MicroRNA‐10b is overexpressed in malignant glioma and associated with tumor invasive factors, uPAR and RhoC

Sasayama, Takashi; Nishihara, Masamitsu; Kondoh, Takeshi; Hosoda, Kohkichi; Kohmura, Eiji

doi:10.1002/ijc.24522

Cited by 276 publications

(231 citation statements)

References 29 publications

Supporting

Mentioning

214

Contrasting

Unclassified

Order By: Relevance

“…Although there was no significant difference in miR-195 levels between the healthy control and breast cancer, both miR-362-3p and miR-329 showed lower expression levels in tumors compared with the matching control tissues (Figure 4b). In line with other reports showing downregulation of miR-329 in neuroblastoma and glioma, [20][21][22] we found that both miR-362-3p and miR-329 were significantly downregulated in human breast cancer tissues. To confirm the observed change of miRs expression in individual patients, we processed small-RNA expression data of estrogen receptor-positive (ER-positive) patient samples from the cancer genome atlas (TCGA).…”

supporting

confidence: 93%

Downregulation of microRNA-362-3p and microRNA-329 promotes tumor progression in human breast cancer

Kang

et al. 2015

Cell Death Differ

View full text Add to dashboard Cite

p130Cas regulates cancer progression by driving tyrosine receptor kinase signaling. Tight regulation of p130Cas expression is necessary for survival, apoptosis, and maintenance of cell motility in various cell types. Several studies revealed that transcriptional and post-translational control of p130Cas are important for maintenance of its expression and activity. To explore novel regulatory mechanisms of p130Cas expression, we studied the effect of microRNAs (miRs) on p130Cas expression in human breast cancer MCF7 cells. Here, we provide experimental evidence that miR-362-3p and miR-329 perform a tumor-suppressive function and their expression is downregulated in human breast cancer. miR-362-3p and miR-329 inhibited cellular proliferation, migration, and invasion, thereby suppressing tumor growth, by downregulating p130Cas. Ectopic expression of p130Cas attenuated the inhibitory effects of the two miRs on tumor progression. Relative expression levels of miR-362-3p/329 and p130Cas between normal and breast cancer correlated inversely; miR-362-3p/329 expression was decreased, whereas that of p130Cas increased in breast cancers. Furthermore, we showed that downregulation of miR-362-3p and miR-329 was caused by differential DNA methylation of miR genes. Enhanced DNA methylation (according to methylation-specific PCR) was responsible for downregulation of miR-362-3p and miR-329 in breast cancer. Taken together, these findings point to a novel role for miR-362-3p and miR-329 as tumor suppressors; the miR-362-3p/miR-329-p130Cas axis seemingly has a crucial role in breast cancer progression. Thus, modulation of miR-362-3p/miR-329 may be a novel therapeutic strategy against breast cancer. Cell Death and Differentiation (2016) 23, 484-495; doi:10.1038/cdd.2015; published online 4 September 2015 p130Cas/breast cancer anti-estrogen resistance 1 is a member of the Cas (Crk-associated substrate) family of adaptor proteins and has a central role in tyrosine kinasebased signaling related to cell adhesion, migration, cell cycle control, apoptosis, development, and cancer progression.

show abstract

supporting

confidence: 93%

Downregulation of microRNA-362-3p and microRNA-329 promotes tumor progression in human breast cancer

Kang

et al. 2015

Cell Death Differ

View full text Add to dashboard Cite

show abstract

“…Overexpression of miR-10b in otherwise nonmetastatic breast tumors initiated robust invasion and metastasis [8]. miR-10b is a unique miRNA expressed specifically in glioma tumors but not in normal brain cells: neither neural progenitor cells nor mature glia or neurons [9,10]. It has been reported that miR-10b was upregulated in all glioma samples compared with nonneoplastic brain tissues; the expression level of miR-10b was associated with higher-grade glioma and the tumor invasive factors uPAR and RhoC [9].…”

