammatory processes in human diseases. In this study, we found a decrease in miR-29a in experimental and human chronic pancreatitis, leading us to investigate the regulatory role of the miR-29a/b1 ... ...

    Abstract MicroRNA-29 (miR-29) is a critical regulator of fibroinflammatory processes in human diseases. In this study, we found a decrease in miR-29a in experimental and human chronic pancreatitis, leading us to investigate the regulatory role of the miR-29a/b1 cluster in acute pancreatitis (AP) utilizing a conditional miR-29a/b1-KO mouse model. miR-29a/b1-sufficient (WT) and -deficient (KO) mice were administered supramaximal caerulein to induce AP and characterized at different time points, utilizing an array of IHC and biochemical analyses for AP parameters. In caerulein-induced WT mice, miR-29a remained dramatically downregulated at injury. Despite high-inflammatory milieu, fibrosis, and parenchymal disarray in the WT mice during early AP, the pancreata fully restored during recovery. miR-29a/b1-KO mice showed significantly greater inflammation, lymphocyte infiltration, macrophage polarization, and ECM deposition, continuing until late recovery with persistent parenchymal disorganization. The increased pancreatic fibrosis was accompanied by enhanced TGFβ1 coupled with persistent αSMA+ PSC activation. Additionally, these mice exhibited higher circulating IL-6 and inflammation in lung parenchyma. Together, this collection of studies indicates that depletion of miR-29a/b1 cluster impacts the fibroinflammatory mechanisms of AP, resulting in (a) aggravated pathogenesis and (b) delayed recovery from the disease, suggesting a protective role of the molecule against AP.
    MeSH term(s) Animals ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Fibrosis/genetics ; Fibrosis/metabolism ; Fibrosis/pathology ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Mice ; Mice, Knockout ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Pancreatitis/genetics ; Pancreatitis/pathology ; Pancreatitis, Chronic/metabolism
    Chemical Substances MIRN29 microRNA, mouse ; MIRN29a microRNA, human ; MicroRNAs
    Language English
    Publishing date 2021-10-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.149539
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The Role and Therapeutic Potential of miRNAs in Colorectal Liver Metastasis.

    Sahu, Smiti S / Dey, Shatovisha / Nabinger, Sarah C / Jiang, Guanglong / Bates, Alison / Tanaka, Hiromi / Liu, Yunlong / Kota, Janaiah

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 15803

    Abstract: Colorectal cancer (CRC) is the fourth leading cause of cancer-related deaths worldwide. Liver metastasis is the major cause of CRC patient mortality, occurring in 60% patients with no effective therapies. Although studies have indicated the role of ... ...

    Abstract Colorectal cancer (CRC) is the fourth leading cause of cancer-related deaths worldwide. Liver metastasis is the major cause of CRC patient mortality, occurring in 60% patients with no effective therapies. Although studies have indicated the role of miRNAs in CRC, an in-depth miRNA expression analysis is essential to identify clinically relevant miRNAs and understand their potential in targeting liver metastasis. Here we analyzed miRNA expressions in 405 patient tumors from publicly available colorectal cancer genome sequencing project database. Our analyses showed miR-132, miR-378f, miR-605 and miR-1976 to be the most significantly downregulated miRNAs in primary and CRC liver metastatic tissues, and CRC cell lines. Observations in CRC cell lines indicated that ectopic expressions of miR-378f, -605 and -1976 suppress CRC cell proliferation, anchorage independent growth, metastatic potential, and enhance apoptosis. Consistently, CRC patients with higher miR-378f and miR-1976 levels exhibited better survival. Together, our data suggests an anti-tumorigenic role of these miRNAs in CRC and warrant future in vivo evaluation of the molecules for developing biomarkers or novel therapeutic strategies.
    MeSH term(s) Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Female ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/secondary ; Male ; MicroRNAs/metabolism
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2019-11-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-52225-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: miR-29a Is Repressed by MYC in Pancreatic Cancer and Its Restoration Drives Tumor-Suppressive Effects via Downregulation of LOXL2.

