MicroRNA-133b inhibits hepatocellular carcinoma cell progression by targeting Sirt1

Tian, Zhijie; Jiang, Huijie; Liu, Ying; Huang, Yong; Xiong, Xin; Wu, Hongwei; Dai, Xiaozhen

doi:10.1016/j.yexcr.2016.03.027

Cited by 33 publications

(31 citation statements)

References 56 publications

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“…SIRT1 activates transcription silencing, DNA repair, recombination of ribosomal DNA, nuclear receptors to stimulate mitochondrial biogenesis, circadian clock, and lipid homeostasis [ 25 ]. In HCC, SIRT1 is aberrantly overexpressed and activates TERT gene promoter [ 10 ], YAP/TEAD4 association [ 11 ], c-Myc stabilization [ 12 ], NF-kB [ 26 ], wnt/β-catenin [ 13 ], and PI3K/AKT [ 27 ] signaling to stimulate cell proliferation and metastasis [ 7 , 28 , 29 ]. Moreover, SIRT1 induces expression of the transcription factor SOX2 to stimulate the self-renewal of liver cancer stem cells [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

“…In HCC, SIRT1 can activate telomerase reverse transcriptase (TERT) gene promoter [ 10 ], promote YAP/TEAD4 association [ 11 ], and stabilize c-Myc protein [ 12 ]. Moreover, microRNA-133b can inhibit HCC progression by directly targeting SIRT1 [ 13 ]. SIRT1 inhibition enhances the antitumor effect of doxorubicin [ 7 ], cisplatin [ 14 ], and irradiation [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

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Prognostic and clinicopathologic significance of SIRT1 expression in hepatocellular carcinoma

et al. 2016

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The clinical value of SIRT1 in hepatocellular carcinoma (HCC) remains controversial. This meta-analysis was performed to investigate the prognostic and clinicopathological significance of the histone deacetylase SIRT1 in HCC. Pooled hazard ratios (HRs) for survival outcomes and pooled odds ratios (ORs) for clinical parameters associated with SIRT1 were calculated in nine studies using Review Manager. Meta-analysis showed that increased SIRT1 expression is associated with poor overall survival (OS) (HR=1.82, 95% confidence interval (CI): 1.49-2.22, P<0.00001) and disease-free survival (DFS) (HR=1.44, 95%CI: 1.06-1.96, P=0.02) in HCC. Increased expression of SIRT1 is more common in female than male HCC patients (OR=0.47, 95%CI: 0.32-0.70, P=0.0001). The increased SIRT1 expression correlates with hepatitis B virus (HBV) infection (OR=1.63, 95%CI: 1.04-2.57, P=0.03), large tumor size (OR=1.81, 95%CI: 1.05-3.13, P=0.03), high p53 expression (OR=2.71, 95%CI: 1.39-5.29, P=0.003), high levels of alpha-fetoprotein (AFP; cutoff value: 400 ng/ml, OR=1.84, 95%CI: 1.26-2.69, P=0.002), and tumor stage (OR=1.72, 95%CI: 1.27-2.32, P=0.0004). Re-sampling statistics for 5,000,000 samples revealed that increased SIRT1 expression is associated with higher TNM stage (OR=1.70, 95%CI: 1.69-1.70, P<0.00001). These results indicate that SIRT1 is a new biomarker off HCC as well as a potentially effective therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Prognostic and clinicopathologic significance of SIRT1 expression in hepatocellular carcinoma

et al. 2016

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“…Likewise, recent study has demonstrated the tumor-suppressor activity of miRNA-214 by inhibiting CDK6, CDK3, and E2F2 [149]. In addition to inhibition of cell proliferation of HCC by miRNA-449a, lentivirus mediated overexpression of miRNA-199a, miRNA-133b, and miRNA-185 has also been reported [53, 59, 150, 151]. Oncogenic miRNA-221 and miRNA-1180 target cell cycle inhibitors (CDKN1C/p57, CDKN1B/p27) and repress TNIP2 expression, respectively, resulting in increased proliferation of HCC cells [39, 152].…”

Section: Noncoding Rnasmentioning

confidence: 99%

New Insights into the Epigenetics of Hepatocellular Carcinoma

Wahid

Ali

Rafique

et al. 2017

BioMed Research International

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Hepatocellular Carcinoma (HCC) is one of the most predominant malignancies with high fatality rate. This deadly cancer is rising at an alarming rate because it is quite resistant to radio- and chemotherapy. Different epigenetic mechanisms such as histone modifications, DNA methylation, chromatin remodeling, and expression of noncoding RNAs drive the cell proliferation, invasion, metastasis, initiation, progression, and development of HCC. These epigenetic alterations because of potential reversibility open way towards the development of biomarkers and therapeutics. The contribution of these epigenetic changes to HCC development has not been thoroughly explored yet. Further research on HCC epigenetics is necessary to better understand novel molecular-targeted HCC treatment and prevention. This review highlights latest research progress and current updates regarding epigenetics of HCC, biomarker discovery, and future preventive and therapeutic strategies to combat the increasing risk of HCC.