Section: Introductionmentioning

confidence: 99%

DNA methylation downregulated mir-10b acts as a tumor suppressor in gastric cancer

et al. 2014

View full text Add to dashboard Cite

Background MicroRNAs act as tumor suppressors or oncogenes. The pathological roles of miRNAs in gastric tumorigenesis are largely unknown. Although miR-10b was identified as an miRNA deregulator expressed in gastric cancer (GC), there also exists some debate on whether miR-10b is acting as tumor suppressor or oncogene in GC. Methods Quantitative RT-PCR was employed to investigate the level of miR-10b in GC tissues and matched adjacent normal tissues (n = 100). In vitro cell proliferation, apoptosis assays, cell migration, and invasion assays were performed to elucidate the biological effects of miR10b. Because silencing of miRNA by promoter CpG island methylation may be an important mechanism in tumorigenesis, GC cells were treated with 5-aza-2 0 -deoxycytidine and trichostatin A, and expression changes of miR-10b were subsequently examined by quantitative RT-PCR. Furthermore, the methylation status of the CpG island upstream of miR-10b was analyzed by methylation-specific PCR in GC tissues (n = 29). Results We showed here that miR-10b was significantly downregulated in GC cell lines and tissues as demonstrated by quantitative real-time PCR. Overexpression of miR-10b in MGC-803 and HGC-27 dramatically suppressed cell proliferation, migration, invasion, and induced apoptosis. Moreover, we demonstrated that T-cell lymphoma invasion and metastasis (Tiam1) was a target of miR-10b. Furthermore, 5-aza-2 0 -deoxycytidine and trichostain A increased miR-10b expression, and the methylation level was high in the CpG islands upstream of miR-10b gene. Conclusions Taken together, these findings suggest that miR-10b may function as a novel tumor suppressor and is partially silenced by DNA hypermethylation in GC.

show abstract

“…Several other studies subsequently found increased expression of miR-10b to be associated with aggressive behavior in various cancers. [34][35][36][37][38] In melanoma, miR-10b was identified in miRNA discovery studies 9,39 but no studies have focused on miR-10b as the primary melanoma candidate biomarker. Segura et al 9 conducted a discovery analysis in melanoma and miR-10b was associated with increased post-recurrence survival, which contradicts our findings.…”

Section: Discussionmentioning

confidence: 99%

microRNA-10b is a prognostic biomarker for melanoma

et al. 2016

View full text Add to dashboard Cite

Malignant melanoma is an aggressive form of skin cancer. Recently, drug therapy of advanced disease has been revolutionized by new agents. More therapeutic options, coupled with the desire to extend treatment to the adjuvant setting mean that prognostic biomarkers that can be assayed from formalin-fixed paraffin-embedded clinical would be valuable. microRNAs have potential to fill this need. We analyzed 377 microRNAs in 79 primary melanomas and 32 metastases using a split sample discovery strategy. From a discovery analysis using 40 thick primary melanomas (20 cases with metastasis and 20 controls without metastasis at 5 years), microRNA expression was measured by quantitative RT-PCR (QRT-PCR). MiR-10b emerged as a candidate prognostic microRNA. This was confirmed in an independent validation set of thick primary melanomas (20 cases with metastasis and 19 controls without metastasis at 5 years). In the combined discovery and validation cohorts (n = 79), miR-10b expression showed a 3.7-fold increase in expression between cases and controls (P = 0.005) and showed a trend of increasing expression between primary melanomas and their matched metastases (Po 0.001). In situ hybridization showed expression was in melanoma cells and correlated with expression measured by QRT-PCR (P = 0.0005). We used the combined discovery and validation samples to verify the prognostic value of additional candidate microRNAs identified from other studies, and proceeded to analyze miR-200b. We demonstrated that miR-10b and miR-200b showed independent prognostic value (P = 0.002 and 0.047, respectively) in multivariable analysis alongside known clinico-pathological prognostic features (eg, Breslow thickness) using a Cox proportional hazards regression model. Furthermore, the addition of these microRNAs to the clinico-pathological features led to an improved regression model with better identification of aggressive thick melanomas. Taken together, these data suggest that miR-10b is a new prognostic microRNA for melanoma and that there could be a place for microRNA analysis in stratifying melanoma for therapy.

show abstract

MicroRNA‐10b is overexpressed in malignant glioma and associated with tumor invasive factors, uPAR and RhoC

Cited by 276 publications

References 29 publications

Downregulation of microRNA-362-3p and microRNA-329 promotes tumor progression in human breast cancer

Downregulation of microRNA-362-3p and microRNA-329 promotes tumor progression in human breast cancer

DNA methylation downregulated mir-10b acts as a tumor suppressor in gastric cancer

microRNA-10b is a prognostic biomarker for melanoma

Contact Info

Product

Resources

About