Down-regulated miR-28-5p in human hepatocellular carcinoma correlated with tumor proliferation and migration by targeting insulin-like growth factor-1 (IGF-1)

Shi, Xiaohong; Teng, Fei

doi:10.1007/s11010-015-2506-z

Cited by 52 publications

(44 citation statements)

References 33 publications

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“…Through gene expression profiles and bioinformatics analysis, we identified IL‐34 as a direct target for miR‐28‐5p, and we further confirmed that the impact of miR‐28‐5p deficiency on regulation of HCC progression in vivo was dependent on this target. A recent report revealed that overexpression of miR‐28‐5p and an miR‐28‐5p mimic suppressed proliferation of HCC cells by targeting insulin‐like growth factor 1 . This observation, which contradicts our study results, may stem from the difference between cell lines and the vectors that were used to overexpress miR‐28‐5p.…”

Section: Discussioncontrasting

confidence: 99%

miR‐28‐5p‐IL‐34‐macrophage feedback loop modulates hepatocellular carcinoma metastasis

et al. 2016

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MicroRNAs (miRNAs) play a critical role in regulation of tumor metastasis. However, the role of these molecules in hepatocellular carcinoma (HCC) has not been fully elucidated. In this study, we employed miRNA-sequencing and identified 22 miRNAs involved in HCC metastasis. One of these, miR-28-5p, was down-regulated in HCCs. This downregulation correlated with tumor metastasis, recurrence, and poor survival. Biofunctional investigations revealed that miR-28-5p deficiency promoted tumor growth and metastasis in nude mice without altering the in vitro biological characteristics of HCC cells. Through gene expression profiles and bioinformatics analysis, we identified interleukin-34 (IL-34) as a direct target of miR-28-5p, and the effects of miR-28-5p deficiency on HCC growth and metastasis was dependent on IL-34-mediated tumor-associated macrophage (TAM) infiltration. Moreover, we found that TAMs induced by miR-28-5p-IL-34 signaling inhibit miR-28-5p expression on HCC cells by transforming growth factor beta 1, resulting in an miR-28-5p-IL-34-macrophage-positive feedback loop. In clinical HCC samples, miR-28-5p levels were inversely correlated with IL-34 expression and the number of TAMs. Patients with low miR-28-5p expression, high IL-34 levels, and high numbers of TAMs had a poor prognosis with shorter overall survival and time to recurrence. Conclusion: A miR-28-5p-IL-34-macrophage feedback loop modulates HCC metastasis and serves as a novel prognostic factor as well as a therapeutic target for HCC. (HEPATOLOGY 2016;63:1560-1575 M etastasis accounts for approximately 90% of cancer-related mortality. (1) The process of metastasis is complex and involves the escape of tumor cells from a primary carcinoma, local invasion of the surrounding tissue, entrance into the systemic circulation, survival during transit through the vasculature, extravasation into the parenchyma of distant tissues, establishment of micrometastases, and ultimately outgrowth of metastatic tumors. (1,2) Multiple studies have explored the intrinsic mechanisms of cancer cells and the extrinsic microenvironmental factors that influence such tumor metastasis (3)(4)(5) ; however, our understanding of these mechanisms remains incomplete.MicroRNAs (miRNAs) comprise a class of small, noncoding RNAs that regulate comprehensive biological processes by changing the expression and translation of their target messenger RNA (mRNA) genes. (6) Deregulation of miRNAs has been confirmed in a number of human diseases, and a crucial role for miRNAs in the development and progression of human

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Section: Discussioncontrasting

confidence: 99%

miR‐28‐5p‐IL‐34‐macrophage feedback loop modulates hepatocellular carcinoma metastasis

et al. 2016

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“…The results displayed by our present work support the conclusion that miR-28 may mediate oxidative stress-induced cellular injury. Previous investigations on cancers demonstrated that miR-28 serves to inhibit cancer development or progression (Almeida et al 2012;Shi and Teng 2015;Zhou et al 2016), and the pro-apoptotic effect of miR-28 on cardiomyocytes in the present study stands in accordance with these studies, further reinforcing the current understanding of the function of miR-28.…”

Section: Discussionsupporting

confidence: 91%

“…In addition, several microRNAs, such as miR-21, miR-874, and miR-484, which control the tumorigenicity are also found to exert critical effects in the cell death of cardiomyocytes (Wang et al , 2013Wei et al 2014). Recent studies have shown that miR-28 is involved in multiple cancers, and it has tumor-suppressive functions in B cell lymphomas and hepatocellular carcinoma (Schneider et al 2014;Shi and Teng 2015). The role of miR-28 in the heart has not been examined.…”

