IL-6 upregulation contributes to the reduction of miR-26a expression in hepatocellular carcinoma cells

Zhang, Yafei; Zhang, Bicheng; Zhang, Anran; Li, Xiaohua; Liu, Jian; Zhao, Jie; Zhao, Yong; Gao, Jian‐Fei; Fang, Dian‐Chun; Rao, Zhiguo

doi:10.1590/s0100-879x2012007500155

Cited by 17 publications

(11 citation statements)

References 30 publications

(45 reference statements)

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“…The decreased total liver weight, hepatic triglyceride deposition and serum ALT concentration induced by Mir-26a was also abrogated completely by IL-6 overexpression. All these were consistent with a previous paper demonstrating that Mir-26a inhibited tumour growth and allograft rejection in part by suppressing IL-6 [7,35,36].…”

Section: Discussionsupporting

confidence: 93%

MicroRNA-26a–interleukin (IL)-6–IL-17 axis regulates the development of non-alcoholic fatty liver disease in a murine model

et al. 2016

Clinical and Experimental Immunology

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SummaryNon-alcoholic fatty liver disease (NAFLD) is a hepatic presentation of obesity and metabolic syndrome. MicroRNA 26a (Mir-26a) has been reported to play functions in cellular differentiation, cell growth, cell apoptosis and metastasis. A recent paper indicated that Mir-26a regulated insulin sensitivity and metabolism of glucose and lipids. However, the role of Mir-26a in NAFLD still needs to be investigated further. In our current study, vectors encoding pre-Mir-26a (LV-26a) and an empty lentiviral vector (LV-Con) delivered approximately 2 3 10 7 transforming units of recombinant lentivirus were injected into mice through the tail vein. LV-26a-infected mice were protected from glucose dysmetabolism and showed markedly decreased total liver weight, hepatic triglyceride deposition and serum alanine transaminase (ALT) concentration when compared with LV-Con-treated mice. LV-26a-treated mice also exhibited decreased infiltration of immune cells in the liversomething attributed to reduce infiltration of T cell receptor (TCR)-gd 1 , granulocyte-differentiation antigen-1 (Gr-1) 1 cells and CD11b 1 cells. Next, we found that Mir-26a inhibited the expression of interleukin (IL)217 and IL-6 in vivo and in vitro. Furthermore, the decreased expression of IL-17 in the liver tissue induced by Mir-26a was abrogated completely by IL-6 overexpression. The decreased total liver weight, hepatic triglyceride deposition and serum ALT concentration induced by Mir-26a was also abrogated completely by IL-6 over-expression. In conclusion, the Mir-26a-IL-6-IL-17 axis regulates the development of NAFLD in a murine model.

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Section: Discussionsupporting

confidence: 93%

MicroRNA-26a–interleukin (IL)-6–IL-17 axis regulates the development of non-alcoholic fatty liver disease in a murine model

et al. 2016

Clinical and Experimental Immunology

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“…However, no direct relationship between the expression of miR‐26a and MEG3 has been reported previously. Yet, a relationship between the expression of miR‐29a and MEG3 was reported in hepatocellular cancer, and although miR‐26a is downregulated in hepatocellular cancer, reportedly through the upregulation of IL‐6, miR‐26a can also affect the pathogenesis of hepatocellular cancer by targeting the interleukin‐6‐Stat3 pathway . In our study, molecular analysis in the TSCC cell lines showed that increased miR‐26a results in increased MEG3 expression through the reduced expression of its target DNMT3B, highlighting an elegant inter‐relationship between three classes of ncRNAs, miRNAs and lncRNAs and epigenetic regulation of gene expression.…”

Section: Discussionmentioning

confidence: 52%

Expression, regulation and roles of miR‐26a and MEG3 in tongue squamous cell carcinoma

