Over-Expression of miR-106b Promotes Cell Migration and Metastasis in Hepatocellular Carcinoma by Activating Epithelial-Mesenchymal Transition Process

Yau, Wing Lung; Lam, Carol S. F.; Ng, Lui; Chow, Albert H.L.; Chan, Sylvia Tsz Ching; Chan, Jacky Yu Ki; Wo, Jana Y.; Ng, Ka Man; Man, Kwan; Poon, Ronnie Tung Ping; Pang, Roberta

doi:10.1371/journal.pone.0057882

Cited by 98 publications

(71 citation statements)

References 28 publications

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“…Upregulation of microRNA-1290 impaired cytokinesis and affected the reprogramming of colon cancer cells (16). Overexpression of miR-106b promoted metastasis of hepatocellular carcinoma and correlated with higher tumor grade (17). In the present study miR-106b and miR-1290 had a significantly higher expression in tumor with compared to without lymphatic metastasis, suggesting that interference of the two miRNAs might depress the lymphatic metastasis of supraglottic LSCC.…”

Section: Discussionsupporting

confidence: 46%

MicroRNA expression and its detection in human supraglottic laryngeal squamous cell carcinoma

et al. 2013

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Abstract. Laryngeal squamous cell carcinoma (LSCC) is one of the most common head and neck malignancies with a poor prognosis. The aim of this study was to detect the expression of microRNAs (miRNAs) in supraglottic LSCC and attached normal mucosa using microarray assay, and explore the role of miRNAs in supraglottic LSCC. Fresh-frozen samples of five supraglottic LSCC and attached normal mucosa were obtained, and their various endogenous miRNAs were screened by microarray. miRNAs of interest were confirmed by quantitative real-time polymerase chain reaction (qRT-PCR) in 48 supraglottic LSCC tumors and 10 normal mucosa tissues. In total, 38 miRNAs were differentially expressed in supraglottic LSCC, with 22 miRNAs being upregulated and 16 downregulated. Of the six miRNAs selected for qRT-PCR, miR-375, miR-139-3P, miR-1290 and miR-106b were differentially expressed in supraglottic LSCC with and without lymphatic metastasis.

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Section: Discussionsupporting

confidence: 46%

MicroRNA expression and its detection in human supraglottic laryngeal squamous cell carcinoma

et al. 2013

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“…Their study provided the evidence that miR-106b might serve as a causative agent in the malignant progression of pediatric BSG, thereby serving as a novel target for constraining the rapid and fatal course of pediatric BSG (Wang et al, 2012). Additionally, the study by Yau et al (2013) demonstrated that miR-106b was overexpressed in HCC tissues as compared with adjacent non-tumor tissue (P = 0.0005), and overexpression of miR-106b was significantly correlated with a higher tumor grade (P = 0.018). Further functional studies demonstrated that miR-106b could promote cell migration and stress fiber formation by overexpressing the RhoGTPases, RhoA and RhoC.…”

Section: Discussionmentioning

confidence: 97%

“…Further functional studies demonstrated that miR-106b could promote cell migration and stress fiber formation by overexpressing the RhoGTPases, RhoA and RhoC. In vivo functional studies also showed that overexpression of miR-106b promoted HCC metastasis (Yau et al, 2013). Moreover, Slaby et al (2010) found that miRNA-106b was significantly overexpressed in renal cell carcinoma (RCC) tissues (P < 0.0001).…”