Section: Introductionmentioning

confidence: 99%

MiR-28 inhibits cardiomyocyte survival through suppressing PDK1/Akt/mTOR signaling

Zhu

Zhang

Zou

et al. 2016

In Vitro Cell.Dev.Biol.-Animal

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MicroRNAs play critical roles in regulating cell survival under multiple pathological conditions of heart diseases. Oxidative stress-induced apoptosis contributes greatly to heart ischemia-reperfusion injury. Herein, we describe a novel regulatory role of miR-28 on the survival of cardiomyocytes. We show that miR-28 was upregulated in cardiomyocytes treated with hydrogen peroxide (HO). MiR-28 gain of function sensitized cell apoptosis, whereas miR-28 loss of function partially rescued cell apoptosis induced by HO. Importantly, we observed a significant reduction in Akt/mammalian target of rapamycin (mTOR) signaling activity after miR-28 treatment. Luciferase activity assay and western blot analysis both revealed that, phosphoinositide-dependent kinase-1 (PDK1), which is critical for Akt activation, was directly and negatively modulated by miR-28. Our results therefore indicate that miR-28 regulates oxidative stress-induced cell apoptosis in heart muscle cells, which possibly involves a PDK1/Akt/mTOR-dependent mechanism. MIR-28 could serve as a critical therapeutic target to diminish oxidative stress-induced cell death in the heart.

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“…In CRC, metastasis is the most fatal event during disease progression; it accounts for approximately 90% of patient deaths. 52 In this study, miR-28-5p expression was down-regulated in CRC samples compared with that in normal colon samples, and the down-regulation of miR-28-5p forecasted a poor prognosis for CRC patients, suggesting that this miRNA plays a tumour-suppressive role. 43 Metastasis formation is a major obstacle in CRC therapy.…”

Section: Discussionmentioning

confidence: 55%

SSRP1 promotes colorectal cancer progression and is negatively regulated by miR‐28‐5p

Guo

et al. 2019

J Cellular Molecular Medi

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In this study, microarray data analysis, real‐time quantitative PCR and immunohistochemistry were used to detect the expression levels of SSRP1 in colorectal cancer (CRC) tissue and in corresponding normal tissue. The association between structure‐specific recognition protein 1 (SSRP1) expression and patient prognosis was examined by Kaplan‐Meier analysis. SSRP1 was knocked down and overexpressed in CRC cell lines, and its effects on proliferation, cell cycling, migration, invasion, cellular energy metabolism, apoptosis, chemotherapeutic drug sensitivity and cell phenotype‐related molecules were assessed. The growth of xenograft tumours in nude mice was also assessed. MiRNAs that potentially targeted SSRP1 were determined by bioinformatic analysis, Western blotting and luciferase reporter assays. We showed that SSRP1 mRNA levels were significantly increased in CRC tissue. We also confirmed that this upregulation was related to the terminal tumour stage in CRC patients, and high expression levels of SSRP1 predicted shorter disease‐free survival and faster relapse. We also found that SSRP1 modulated proliferation, metastasis, cellular energy metabolism and the epithelial‐mesenchymal transition in CRC. Furthermore, SSRP1 induced apoptosis and SSRP1 knockdown augmented the sensitivity of CRC cells to 5‐fluorouracil and cisplatin. Moreover, we explored the molecular mechanisms accounting for the dysregulation of SSRP1 in CRC and identified microRNA‐28‐5p (miR‐28‐5p) as a direct upstream regulator of SSRP1. We concluded that SSRP1 promotes CRC progression and is negatively regulated by miR‐28‐5p.

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Down-regulated miR-28-5p in human hepatocellular carcinoma correlated with tumor proliferation and migration by targeting insulin-like growth factor-1 (IGF-1)

Cited by 52 publications

References 33 publications

miR‐28‐5p‐IL‐34‐macrophage feedback loop modulates hepatocellular carcinoma metastasis

miR‐28‐5p‐IL‐34‐macrophage feedback loop modulates hepatocellular carcinoma metastasis

MiR-28 inhibits cardiomyocyte survival through suppressing PDK1/Akt/mTOR signaling

SSRP1 promotes colorectal cancer progression and is negatively regulated by miR‐28‐5p

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