MiR‐96‐5p influences cellular growth and is associated with poor survival in colorectal cancer patients

Ress, Anna Lena; Stiegelbauer, Verena; Winter, Elke; Schwarzenbacher, Daniela; Kiesslich, Tobias; Lax, Sigurd; Jahn, S W; Deutsch, Alexander; Bauernhofer, Thomas; Ling, Hui; Samonigg, Hellmut; Gerger, Armin; Höefler, Gerald; Pichler, Martin

doi:10.1002/mc.22218

Cited by 74 publications

(60 citation statements)

References 30 publications

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“…We also validated the up‐regulation of miR‐96‐5p in the present study, which has been observed in many types of cancers, including triple‐negative breast cancer . It was found that up‐regulated miR‐96‐5p is associated with poor survival in patients with colorectal cancer and that it resulted in reduced cell proliferation . These findings indicate the role of miR‐96‐5p in tumor growth.…”

Section: Discussionsupporting

confidence: 86%

Identification of microRNA expression in sentinel lymph nodes from patients with breast cancer via RNA sequencing for diagnostic accuracy

Sun

Zhong

Wei

et al. 2019

The Journal of Gene Medicine

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Background Sentinel lymph node (SLN) property assessment (with or without metastasis) is important when deciding the surgery for breast cancer; however, the current diagnosis of SLN metastasis remains to be studied. microRNAs (miRNAs) have been confirmed previously as a molecular marker for the diagnosis, development and prognosis of tumors. However, the detailed role of miRNAs in the diagnosis of SLN metastasis has not been reported. Methods The present study aimed to explore the potential use of miRNAs in the diagnosis of SLN using RNA sequencing (RNA‐seq) and a quantitative real‐time polymerase chain reaction (qRT‐PCR) to compare the expression profiles of miRNAs in patients with breast cancer with or without SLN metastasis. Results The RNA‐seq results revealed that 1993 miRNAs were differentially expressed in patients with breast cancer with SLN metastasis. Among these miRNAs, 1960 were up‐regulated and 33 were down‐regulated. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses revealed that these differentially expressed miRNAs were associated with tumor growth and metastasis and were also predicted to regulate a series of tumorigenesis and metastasis genes. In particular, the most differentially expressed miRNAs were validated by qRT‐PCR, such that miR‐200a‐3p and miR‐96‐5p were up‐regulated and miR‐1‐3p and miR‐486‐3p were down‐regulated in patients with breast cancer with SLN metastasis. Conclusions The findings of the present study suggest that there is an association of miRNAs with SLN metastasis and also that miRNAs function as biomarkers with respect to the choice of therapy and disease prognosis.

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Section: Discussionsupporting

confidence: 86%

Identification of microRNA expression in sentinel lymph nodes from patients with breast cancer via RNA sequencing for diagnostic accuracy

Sun

Zhong

Wei

et al. 2019

The Journal of Gene Medicine

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“…Another miR that was highly dysregulated in TNBC samples was miR-96. Previous studies have shown miR-96 as a potential biomarker for bladder, colorectal, non-small cell lung cancer and acute myeloid leukemia 35-40. On the other hand, many of the miRs were found to be significantly downregulated in TNBC samples compared to adjacent normal tissues.…”

Section: Resultsmentioning

confidence: 91%

A Comprehensive NGS Data Analysis of Differentially Regulated miRNAs, piRNAs, lncRNAs and sn/snoRNAs in Triple Negative Breast Cancer