Jia

Wei

Gan

et al. 2014

Intl Journal of Cancer

190

192

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MicroRNA miR-26a and long noncoding RNA (lncRNA) MEG3 gene have been independently reported to be tumor suppressor genes in various cancers, but neither has been previously associated with tongue squamous cell carcinoma (TSCC). We report here that miR-26a and lncRNA MEG3 gene expression were both strongly reduced in TSCC compared with levels in matched nonmalignant tissues, and combined low expression levels of both miR-26a and MEG3 emerged as an independent prognostic factor for poor clinical outcome in TSCC patients. Assays in the human TSCC cell lines SCC-15 and CAL27 showed that miR26a targets the DNA methyltransferase 3B transcript and that its inhibition may result in the upregulation of MEG3, providing a plausible link between the observed reduction of miR-26a and MEG3 in TSCC tissue. Furthermore, the overexpression of miR-26a or MEG3 in SCC-15 and CAL27 cells inhibited cell proliferation and cell cycle progression, and promoted cell apoptosis. Considering the poor prognostic outcomes associated with reduced miR-26a and MEG3, our findings imply that these factors likely play important antitumor effects in TSCC pathogenesis. Furthermore, they represent potential prognostic biomarkers for stratification of TSCC patients.Tongue squamous cell carcinoma (TSCC) is the most common type of oral cancer and is well known for its high rate of proliferation and lymph nodal metastasis. 1 In clinical practice, the prediction of prognosis and planning of treatment for patients suffering from oral cancers are predominantly based on the tumor node metastasis (TNM) staging system. 2 However, in many cases of TSCC, these conventional clinical prognostic factors remain inadequate, and are unable to discriminate tumors of the same clinical stage that may have distinct clinical outcomes and different responses to the same treatments. Therefore, the identification and application of additional biomarkers into the prognostic system that better reflect the biologic diversity of TSCC and consequently predict clinical outcomes more accurately is desirable. 3 Differentially expressed genes identified from hundreds of cancer profiling studies over the last several years have yielded numerous biomarkers that have improved the subtyping, classification and diagnosis of tumors for both research and the clinic. However, the human transcriptome comprises not only large numbers of protein-coding messenger RNAs (mRNAs) but also a large set of noncoding RNAs (ncRNAs) that have structural, regulatory or unknown functions. 4 In TSCC many microRNAs (miRNAs), such as miR-195/184/ 138/21, have been shown to be dysregulated and are believed to contribute to its development and progression. [5][6][7][8] In contrast, long noncoding RNAs (lncRNAs), tentatively defined as ncRNAs more than 200 nt in length, 9 are also known to play key roles in cancer development, 10,11 and aberrant expression of lncRNAs has been functionally associated with lung, breast and prostate carcinomas. 12-14 However, whether lncRNA has relevance to TSCC biology had not been p...

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“…Aside from miR-124, the tumor suppressor miR-126a can reduce IL6, furthermore decreasing STAT3 (41). Furthermore, IL6 in HCC can in turn suppress miR-126a (42). …”

Section: Introductionmentioning

confidence: 99%

Molecular mechanisms of oncogene-induced inflammation and inflammation-sustained oncogene activation in gastrointestinal tumors: An underappreciated symbiotic relationship

Dibra

Mishra

2014

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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Inflammation plays an integral part in tumor initiation. Specifically, patients with colitis, pancreatitis, or hepatitis have an increased susceptibility to cancer. The activation, mutation, and overexpression of oncogenes have been well documented in cell proliferation and transformation. Recently, oncogenes were found to also regulate the inflammatory milieu in tumors. Similarly, the inflammatory milieu can promote oncogene activation. In this review, we summarize advances of the symbiotic relationship oncogene activation and inflammation in gastrointestinal tumors such as colorectal, hepatic, and pancreatic tumors. NF-κB and STAT3 are the two most common pathways that are deregulated via these oncogenes. Understanding these interactions may yield effective therapeutic strategies for tumor prevention and treatment.

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IL-6 upregulation contributes to the reduction of miR-26a expression in hepatocellular carcinoma cells

Cited by 17 publications

References 30 publications

MicroRNA-26a–interleukin (IL)-6–IL-17 axis regulates the development of non-alcoholic fatty liver disease in a murine model

MicroRNA-26a–interleukin (IL)-6–IL-17 axis regulates the development of non-alcoholic fatty liver disease in a murine model

Expression, regulation and roles of miR‐26a and MEG3 in tongue squamous cell carcinoma

Molecular mechanisms of oncogene-induced inflammation and inflammation-sustained oncogene activation in gastrointestinal tumors: An underappreciated symbiotic relationship

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