miR-339-5p inhibits cell migration and invasion in vitro and may be associated with the tumor-node-metastasis staging and lymph node metastasis of non-small cell lung cancer

Li, Yun; Zhao, Weiguo; Bao, Pengtao; Li, Chunsun; Qing, Xiu; Li, Yanqing; Chen, Liangan

doi:10.3892/ol.2014.2165

Cited by 33 publications

(44 citation statements)

References 28 publications

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“…Furthermore, its upregulation could inhibit NSCLC cell migration and invasion in vitro. Bioinformatics analyses also demonstrated that the B-cell CLL/lymphoma 6 (BCL6) and valosin-containing protein genes may be potential targets of miR-339-5p (11). The present study aimed to confirm that BCL6 is the target gene of miR-339-5p, and that miR-339-5p represses the epithelial-to-mesenchymal transition (EMT) of NSCLC cells via BCL6 regulation.…”

Section: Introductionsupporting

confidence: 50%

“…Our previous study suggested that miR-339-5p inhibited NSCLC cell migration and invasion; in patients with NSCLC, the expression of miR-339-5p was decreased in cancer tissues compared with normal lung tissues. Furthermore, statistical analysis demonstrated that miR-339-5p expression was inversely correlated with TNM stage and lymph node metastasis (11). In the present study, BCL6 was verified as the direct target gene of miR-339-5p, and miR-339-5p was shown to regulate EMT through BCL6.…”

Section: Discussionmentioning

confidence: 60%

“…In our previous study, target prediction programs, TargetScan and miRanda, determined that BCL6 was a potential target gene of miR-339-5p (11). To confirm this, Dual-Luciferase assays were performed in A549 and H1299 cell lines transfected with reporter vectors containing the wild-type or mutated forms of the BCL6 3'-UTR (Fig.…”

Section: Mir-339-5p Inhibits Bcl6 Expression By Targeting Its 3'-utrmentioning

confidence: 99%

“…Our previous study (11) identified that miR-339-5p was downregulated in non-small cell lung cancer (NSCLC) cells and tissue samples, and that its expression was inversely associated with tumor-node-metastasis (TNM) stage. Furthermore, its upregulation could inhibit NSCLC cell migration and invasion in vitro.…”

Section: Introductionmentioning

confidence: 99%

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miR-339-5p inhibits metastasis of non-small cell lung cancer by regulating the epithelial-to-mesenchymal transition

Zhang

Yang

et al. 2017

Oncol Lett

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Abstract. Metastasis is a common event in cancer pathology, and represents the primary cause of cancer-associated mortality. Metastasis, which is the process in which cancer cells at the primary tumor site spread to a different location in the body and form a new tumor, is regulated by multiple factors and includes a number of steps and stages. In our previous study, it was demonstrated miR-339-5p inhibits cell migration and invasion in vitro and is associated with the tumor-node-metastasis stage and the lymph node metastasis status of non-small cell lung cancer. In the present study, expression of miR-339-5p was first determined in the tissues and peripheral blood of patients with non-small cell lung cancer (NSCLC) and in NSCLC cell lines. It was then demonstrated that miR-339-5p inhibits A549 and H1299 cell invasion. The underlying molecular events of miR-339-5p action in NSCLC were also explored. By luciferase assay and western blot analysis, B-cell CLL/lymphoma 6 (BCL6) was verified as the direct target gene of miR-339-5p. miR-339-5p may inhibit lung cancer cell invasion and migration by regulating the epithelial-to-mesenchymal transition via BCL6 in vitro. It was also demonstrated that the relative expression of miR-339-5p in the peripheral blood is associated with cancer metastasis in patients with non-small cell lung cancer.

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Section: Introductionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 60%

Section: Mir-339-5p Inhibits Bcl6 Expression By Targeting Its 3'-utrmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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miR-339-5p inhibits metastasis of non-small cell lung cancer by regulating the epithelial-to-mesenchymal transition

Zhang

Yang

et al. 2017

Oncol Lett

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“…Similarly, miR-339-5p markedly decreased the ability of migration and invasion of lung cancer cells [14]. Moreover, overexpression of NOVA1attenuates the suppressive role of miR-339, suggested that miR-339 modulates tumor growth through targeting NOVA1 in GC.…”

Section: Discussionmentioning

confidence: 94%

MicroRNA‐339, an epigenetic modulating target is involved in human gastric carcinogenesis through targeting NOVA1

Shen

Zhang

et al. 2015

FEBS Letters

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a b s t r a c tThe role of miR-339 in human gastric cancer (GC) remains unclear. Here, we found that miR-339 is remarkably decreased in primary GC tissues. Overexpression of miR-339 in GC cells significantly suppressed proliferation, migration, invasion, and tumorigenicity. Furthermore, NOVA1 was confirmed as a target of miR-339. Restoration of NOVA1 in miR-339-overexpressing GC cells partially impaired the inhibitory effects of miR-339. More importantly, epigenetic modification may be involved in the modulation of miR-339 expression. These findings uncover a novel role for miR-339 in gastric carcinogenesis, and restoration of miR-339 could be considered as a potential therapeutic strategy for GC treatment.

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miR‐339‐5p downregulation contributes to Taxol resistance in small‐cell lung cancer by targeting α1,2‐fucosyltransferase 1

Gan

Luo

et al. 2017

IUBMB Life

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Lung cancer is a leading cause of cancer-related mortality, and non-small-cell lung carcinoma is responsible for almost 80% of lung cancer-related deaths. In recent years, lung cancer has shown increasing incidence but poor prognosis, and many studies have demonstrated that microRNAs play crucial roles in the development of lung carcinoma and chemoresistance. This study investigated the role of miR-339-5p involvement in lung carcinoma cell lines and chemoresistance to Taxol. We observed that miR-339-5p was significantly downregulated in Taxol-A549 cells compared with A549 cells. In vitro studies further indicated that miR-339-5p could promote colony formation and attenuate apoptosis of lung carcinoma cell lines through targeting a1,2-fucosyltransferase 1 and regulation of the downstream protein Lewis y. Furthermore, miR-339-5p was found to enhance the proliferation inhibition ability of Taxol in lung carcinoma cell lines as well as in the Taxol-A549 subclone. An in vivo study indicated that both miR-339-5p and Taxol could attenuate the growth of lung carcinoma; moreover, miR-339-5p could synergistically promote this inhibitory function of Taxol. In summary, our results suggest a miR-339-5p molecular network that is involved in controlling lung carcinoma progression.

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miR-339-5p inhibits cell migration and invasion in vitro and may be associated with the tumor-node-metastasis staging and lymph node metastasis of non-small cell lung cancer

Cited by 33 publications

References 28 publications

miR-339-5p inhibits metastasis of non-small cell lung cancer by regulating the epithelial-to-mesenchymal transition

miR-339-5p inhibits metastasis of non-small cell lung cancer by regulating the epithelial-to-mesenchymal transition

MicroRNA‐339, an epigenetic modulating target is involved in human gastric carcinogenesis through targeting NOVA1

miR‐339‐5p downregulation contributes to Taxol resistance in small‐cell lung cancer by targeting α1,2‐fucosyltransferase 1

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