Koduru¹,

Tiwari²,

Leberfinger³

et al. 2017

J. Cancer

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Cancer is the second leading cause of death in the United States and is a major public health concern worldwide. Basic, clinical and epidemiological research is leading to improved cancer detection, prevention, and outcomes. Recent technological advances have allowed unbiased and comprehensive screening of genome-wide gene expression. Small non-coding RNAs (sncRNAs) have been shown to play an important role in biological processes and could serve as a diagnostic, prognostic and therapeutic biomarker for specific diseases. Recent findings have begun to reveal and enhance our understanding of the complex architecture of sncRNA expression including miRNAs, piRNAs, lncRNAs, sn/snoRNAs and their relationships with biological systems. We used publicly available small RNA sequencing data that was derived from 24 triple negative breast cancers (TNBC) and 14 adjacent normal tissue samples to remap various types of sncRNAs. We found a total of 55 miRNAs were aberrantly expressed (p<0.005) in TNBC samples (8 miRNAs upregulated; 47 downregulated) compared to adjacent normal tissues whereas the original study reported only 25 novel miRs. In this study, we used pathway analysis of differentially expressed miRNAs which revealed TGF-beta signaling pathways to be profoundly affected in the TNBC samples. Furthermore, our comprehensive re-mapping strategy allowed us to discover a number of other differentially expressed sncRNAs including piRNAs, lncRNAs, sn/snoRNAs, rRNAs, miscRNAs and nonsense-mediated decay RNAs. We believe that our sncRNA analysis workflow is extremely comprehensive and suitable for discovery of novel sncRNAs changes, which may lead to the development of innovative diagnostic and therapeutic tools for TNBC.

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“…Among them, the role and biological significance of miR-96 have focused mainly on the oncogenesis and cancer progression in various malignancies, such as the liver, stomach, and breast cancer [29–31]. Therefore, miR-96 is recognized as an oncomiR that facilitates the development of malignancies by promoting the growth, proliferation, and survival of cancer cells [32, 33]. On the other hand, the metabolic influence of miR-96 was first reported in pancreatic β-cells [34].…”

Section: Discussionmentioning

confidence: 99%

Induction of miR-96 by Dietary Saturated Fatty Acids Exacerbates Hepatic Insulin Resistance through the Suppression of INSR and IRS-1

2016

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Obesity is defined as the excessive accumulation of body fat that ultimately leads to chronic metabolic diseases. Diets rich in saturated fatty acids (SFA) exacerbate obesity and hepatic steatosis, which increase the risk of hepatic insulin resistance and type 2 diabetes (T2DM). Although microRNAs (miRNAs) play an important role in a range of biological processes, the implications of SFA-induced miRNAs in metabolic dysregulation, particularly in the pathogenesis of hepatic insulin resistance, are not well understood. This study investigated the implications of miR-96, which is induced strongly by SFA, in the development of hepatic insulin resistance. The liver of HFD mice and the palmitate-treated hepatocytes exhibited an impairment of insulin signaling due to the significant decrease in INSR and IRS-1 expression. According to expression profiling and qRT-PCR analysis of the miRNAs, the expression level of miR-96 was higher in hepatocytes treated with palmitate. Moreover, miR-96 was also upregulated in the liver of HFD mice. Interestingly, miR-96 targeted the 3’UTRs of INSR and IRS-1 directly, and repressed the expression of INSR and IRS-1 at the post-transcriptional level. Accordingly, the overexpression of miR-96 was found to cause a significant decrease in INSR and IRS-1 expression, thereby leading to an impairment of insulin signaling and glycogen synthesis in hepatocytes. These results reveal a novel mechanism whereby miR-96 promotes the pathogenesis of hepatic insulin resistance resulted from SFA or obesity.

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MiR‐96‐5p influences cellular growth and is associated with poor survival in colorectal cancer patients

Cited by 74 publications

References 30 publications

Identification of microRNA expression in sentinel lymph nodes from patients with breast cancer via RNA sequencing for diagnostic accuracy

Identification of microRNA expression in sentinel lymph nodes from patients with breast cancer via RNA sequencing for diagnostic accuracy

A Comprehensive NGS Data Analysis of Differentially Regulated miRNAs, piRNAs, lncRNAs and sn/snoRNAs in Triple Negative Breast Cancer

Induction of miR-96 by Dietary Saturated Fatty Acids Exacerbates Hepatic Insulin Resistance through the Suppression of INSR and IRS-1

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