Downregulation of microRNA-211 is involved in expression of preferentially expressed antigen of melanoma in melanoma cells

Sakurai, Eiichi; Maesawa, Chihaya; Shibazaki, Masahiko; Yasuhira, Shinji; Oikawa, Hiroki; Sato, Masayuki; Tsunoda, Kenji; Ishikawa, Yuichi; Watanabe, Ayano; Takahashi, Kazuhiro; Akasaka, Toshihide; Masuda, Tomoyuki

doi:10.3892/ijo.2011.1084

Cited by 24 publications

(19 citation statements)

References 32 publications

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“…Furthermore, enforced expression of miR-211 promoted tumor cell growth at least in part by down-regulating the CHD5 tumor suppressor [ 31 ]. On the other hand, another study showed that miR-211 was a suppressor of melanoma invasion during human melanoma progression [ 34 , 37 , 38 ]. To our knowledge, the role and mechanism of miR-211 in HCC have not been completely understood.…”

Section: Discussionmentioning

confidence: 99%

miR-211 suppresses hepatocellular carcinoma by downregulating SATB2

Jiang

Cui

et al. 2015

Oncotarget

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Dysregulation of microRNAs (miRs) is involved in carcinogenesis. Deregulation of miR-211 has recently been observed in many tumors, but its function in hepatocellular carcinoma (HCC) is still unknown. Here we found that miR-211 was decreased in HCC cancer tissues compared with adjacent normal tissues. We also found that overexpression of miR-211 repressed proliferation and invasion in HepG2 and SMMC7721 cells. Luciferase reporter assays and western blot indicated that special AT-rich sequence-binding protein-2 (SATB2), is a direct target of miR-211. The expression of SATB2 was upregulated in HCC cancer tissues and cell lines and miR-211 levels inversely correlated with SATB2 levels in HCC. Importantly, SATB2 rescued the miR-211-mediated inhibition of cell invasion and proliferation. Finally, reintroduction of miR-211 repressed tumor formation of HCC in xenograft mice. This study provides insights into molecular mechanisms that miR-211 contributed to HCC.

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Section: Discussionmentioning

confidence: 99%

miR-211 suppresses hepatocellular carcinoma by downregulating SATB2

Jiang

Cui

et al. 2015

Oncotarget

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“…3A). miR-211, a melanocyte lineage-specific small non-coding miRNA, acts as a tumor suppressor by regulating the activity of oncogenes such as PRAME and KCNMA1 (Mazar et al, 2010; Sakurai et al, 2011). miR-211 suppresses the invasion potential of melanoma cells (Levy et al, 2010; Mazar et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

miR-335 Targets SIAH2 and Confers Sensitivity to Anti-Cancer Drugs by Increasing the Expression of HDAC3

Kim¹,

Kim²,

Park³

et al. 2015

Molecules and Cells

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We previously reported the role of histone deacetylase 3 (HDAC3) in response to anti-cancer drugs. The decreased expression of HDAC3 in anti-cancer drug-resistant cancer cell line is responsible for the resistance to anti-cancer drugs. In this study, we investigated molecular mechanisms associated with regulation of HDAC3 expression. MG132, an inhibitor of proteasomal degradation, induced the expression of HDAC3 in various anti-cancer drug-resistant cancer cell lines. Ubiquitination of HDAC3 was observed in various anti-cancer drug-resistant cancer cell lines. HDAC3 showed an interaction with SIAH2, an ubiquitin E3 ligase, that has increased expression in various anti-cancer drug-resistant cancer cell lines. miRNA array analysis showed the decreased expression of miR-335 in these cells. Targetscan analysis predicted the binding of miR-335 to the 3′-UTR of SIAH2. miR-335-mediated increased sensitivity to anti-cancer drugs was associated with its effect on HDAC3 and SIAH2 expression. miR-335 exerted apoptotic effects and inhibited ubiquitination of HDAC3 in anti-cancer drug-resistant cancer cell lines. miR-335 negatively regulated the invasion, migration, and growth rate of cancer cells. The mouse xenograft model showed that miR-335 negatively regulated the tumorigenic potential of cancer cells. The down-regulation of SIAH2 conferred sensitivity to anti-cancer drugs. The results of the study indicated that the miR-335/SIAH2/HDAC3 axis regulates the response to anti-cancer drugs.

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“…A number of recent studies have reported modified expression levels of miR-211 in melanoma cells and/or have investigated the functional roles of miR-211 and its target genes [10]–[12], [17], [18]. A clear correlation has been demonstrated between MITF and miR-211, which we also confirm here: MITF transcriptionally activates, amongst many other genes, the calcium channel TRPM1 (melastatin) and by doing so, the intronic miR-211 is simultaneously up-regulated.…”

Section: Discussionmentioning

confidence: 99%

New Target Genes of MITF-Induced microRNA-211 Contribute to Melanoma Cell Invasion

et al. 2013

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The non-coding microRNAs (miRNA) have tissue- and disease-specific expression patterns. They down-regulate target mRNAs, which likely impacts on most fundamental cellular processes. Differential expression patterns of miRNAs are currently being exploited for identification of biomarkers for early disease diagnosis, prediction of progression for melanoma and other cancers and as promising drug targets, since they can easily be inhibited or replaced in a given cellular context. Before successfully manipulating miRNAs in clinical settings, their precise expression levels, endogenous functions and thus their target genes have to be determined. MiR-211, a melanocyte lineage-specific small non-coding miRNA, is located in an intron of TRPM1, a target gene of the microphtalmia-associated transcription factor (MITF). By transcriptionally up-regulating TRPM1, MITF, which is critical for both melanocyte differentiation and survival and for melanoma progression, indirectly drives the expression of miR-211. Expression of this miRNA is often reduced in melanoma samples. Here, we investigated functional roles of miR-211 by identifying and studying new target genes. We show that MITF-correlated miR-211 expression levels are mostly but not always reduced in a panel of 11 melanoma cell lines and in primary and metastatic melanoma compared to normal melanocytes and nevi, respectively. MiR-211 itself only marginally impacted on cell invasion and migration, while perturbation of some new miR-211 target genes, such as AP1S2, SOX11, IGFBP5, and SERINC3 significantly increased invasion. These results and the variable expression levels of miR-211 raise serious doubts on the value of miR-211 as a melanoma tumor-suppressing miRNA and/or as a biomarker for melanoma.

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Downregulation of microRNA-211 is involved in expression of preferentially expressed antigen of melanoma in melanoma cells

Cited by 24 publications

References 32 publications

miR-211 suppresses hepatocellular carcinoma by downregulating SATB2

miR-211 suppresses hepatocellular carcinoma by downregulating SATB2

miR-335 Targets SIAH2 and Confers Sensitivity to Anti-Cancer Drugs by Increasing the Expression of HDAC3

New Target Genes of MITF-Induced microRNA-211 Contribute to Melanoma Cell Invasion

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