    Dey, Shatovisha / Kwon, Jason J / Liu, Sheng / Hodge, Gabriel A / Taleb, Solaema / Zimmers, Teresa A / Wan, Jun / Kota, Janaiah

    Molecular cancer research : MCR

    2019  Volume 18, Issue 2, Page(s) 311–323

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is an intractable cancer with a dismal prognosis. miR-29a is commonly downregulated in PDAC; however, mechanisms for its loss and role still remain unclear. Here, we show that in PDAC, repression of miR-29a is ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is an intractable cancer with a dismal prognosis. miR-29a is commonly downregulated in PDAC; however, mechanisms for its loss and role still remain unclear. Here, we show that in PDAC, repression of miR-29a is directly mediated by MYC via promoter activity. RNA sequencing analysis, integrated with miRNA target prediction, identified global miR-29a downstream targets in PDAC. Target enrichment coupled with gene ontology and survival correlation analyses identified the top five miR-29a-downregulated target genes (
    MeSH term(s) Amino Acid Oxidoreductases/genetics ; Amino Acid Oxidoreductases/metabolism ; Animals ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; Disease Models, Animal ; Down-Regulation ; Humans ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Transfection
    Chemical Substances MIRN29 microRNA, mouse ; MIRN29a microRNA, human ; MYC protein, human ; MicroRNAs ; Myc protein, mouse ; Proto-Oncogene Proteins c-myc ; Amino Acid Oxidoreductases (EC 1.4.-) ; LOXL2 protein, human (EC 1.4.3.-) ; Loxl2 protein, mouse (EC 1.4.3.-)
    Language English
    Publishing date 2019-10-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-19-0594
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5744: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Novel role of miR-29a in pancreatic cancer autophagy and its therapeutic potential.

    Kwon, Jason J / Willy, Jeffrey A / Quirin, Kayla A / Wek, Ronald C / Korc, Murray / Yin, Xiao-Ming / Kota, Janaiah

    Oncotarget

    2016  Volume 7, Issue 44, Page(s) 71635–71650

    Abstract: Pancreatic Ductal Adenocarcinoma (PDAC) is a highly lethal malignancy that responds poorly to current therapeutic modalities. In an effort to develop novel therapeutic strategies, we found downregulation of miR-29 in pancreatic cancer cells, and ... ...

    Abstract Pancreatic Ductal Adenocarcinoma (PDAC) is a highly lethal malignancy that responds poorly to current therapeutic modalities. In an effort to develop novel therapeutic strategies, we found downregulation of miR-29 in pancreatic cancer cells, and overexpression of miR-29a sensitized chemotherapeutic resistant pancreatic cancer cells to gemcitabine, reduced cancer cell viability, and increased cytotoxicity. Furthermore, miR-29a blocked autophagy flux, as evidenced by an accumulation of autophagosomes and autophagy markers, LC3B and p62, and a decrease in autophagosome-lysosome fusion. In addition, miR-29a decreased the expression of autophagy proteins, TFEB and ATG9A, which are critical for lysosomal function and autophagosome trafficking respectively. Knockdown of TFEB or ATG9A inhibited autophagy similar to miR-29a overexpression. Finally, miR-29a reduced cancer cell migration, invasion, and anchorage independent growth. Collectively, our findings indicate that miR-29a functions as a potent autophagy inhibitor, sensitizes cancer cells to gemcitabine, and decreases their invasive potential. Our data provides evidence for the use of miR-29a as a novel therapeutic agent to target PDAC.
    MeSH term(s) Autophagy ; Autophagy-Related Proteins/antagonists & inhibitors ; Autophagy-Related Proteins/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/antagonists & inhibitors ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/pathology ; Cell Line, Tumor ; Deoxycytidine/analogs & derivatives ; Deoxycytidine/therapeutic use ; Epithelial-Mesenchymal Transition ; Humans ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/genetics ; MicroRNAs/physiology ; Neoplasm Invasiveness ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/pathology ; Vesicular Transport Proteins/antagonists & inhibitors ; Vesicular Transport Proteins/genetics ; Gemcitabine
    Chemical Substances ATG9A protein, human ; Autophagy-Related Proteins ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; MIRN29a microRNA, human ; Membrane Proteins ; MicroRNAs ; TFEB protein, human ; Vesicular Transport Proteins ; Deoxycytidine (0W860991D6) ; Gemcitabine
    Language English
    Publishing date 2016-09-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.11928
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  9. Article ; Online: Gene targets of mouse miR-709: regulation of distinct pools.

    Surendran, Sneha / Jideonwo, Victoria N / Merchun, Chris / Ahn, Miwon / Murray, John / Ryan, Jennifer / Dunn, Kenneth W / Kota, Janaiah / Morral, Núria

    Scientific reports

    2016  Volume 6, Page(s) 18958

    Abstract: MicroRNA (miRNA) are short non-coding RNA molecules that regulate multiple cellular processes, including development, cell differentiation, proliferation and death. Nevertheless, little is known on whether miRNA control the same gene networks in ... ...

