miR-203 inhibits tumor cell migration and invasion via caveolin-1 in pancreatic cancer cells

Miao, Lifeng; Xiong, Xian‐Ze; Lin, Yixin; Cheng, Yao; Lu, Jiong; Zhang, Jie; Cheng, Nan-Sheng

doi:10.3892/ol.2014.1807

Cited by 47 publications

(42 citation statements)

References 18 publications

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“…Whether miRNAs act as oncogenes or tumor suppressor genes depends on the context. For example, miR-203 behaves as a tumor suppressor and is downregulated in pancreatic, glioma and esophageal cancer, while it is upregulated in epithelial ovarian cancer and acts as an oncogene (9,(20)(21)(22). The present study demonstrated that miR-203 was downregulated in NSCLC specimens, which is in agreement with a …”

Section: Discussionsupporting

confidence: 81%

MicroRNA-203 inhibits cellular proliferation and invasion by targeting Bmi1 in non-small cell lung cancer

Chen

Ding

et al. 2015

Oncology Letters

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Abstract. MicroRNAs are proposed to serve vital functions in the regulation of tumor progression and invasion. However, the expression levels of miR-203 in non-small cell lung cancer (NSCLC) and its clinical significance remain unknown. In the present study, the association between B-cell-specific moloney murine leukemia virus insertion site 1 (Bmi1) and miR-203 was investigated. miR-203 was demonstrated to act as a tumor suppressor by regulating the expression of Bmi1. miR-203 expression levels were downregulated in NSCLC tissues while Bmi1 expression was upregulated in NSCLC tissues and cell lines. Furthermore, downregulated Bmi1 or enhanced miR-203 expression inhibited NSCLC cell proliferation and invasion in vitro. In addition, a dual-luciferase reporter assay was performed, which identified Bmi1 as a novel target of miR-203. In conclusion, the present study demonstrated that miR-203 functions as a tumor suppressor and is important in inhibiting the proliferation of NSCLC cells through targeting Bmi1. These findings indicate that miR-203 may be useful as a novel potential therapeutic target for NSCLC.

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Section: Discussionsupporting

confidence: 81%

MicroRNA-203 inhibits cellular proliferation and invasion by targeting Bmi1 in non-small cell lung cancer

Chen

Ding

et al. 2015

Oncology Letters

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“…In addition, we demonstrated that overexpressed miR-203 improved gemcitabine sensitivity; a finding consistent with other data which showed that miR-203 inhibits cell proliferation and invasiveness in prostate carcinoma, and induces apoptosis in transitional cell carcinom (38). Moreover, Feber et al revealed that miR-203 suppresses cell proliferation in esophageal carcinoma (22), while Miao et al showed that miR-203 inhibits cell migration, invasion, and the epithelial-mesenchymal transition (EMT) via caveolin-1 in pancreatic carcinoma (39). Considering these data, our results support the hypothesis that miR-203 acts as a tumor suppressor gene by regulating Puma expression in both colon and lung cancer cells.…”

Section: Overexpressed Mir-203 Induces Apoptosis and Decreases Cell Isupporting

confidence: 78%

MicroRNA-203 induces apoptosis by upregulating Puma expression in colon and lung cancer cells

Funamizu

Lacy

Kamada

et al. 2015

International Journal of Oncology

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Abstract. The present study investigated the relationship between and the p53 upregulated modulator of apoptosis (Puma) in colon (HCT116) and lung cancer (A549) cells. Colon and lung cancer cell lines were selected for this study since a relationship between p53/miR-203 and p53/Puma has been established in both cancers. In the present study, adriamycin and nutlin-3 were used to activate p53, which induced both miR-203 and Puma expression in HCT116 cells. In contrast, HCT 116 cells with downregulated p53 showed decreased miR-203 and Puma expression. Importantly, we found that overexpressed miR-203 in HCT116 cells resulted in significantly increased Puma expression (P<0.05). Based on these findings, we hypothesized that another limb of the p53/Puma axis depends on miR-203 expression. To further validate this relationship, we used lung cancer cells (A549) and found that activated p53 increased both miR-203 and Puma expression. In addition, we found that Puma expression remained elevated in cells with overexpressed miR-203 in the presence of p53 downregulation. Cumulatively, our data purport that p53 not only increased Puma expression directly, but that it may also do so through miR-203. Additionally, functional studies revealed that miR-203 overexpression induced apoptosis and inhibited cell invasiveness.

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“…These data suggest that oridonin preferentially be an anti-OvCa reagent. Further, we examine whether oridonin affected cell cycle progression and apoptosis and our results revealed that it induced a Oridonin inhibits migration, invasion of SKOV3 cells Tumor migration and invasion are the essential steps in tumorigenesis (Miao et al, 2014). We determined the effects of oridonin on the chemotactic motility of SKOV3 cells using wound-healing migration and transwell cell invasion assays.…”

Section: Inhibition Of Ovarian Cancer Cell Lines Proliferation By Orimentioning

confidence: 99%

Oridonin Suppresses Proliferation of Human Ovarian Cancer Cells via Blockage of mTOR Signaling

Xiao¹,

Chen²,

Qin³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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Oridonin, an ent-kaurane diterpenoid compound isolated from the traditional Chinese herb Rabdosia rubescens, has shown various pharmacological and physiological effects such as anti-tumor, anti-bacterial, and anti-inflammatory properties. However, the effect of oridonin on human ovarian cancer cell lines has not been determined. In this study, we demonstrated that oridonin inhibited ovarian cancer cell proliferation, migration and invasion in a dose-dependent manner. Furthermore, we showed oridonin inhibited tumor growth of ovarian cancer cells (SKOV3) in vivo. We then assessed mechanisms and found that oridonin specifically abrogated the phosphorylation/activation of mTOR signaling. In summary, our results indicate that oridonin is a potential inhibitor of ovarian cancer by blocking the mTOR signaling pathway. Keywords

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miR-203 inhibits tumor cell migration and invasion via caveolin-1 in pancreatic cancer cells

Cited by 47 publications

References 18 publications

MicroRNA-203 inhibits cellular proliferation and invasion by targeting Bmi1 in non-small cell lung cancer

MicroRNA-203 inhibits cellular proliferation and invasion by targeting Bmi1 in non-small cell lung cancer

MicroRNA-203 induces apoptosis by upregulating Puma expression in colon and lung cancer cells

Oridonin Suppresses Proliferation of Human Ovarian Cancer Cells via Blockage of mTOR Signaling

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