miR-324-3p suppresses migration and invasion by targeting WNT2B in nasopharyngeal carcinoma

Liu, Chao; Guo, Li; N, Yang; Su, Zhi; Zhang, Shuiting; Deng, Tengbo; Ren, Shuling; Lu, Shanhong; Tian, Yongquan; Liu, Yong; Qiu, Yuanzheng

doi:10.1186/s12935-016-0372-8

Cited by 58 publications

(45 citation statements)

References 30 publications

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“…Therefore, we confirmed the migration capacity of T98G-R and U87-R cells, and similarly found significant reduction of the scratch marks compared to that of T98G and U87 cells ( Figures 1F,G ). Meanwhile, the protein expression of E-cadherin, a migration inhibitor, and Vimentin, a pro-migration factor ( Liu et al, 2017 ), was also examined by western blot to estimate the degree of epithelial-to-mesenchymal transition (EMT). As expected, we found that T98G-R and U87-R displayed a lower level of E-cadherin and much higher level of Vimentin compared to their parental T98G and U87 cells ( Figure 1H ).…”

Section: Resultsmentioning

confidence: 99%

SCD1 Confers Temozolomide Resistance to Human Glioma Cells via the Akt/GSK3β/β-Catenin Signaling Axis

Dai

Yan

et al. 2018

Front. Pharmacol.

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Resistance to temozolomide (TMZ), the standard chemotherapy agent for glioblastoma (GBM), poses a major clinical challenge to GBM prognosis. Understanding the mechanisms of TMZ resistance can help to identify novel drug targets and more effective therapies. Recent studies suggest that bioenergetic alterations of cancer cells play important roles in drug resistance. In our study, the altered metabolism of cancer cells was observed using a metabolic PCR array. We found that stearoyl-coenzyme A desaturase 1 (SCD1), a key rate-limiting enzyme for synthesis of monounsaturated fatty acids, was significantly upregulated in TMZ-resistant GBM cells compared to their parental counterparts. Overexpression of SCD1 promoted resistance to TMZ in parental GBM cells, whereas SCD1 downregulation by siRNA could re-sensitize TMZ-resistant cells in vitro. Combinational treatment of TMZ and an SCD1-specific inhibitor showed a combined inhibitory effect on TMZ-resistant glioma cells. We also observed that overexpression of SCD1 promoted Akt/GSK3β/β-catenin signaling, while silencing of SCD1 inhibited the signaling. The combination of an Akt activator with exogenous SCD1 or the combined inhibition of Akt and enforced expression of SCD1 resulted in the most significant changes of Akt signaling. Functionally, significantly lower viability and mobility rates were observed in TMZ-resistant cells when treated with Akt inhibitors and an SCD1 inhibitor simultaneously compared to when treated individually. In conclusion, our study identified SCD1 along with its functional pathway as a novel target in the development of TMZ resistance. SCD1 inhibition used alone or in combination with Akt inhibition could effectively overcome TMZ resistance in gliomas.

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Section: Resultsmentioning

confidence: 99%

SCD1 Confers Temozolomide Resistance to Human Glioma Cells via the Akt/GSK3β/β-Catenin Signaling Axis

Dai

Yan

et al. 2018

Front. Pharmacol.

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“…Wnt/β-catenin signaling pathway is a key driver for cancer behaviors in numerous malignancies 30 , which is also intensively studied in our previous researches about radioresistance and metastasis of SCCHN 26 , 31 , 32 . Recent publication indicates that PVT1 promotes chemoresistance in bladder urothelial carcinoma via Wnt/β-catenin signaling pathway 33 .…”

Section: Resultsmentioning

confidence: 99%

LncRNA PVT1 promotes malignant progression in squamous cell carcinoma of the head and neck