    Abstract MicroRNA (miRNA) are short non-coding RNA molecules that regulate multiple cellular processes, including development, cell differentiation, proliferation and death. Nevertheless, little is known on whether miRNA control the same gene networks in different tissues. miR-709 is an abundant miRNA expressed ubiquitously. Through transcriptome analysis, we have identified targets of miR-709 in hepatocytes. miR-709 represses genes implicated in cytoskeleton organization, extracellular matrix attachment, and fatty acid metabolism. Remarkably, none of the previously identified targets in non-hepatic tissues are silenced by miR-709 in hepatocytes, even though several of these genes are abundantly expressed in liver. In addition, miR-709 is upregulated in hepatocellular carcinoma, suggesting it participates in the genetic reprogramming that takes place during cell division, when cytoskeleton remodeling requires substantial changes in gene expression. In summary, the present study shows that miR-709 does not repress the same pool of genes in separate cell types. These results underscore the need for validating gene targets in every tissue a miRNA is expressed.
    MeSH term(s) Animals ; Base Sequence ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cytoskeletal Proteins/genetics ; Cytoskeletal Proteins/metabolism ; Disease Models, Animal ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Regulatory Networks ; Genes, Reporter ; Hepatocytes/cytology ; Hepatocytes/metabolism ; Humans ; Lipid Metabolism/genetics ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Luciferases/genetics ; Luciferases/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Organ Specificity ; Primary Cell Culture ; Transcriptome ; Transfection
    Chemical Substances Cytoskeletal Proteins ; Extracellular Matrix Proteins ; MIRN709 microRNA, mouse ; MicroRNAs ; Luciferases (EC 1.13.12.-)
    Language English
    Publishing date 2016-01-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep18958
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  10. Article ; Online: Lower expression of tumor microRNA-26a is associated with higher recurrence in patients with hepatocellular carcinoma undergoing surgical treatment.

    Jones, Keaton R / Nabinger, Sarah C / Lee, Sangbin / Sahu, Smiti Snigdha / Althouse, Sandra / Saxena, Romil / Johnson, Mathew S / Chalasani, Naga / Gawrieh, Samer / Kota, Janaiah

    Journal of surgical oncology

    2018  Volume 118, Issue 3, Page(s) 431–439

    Abstract: Background and objectives: Hepatocellular carcinoma (HCC) in patients with hepatitis B virus (HBV) exhibit lower tumor microRNA-26a (miR-26a) expression which is associated with worse outcomes. It is unknown if similar miR-26a loss occurs in HCC ... ...

    Abstract Background and objectives: Hepatocellular carcinoma (HCC) in patients with hepatitis B virus (HBV) exhibit lower tumor microRNA-26a (miR-26a) expression which is associated with worse outcomes. It is unknown if similar miR-26a loss occurs in HCC developed in other liver diseases. We examined tumor miR-26a expression and its impact on recurrence and mortality in a North American HCC cohort.
    Methods: MiR-26a levels from tumor and surrounding nontumor liver tissue in 186 subjects were collected. We defined lower tumor expression of miR-26a as <1-fold that of the adjacent nontumor liver tissue.
    Results: Viral hepatitis (42%; 40% hepatitis C and 2% HBV), alcohol (19%), and nonalcoholic fatty liver disease (NAFLD) (18%) were the most common causes of liver disease. The prevalence of lower tumor miR-26a expression was 68%, and it was evident in HCCs arising in all etiologies (viral hepatitis 60%, alcohol 61%, and NAFLD 76%). Subjects with lower tumor miR-26a expression had significantly higher tumor recurrence (hazard ratio [HR], 2.45; 95% confidence interval [CI], 1.18 to 5.1; P = 0.016) and higher mortality of borderline significance (HR, 1.51; 95% CI, 0.94 to 2.41; P = 0.086).
    Conclusion: Reduced miR-26a expression is a common phenomenon in HCC arising in North American patients with different underlying liver diseases and may increase recurrence and mortality after surgery.
    MeSH term(s) Aged ; Biomarkers, Tumor/blood ; Biomarkers, Tumor/genetics ; Carcinoma, Hepatocellular/pathology ; Carcinoma, Hepatocellular/surgery ; Female ; Follow-Up Studies ; Gene Expression Regulation, Neoplastic ; Hepatectomy/methods ; Humans ; Liver Neoplasms/pathology ; Liver Neoplasms/surgery ; Male ; MicroRNAs/blood ; MicroRNAs/genetics ; Middle Aged ; Neoplasm Recurrence, Local/blood ; Neoplasm Recurrence, Local/diagnosis ; Neoplasm Recurrence, Local/genetics ; Prognosis ; Signal Transduction ; Survival Rate
    Chemical Substances Biomarkers, Tumor ; MIRN26A microRNA, human ; MicroRNAs
    Language English
    Publishing date 2018-08-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 82063-5
    ISSN 1096-9098 ; 0022-4790
    ISSN (online) 1096-9098
    ISSN 0022-4790
    DOI 10.1002/jso.25156
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