Identification of miRNAs associated with tumorigenesis of retinoblastoma by miRNA microarray analysis

Zhao, Jianjun; Yang, Juhua; Lin, Jianhong; Yao, Nan; Chen, Jinyuan; Zheng, Jianlong; Xu, Jianhua; Cheng, Jin Q.; Lin, Jian; Ma, Xu

doi:10.1007/s00381-008-0701-x

Cited by 223 publications

(186 citation statements)

References 30 publications

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“…Evidence has shown that miRNAs could be suitable biomarkers for tumor prognosis and potential therapeutic targets based on the increasing understanding of their mechanisms of action (6)(7)(8)(9)(10). Consistent with a previous study (15), we observed significantly higher expression of miR-320 in RB tissues compared with normal tissues, indicating that miR-320 has a role in RB. As is well known, proliferation and metabolism exhaust intratumoral oxygen, and the hypoxic microenvironment, which is partly controlled by HIF-1α, promotes RB development (18).…”

Section: Discussionsupporting

confidence: 91%

“…miR-320 has been demonstrated to be involved in various types of cancer, including colorectal cancer (11), non-small cell lung cancer (12), cervical cancer (13), and oral cancer (14). In a previous miRNA microarray analysis, miR-320 was identified to be associated with the tumorigenesis of RB for the first time, indicating that miR-320 has a role in the regulation of RB development (15). However, the underlying mechanisms of miR-320 remained unclear in RB.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-320 regulates autophagy in retinoblastoma by targeting hypoxia inducible factor-1α

Liang¹,

Chen²,

Zhu³

2017

Experimental and Therapeutic Medicine

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Abstract. Retinoblastoma (RB) is the most common malignancy in children. Due to refractory mechanisms of chemoresistance and the toxicity of chemotherapies, novel therapies for RB treatment are urgently required. MicroRNA-320 (miR-320) is believed to be associated with the tumorigenesis of RB, although the mechanism remains unclear. Considering the hypoxic intratumoral region, the roles of miR-320 and hypoxia inducible factor-1α (HIF-1α) in the regulation of autophagy were investigated in 30 human RB samples and WERI-RB1 cells. The results demonstrated that HIF-1α was the downstream target of miR-320, and decreased miRNA-320 or HIF-1α lead to the inhibition of autophagy in WERI-RB1 cells. Compared with WERI-RB1 cells that were not transfected, silenced HIF-1α caused a 1.41-fold increase (P<0.01) in p62, a 2.71-fold decrease of Beclin1, and inhibited miRNA-320. Silenced HIF-1α also resulted in 7.29-and 7.43-fold increases in phosphorylated-mechanistic target of rapamycin (mTOR) and mTOR, respectively. In conclusion, the present results suggest that miRNA-320 may regulate the development of autophagy by targeting HIF-1α and autophagy-related proteins in RB under hypoxic conditions.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

MicroRNA-320 regulates autophagy in retinoblastoma by targeting hypoxia inducible factor-1α

Liang¹,

Chen²,

Zhu³

2017

Experimental and Therapeutic Medicine

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“…CDC40 plays a role in cell cycle progression through G1/S and G2/M and pre-mRNA splicing (Dahan and Kupiec, 2004). Some of the miRNAs (miR-363, miR-497, miR-28-5p, miR-27b, miR-218, miR-30a, miR-9*,miR-10b, miR-122, miR-144*, miR-365, miR-494, and miR-500) deregulated in CRC in this study have been reported in other cancers but not previously in colorectal cancer Guo et al, 2009;Nass et al, 2009;Pizzimenti et al, 2009;Yamamoto et al, 2009;Zhao et al, 2009;Leidinger et al, 2010).…”

Section: Mirna Profiling In Crc Versus Normal Colon Tissuesupporting

confidence: 49%

MicroRNA profiling differentiates colorectal cancer according to KRAS status

Mosakhani

Sarhadi

Borze

et al. 2011

Genes Chromosomes & Cancer

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Recent studies have shown the important role of microRNAs (miRNAs) in a variety of biological processes, and in its ability to distinguish tumors according to their prognostic and predictive properties. To identify miRNA signatures associated with colorectal carcinoma (CRC) and with KRAS status, we studied, using Agilent's miRNA microarrays, miRNA expression in primary tumors from 55 metastatic CRC patients, including 15 with mutant and 40 with wild-type KRAS. Comparing these with normal colon tissue, we identified 49 miRNAs-including 19 novel miRNAs-significantly deregulated in tumor tissue. The presence of the KRAS mutation was associated with up-regulation of miR-127-3p, miR-92a, and miR-486-3p and down-regulation of miR-378. Increased expression of miR-127-3p and miR-92a in KRAS mutant tumors was significantly confirmed by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) (P < 0.05). We identified some predicted target genes of differentially expressed miRNAs between mutated and wild-type KRAS, such as RSG3 and TOB1, which are involved in apoptosis and proliferation. Target prediction and pathway analysis suggest a possible role for deregulated miRNAs in nicotinamide adenine dinucleotide phosphate (NADPH) regeneration and G protein-coupled receptor signaling pathways.

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“…An expression profiling-based analysis revealed that miR-483-5p is up-regulated in malignant adrenocortical tumors, compared with in benign ones, indicating that the upregulation of miR-483-5p might be associated with a poorer cancer-specific survival (40). miR-494 was first reported as part of a miRNA expression profile for retinoblastoma, belonging to a cluster of highly expressed miRNAs (41). Recently, in a cultured primary bronchial epithelial cell system exposed to benzo[a]pyrene, miR-494 expression was upregulated in parallel with the down-regulated expression of CDK6 (42).…”

Section: Discussionmentioning

confidence: 99%

A subset of microRNAs potentially acts as a convergent hub for upstream transcription factors in cancer cells

Yoshida¹

2010

Oncol Rep

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Abstract. microRNAs (miRNAs) are non-coding short nucleotides that exhibit a unique function as translational suppressors towards a wide realm of mRNAs. To date, a specific set of miRNAs has been characterized as oncogenes and tumor suppressors based on their expression levels and/or target mRNA functions; however, a comprehensive view of the changes in miRNA expression regulated by pivotal cellular signaling mechanisms remains elusive. Here, we aimed to characterize common and unique miRNAs regulated by transcriptional regulators such as oncogenic HRAS, c-Jun and E2F family members (E2F1~E2F6) in the human cancer cell lines A549 and HeLa. For this purpose, we employed a miRNA microarray and identified several miRNAs that were commonly regulated by transcriptional regulators. Next we tested whether these miRNAs could affect any of the signal pathways by employing luciferase reporters bearing response elements for various cellular signaling pathways. Among those tested, luciferase reporter bearing interferon Á activation site responsive element was solely activated by miR-494, indicating that the overexpression of miR-494 has a limited effect on a specific signal pathway in A549 cells. Taken together, these results suggest that a unique subset of miRNAs could have an integrating effect on upstream pivotal transcriptional regulators influencing decisions regarding proper cellular responses.

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Identification of miRNAs associated with tumorigenesis of retinoblastoma by miRNA microarray analysis

Abstract: These miRNAs are the first to be reported for human retinoblastoma and may play significant roles in regulating tumor genesis.

Cited by 223 publications

References 30 publications

MicroRNA-320 regulates autophagy in retinoblastoma by targeting hypoxia inducible factor-1α

MicroRNA-320 regulates autophagy in retinoblastoma by targeting hypoxia inducible factor-1α

MicroRNA profiling differentiates colorectal cancer according to KRAS status

A subset of microRNAs potentially acts as a convergent hub for upstream transcription factors in cancer cells

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