Yu¹,

Wang

Guo

et al. 2018

J. Cancer

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Long non-coding RNAs (lncRNAs) are potentially critical regulators of cancer malignant behaviours. Aberrant expression and dysfunction of lncRNA PVT1 have been reported in multiple human cancers. However, its role in squamous cell carcinoma of the head and neck (SCCHN) remains largely unknown. Our current study demonstrated that PVT1 expression was increased in SCCHN. High PVT1 expression was positively correlated with SCCHN clinical parameters including T classification, clinical stages and cervical lymph node metastasis. More importantly, high PVT1 expression predicted a poor prognosis in SCCHN patients. Gain-of function and loss-of function studies further indicated that PVT1 promoted the proliferation and invasion of SCCHN both in vitro and in vivo, which was accompanied by epithelial-mesenchymal transition and enhanced cancer stem cell-like properties. Further mechanistic investigation revealed that PVT1 activated Wnt/β-catenin signalling pathway, and inhibition of Wnt/β-catenin signalling reversed the malignant progression caused by PVT1 overexpression. Together, our study reveals that PVT1 accelerates the malignant progression of SCCHN and represents a potential biomarker and therapeutic target in SCCHN.

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“…For example, miR-212 could suppress HCC growth via targeting FOXA1 [ 7 ]. And a research revealed that miR-129-2 might serve as a prognostic indicator for HCC patients and exerted a tumor suppressive role by inhibiting high mobility group box 1 (HMGB1) [ 24 ].What’s more, miR-324-3p has been suggested to be involved in tumorigenesis and tumor development by acting as an oncogene or tumor suppressor in several cancers, such as nasopharyngeal carcinoma [ 9 , 25 ], colorectal cancer [ 26 ] and lung squamous cell carcinoma [ 10 ]. Especially, Wen Y et al highlight that miR-324-3p is significantly overexpressed in the HBV-positive HCC patients compared with the HBV-positive cancer-free controls in both the training and validation sets [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

“…And miR-15b-5p regulates HCC growth and metastasis through the AKT/mTORC1 and β-catenin signaling pathways [ 8 ]. Recently, Liu C et al reported that miR-324-3p could modulate cancer cell growth and apoptosis by targeting SMAD family member 7 (SMAD7) in nasopharyngeal carcinoma [ 9 ]. Gao X et al demonstrated that up-regulated miR-324-3p expression was an independent prognostic predictor for early stage lung squamous cell carcinoma [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

MiR-324-3p promotes tumor growth through targeting DACT1 and activation of Wnt/β-catenin pathway in hepatocellular carcinoma

Tuo

Wang

et al. 2017

Oncotarget

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Recently, it has been reported that miR-324-3p participates in regulation of the carcinogenesis and tumor progression in various cancers. However, the expression and function of miR-324-3p in hepatocellular carcinoma (HCC) remain unclear. In the current study, miR-324-3p expression was significantly up-regulated in HCC tissues and cell lines. HCC patients with high miR-324-3p level showed poor prognostic features and shorter overall survival and disease-free survival. And in vitro and in vivo experiments revealed that miR-324-3p promoted cell viability, colony formation, proliferation and cell cycle progression of HCC cells. Further studies demonstrated that miR-324-3p could directly target DACT1 (dishevelled binding antagonist of beta catenin 1) and negatively regulated its expression in HCC cells. And rescue experiments revealed that DACT1 could reverse the effects of miR-324-3p on HCC cells. Furthermore, the accumulation of both cytoplasmic and nuclear β-catenin as well as its downstream targets including c-Myc and cyclin D1 could be positively regulated by miR-324-3p. The regulatory effects of miR-324-3p on β-catenin, c-Myc and cyclin D1 levels could be reversed by DACT1. Overall, we concluded that miR-324-3p could promote tumor growth through targeting DACT1 and activation of Wnt/β-catenin pathway in HCC. MiR-324-3p may be a ponderable and promising therapeutic target for HCC.

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miR-324-3p suppresses migration and invasion by targeting WNT2B in nasopharyngeal carcinoma

Cited by 58 publications

References 30 publications

SCD1 Confers Temozolomide Resistance to Human Glioma Cells via the Akt/GSK3β/β-Catenin Signaling Axis

SCD1 Confers Temozolomide Resistance to Human Glioma Cells via the Akt/GSK3β/β-Catenin Signaling Axis

LncRNA PVT1 promotes malignant progression in squamous cell carcinoma of the head and neck

MiR-324-3p promotes tumor growth through targeting DACT1 and activation of Wnt/β-catenin pathway in hepatocellular carcinoma

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