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“…Some signaling pathway can be affected by miR-133b, such as c-Met engagement activates multiple oncogenic pathways (RAS, PI3K, STAT3, beta-catenin), which itself is the Immediate target gene of miR-133b in colorectal cancer (CC) and osteosarcoma, its suppression can affected tumor cell proliferation and apoptosis in vitro and in vivo [ 28 , 37 , 38 ]. In glioma and hepatocellular carcinoma, miR-133b inhibit its target gene silent information regulator 1 (Sirt1) and then suppress cell proliferation and invasion together with increasing apoptosis, the specific influence mechanism may be the miR-133b/Sirt1/GPC3/Wnt β-catenin pathway, by which a series of genes such as Bcl-2, Bcl-xL, Mcl-1 and E-cadherin were regulated [ 39 , 40 ]. Anti-apoptotic oncogene Bcl-2, Mcl-1 and cellular inhibitor of apoptosis-2 (c-IAP2) also can be modulated through miR-133b /S1PR1 /STAT3 signaling in nasopharyngeal carcinoma, sphingosine-1-phosphate receptor 1 (S1PR1) was predicted to be a target of miR-133b [ 41 ].…”

Section: Introductionmentioning

confidence: 99%

“…miRNA microarray data and most individual experiments have demonstrated that miR-133b was frequently down-regulated in various cancers and have tumor-suppressive functions [ 93 ], such as firstly been detected in colorectal cancer [ 64 , 94 , 95 ], and subsequently in SCC of tongue [ 47 , 96 ], bladder cancer [ 97 , 98 ], urothelial carcinoma of the bladder [ 78 , 99 , 100 ], lung cancer [ 51 , 77 , 101 ], glioblastoma [ 34 , 60 ], ovarian cancer [ 48 ], prostate cancer [ 23 , 49 ], gastric cancer [ 31 , 80 , 99 , 102 , 103 ], head and neck cancer [ 104 ], GIST [ 62 ], osteosarcoma [ 38 , 105 ], rhabdomyosarcomas [ 106 ], ESCC [ 61 , 102 , 103 , 107 ], uterine sarcomas and mixed epithelial-mesenchymal uterine tumors [ 108 ], renal cell carcinoma [ 109 ], hepatocellular carcinoma [ 39 ], laryngeal cancer [ 110 ]. Some cancers however show that elevation of miR-133b levels promotes cancer progression.…”

Section: Introductionmentioning

confidence: 99%

miR-133b, a particular member of myomiRs, coming into playing its unique pathological role in human cancer

Xia

Chen

et al. 2017

Oncotarget

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MicroRNAs, a family of single-stranded and non-coding RNAs, play a crucial role in regulating gene expression at posttranscriptional level, by which it can mediate various types of physiological and pathological process in normal developmental progress and human disease, including cancer. The microRNA-133b originally defined as canonical muscle-specific microRNAs considering their function to the development and health of mammalian skeletal and cardiac muscles, but new findings coming from our group and others revealed that miR-133b have frequently abnormal expression in various kinds of human cancer and its complex complicated regulatory networks affects the tumorigenicity and development of malignant tumors. Very few existing reviews on miR-133b, until now, are principally about its role in homologous cluster (miR-1, −133 and -206s), however, most of constantly emerging new researches now are focused mainly on one of them, so In this article, to highlight the unique pathological role of miR-133b playing in tumor, we conduct a review to summarize the current understanding about one of the muscle-specific microRNAs, namely miR-133b, acting in human cancer. The review focused on the following four aspects: the overview of miR-133b, the target genes of miR-133b involved in human cancer, the expression of miR-133b and regulatory mechanisms leading to abnormal expression of miR-133b.

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MicroRNA-133b inhibits hepatocellular carcinoma cell progression by targeting Sirt1

Cited by 33 publications

References 56 publications

Prognostic and clinicopathologic significance of SIRT1 expression in hepatocellular carcinoma

Prognostic and clinicopathologic significance of SIRT1 expression in hepatocellular carcinoma

New Insights into the Epigenetics of Hepatocellular Carcinoma

miR-133b, a particular member of myomiRs, coming into playing its unique pathological role in human cancer

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