Section: Discussionmentioning

confidence: 99%

Expression of microRNA-106b and its clinical significance in cutaneous melanoma

et al. 2015

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ABSTRACT. is overexpressed in various types of cancers and is associated with the regulation of carcinogenic processes. However, its clinical significance in cutaneous melanoma has not been reported. qRT-PCR was performed to examine the expression of miR-106b in 15 cases of dysplastic nevi, 17 cases of melanoma metastases, and 97 cases of primary cutaneous melanoma tissue samples. Survival rate was determined with Kaplan-Meier and statistically analyzed with the log-rank method between groups. Survival data were evaluated through multivariate Cox regression analysis. Significant differences in miR-106b expression were shown between dysplastic nevi and primary cutaneous melanomas (P < 0.01), between primary melanomas and metastatic cutaneous melanomas (P < 0.01), and between primary cutaneous melanomas and metastatic cutaneous melanomas (P < 0.001). We found that high miR106b expression was correlated with Breslow thickness (P = 0.002), tumor ulceration (P = 0.002), and advanced clinical stage (P < 0.001). The patients with high miR-106b expression showed shorter 5-year overall survival than those with low miR-106b expression (P = 0.02; log-rank test). Multivariate regression analysis showed that the status of miR-106b expression was an independent prognostic factor for overall survival (HR = 2.09, 95%CI: 1.11-10.26, P = 0.02). This study showed that miR-106b may contribute 16379-16385 (2015) to the progression of cutaneous melanoma and its up-regulation may be independently associated with poor prognosis of cutaneous melanoma. This suggests that miR-106b might serve as a promising biological marker for further risk stratification in the management of cutaneous melanoma.

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“…27 Recently, miR-106b was also known to regulate EMT by the TGF-b/Smad signaling pathway implicated in cancer stem-like cell development. 25,28,29 The newly found target gene of miR-106b is Smad7, which acts as an inhibitor of TGF-b/Smad signaling. Smad7 binds to TGF-b receptor I and interrupts recruitment of TGF-b receptors I and II.…”

Section: Expression Of Cancer Stem Cell Markers and Spherementioning

confidence: 99%

miR-106b modulates cancer stem cell characteristics through TGF-β/Smad signaling in CD44-positive gastric cancer cells

Shin

Lee

et al. 2014

Laboratory Investigation

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Cancer stem cells have the capacity to form new tumors and are thus considered to be a cause of metastasis and tumor recurrence. However, many of the mechanisms determining cancer stem cell characteristics are still unknown. MicroRNAs (miRNAs) are possible modulators of cancer stem cell generation and may be involved in the retention of cancer stem cell characteristics. The aim of this study was to examine the miRNA expression profiles regulating the cancer stem-like cell characteristics in gastric cancer. We sorted gastric cancer stem-like cells using the stem cell marker CD44 by fluorescenceactivated cell sorting. CD44( þ ) cells formed more and larger spheres compared with CD44( À ) cells. Cancer stem cell markers were overexpressed in CD44( þ ) cells. CD44( þ ) cells showed increased expression of mesenchymal cell markers, whereas epithelial markers were downregulated. In miRNA microarray, the miR-106b family comprising miR-106b, miR-93, and miR-25 was significantly upregulated in CD44( þ ) cells than in CD44( À ) cells. Smad7, which inhibits transforming growth factor-b (TGF-b)/Smad signaling as a target of the miR-106b family, was downregulated in CD44( þ ) cells. Furthermore, expression of TGF-b/Smad signal molecules was activated in CD44( þ ) cells, in accordance with the action of the miR-106b family. Inhibition of miR-106b showed suppression of the TGF-b/Smad signaling pathway and decreased self-renewal capacity and cell invasiveness. Our study suggests that CD44( þ ) gastric cancer cells show cancer stem cell properties with epithelial-mesenchymal transition (EMT). Increased miR-106b family expression regulated cancer stemlike cell properties, particularly EMT characteristics, through the TGF-b/Smad signaling pathway in CD44( þ ) stem-like cells. Taken together, these results indicate that targeting miR-106b may be an effective form of cancer therapy in gastric cancer through the modulation of cancer stem cell characteristics.

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Over-Expression of miR-106b Promotes Cell Migration and Metastasis in Hepatocellular Carcinoma by Activating Epithelial-Mesenchymal Transition Process

Cited by 98 publications

References 28 publications

MicroRNA expression and its detection in human supraglottic laryngeal squamous cell carcinoma

MicroRNA expression and its detection in human supraglottic laryngeal squamous cell carcinoma

Expression of microRNA-106b and its clinical significance in cutaneous melanoma

miR-106b modulates cancer stem cell characteristics through TGF-β/Smad signaling in CD44-positive gastric cancer cells

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