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

Li, Yun; Zhang, Xuelin; Yang, Zhen; Li, Yanan; Han, Bingchao; Chen, Liangan

doi:10.3892/ol.2017.7608

Cited by 18 publications

(21 citation statements)

References 39 publications

(37 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MicroRNAs (miRNAs/miRs) are found to be deregulated in various human cancers (6). These small noncoding RNAs can regulate gene expression at the post-transcriptional level and are involved in various cell processes such as proliferation, migration, invasion, differentiation and apoptosis (7,8).…”

Section: Introductionmentioning

confidence: 99%

Ultrasound‑targeted microbubble destruction‑mediated miR‑767 inhibition suppresses tumor progression of non‑small cell lung cancer

et al. 2020

Exp Ther Med

View full text Add to dashboard Cite

MicroRNAs (miRNAs/miRs) have important roles in tumor progression in various human cancers. Ultrasound-targeted microbubble destruction (UTMD)-mediated gene transfection has been considered a useful tool for improving cancer treatment. The present study aimed to investigate the role of miR-767 in non-small cell lung cancer (NSCLC) and further analyze the effects of UTMD-mediated miR-767 inhibition on tumor progression. The expression of miR-767 was measured by reverse transcription-quantitative PCR. UTMD-mediated miR-767 inhibition was achieved by the co-transfection of microbubbles and miR-767 inhibitor in NSCLC cells. Cell proliferation was assessed by a CCK-8 assay and cell migration and invasion were examined by a Transwell assay. The expression of miR-767 was increased in NSCLC serum, tissues and cells compared with controls. The reduction of miR-767 in NSCLC cells led to the inhibition of cell proliferation, migration and invasion. UTMD increased the transfection efficiency of the miR-767 inhibitor in NSCLC cells, and UTMD-mediated miR-767 inhibition resulted in a more significant suppressive effect on tumor cell proliferation, migration and invasion. Taken together, the results indicated that miR-767 expression is upregulated in both NSCLC clinical samples and cells. The downregulation of miR-767 can inhibit tumor cell proliferation, migration and invasion, and these effects are further promoted by UTMD-mediated miR-767 inhibition, which indicated the potential of a UTMD-mediated miR-767 inhibition as a novel therapeutic strategy for NSCLC treatment.

show abstract

Section: Introductionmentioning

confidence: 99%

Ultrasound‑targeted microbubble destruction‑mediated miR‑767 inhibition suppresses tumor progression of non‑small cell lung cancer

et al. 2020

Exp Ther Med

View full text Add to dashboard Cite

show abstract

“…The authors showed that forced expression of BCL6 results in increased proliferation, anchorage-independent growth, migration, invasion and survival of breast cancer cell lines, whereas knockdown of BCL6 expression reduced these oncogenic properties of breast cancer cells (52). Interestingly, miR-339-5p has been shown to inhibit migration and invasion by targeting BCL6 in breast cancer (53), ovarian cancer cell lines (47) and in NSCLC (54). In addition, miR-339-5p down-regulation in NSCLC inhibits metastasis of NSCLC by regulating the epithelial-to-mesenchymal(EMT) transitionvia BCL6 (54).…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, miR-339-5p has been shown to inhibit migration and invasion by targeting BCL6 in breast cancer (53), ovarian cancer cell lines (47) and in NSCLC (54). In addition, miR-339-5p down-regulation in NSCLC inhibits metastasis of NSCLC by regulating the epithelial-to-mesenchymal(EMT) transitionvia BCL6 (54). A recent report has shown that miR-339-5p regulates EMT through regulation of TGF-β (55) in osteosarcoma (51).…”

Section: Discussionmentioning

confidence: 99%

Circulating microRNAs in Early Breast Cancer Patients and Its Association With Lymph Node Metastases

Escuín

López‐Vilaró

Bell

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: In recent years, miRNAs have emerged as important regulators of many cellular processes, including the various steps of the metastatic process. In addition, circulating miRNAs appear to be surprisingly stable in peripheral blood making them ideal noninvasive biomarkers for disease diagnosis. Here, we investigated the expression profile of circulating miRNAs and their association with the metastatic lymph node status in early breast cancer patients. Methods: We designed a proof-of-principle study using 16 plasma samples from patients with known sentinel lymph node status (n=12 positive and n=4 negative). We performed RNA-sequencing and validated the results by qPCR. Gene Ontology term enrichment and KEGG pathway analyses were carried out using DAVID tools.Results: We found16 differentially expressed miRNAs after adjusting for false discovery correction (q < 0.01) in patients with positive samples. Thirteen miRNAs were down-regulated (miR-339-5p, miR-133a-3p, miR-326, miR-331-3p, miR-369-3p, miR-328-3p, miR-26a-3p, miR-139-3p, miR-493-3p, miR-664a-5p, miR-323b-3pmiR-1307-3p and miR-423-3p) and 3 were up-regulated (miR-101-3p, miR-146a-5p and miR-144-3p). Hierarchical clustering using differentially expressed miRNAs clearly distinguished patients according to their lymph node status. We did not find any difference in the miRNA expression profile between plasma samples associated with macrometastasis or micrometastasis. The expression of 9 miRNAs was validated by qPCR. Moreover, gene ontology analysis showed a significant enrichment of biological processes associated with the regulation of the epithelial mesenchymal transition, cell proliferation and transcriptional regulation. Conclusions: Our results indicated the potential role of several circulating miRNAs as surrogate markers of lymph node metastases in early breast cancer patients. Further validation in a larger cohort of patients will be necessary to confirm our results.

show abstract

“…miR-339-5p was reported to inhibit the EMT via targeting B-cell chronic lymphocytic leukemia/ BCL6 and, therefore, restrain cell migration and invasion in NSCLC. 10 In CRC cells, miR-339-5p functions as a tumor suppressor which suppresses cell growth, colony formation and metastasis by downregulating the expression of PRL-1. 30 A study by Jansson et al 31 demonstrated that miR-339-5p downregulates MDM2 expression through directly targeting the 3′-UTR of MDM2 mRNA, and thus promotes p53 function in breast cancer cell MCF-7 and CRC cell HCT-116.…”

Section: Discussionmentioning

confidence: 99%

“…6,7 In recent years, miR-339 has been reported to be a suppressor for various cancers, such as lung cancer, ovarian cancer, colorectal cancer (CRC) and melanoma. [8][9][10][11][12][13][14] However, the mechanism underlying miR-399 inhibiting HCC carcinogenesis remains unclear.…”

Section: Introductionmentioning

confidence: 99%

<p>MicroRNA-339 inhibits human hepatocellular carcinoma proliferation and invasion via targeting ZNF689</p>

Zeng¹,

Zheng²,

Song³

et al. 2019

DDDT

View full text Add to dashboard Cite

Background: Hepatocellular carcinoma (HCC) is the second leading cause of cancer mortality worldwide, however, the prognosis for HCC remains unsatisfactory. This study aimed to explore the role of miR-339-5p in HCC. Methods: We first used quantitative real-time PCR to examine the level of miR-339-5p in HCC tissues. Then we further adopted Western blotting assay, CCK8, cell invasion assays, apoptosis detection assay, and luciferase assay to analyze how it mediate the development of HCC. Results: We found that miR-339 is significantly decreased in primary HCC tissues. Overexpression of miR-339 in HCC cells remarkably suppressed proliferation and invasion and induced apoptosis. However, silencing miR-339 in HCC cells promoted proliferation and invasion, and reduced apoptosis. Moreover, we demonstrated that ZNF689 is a target of miR-339 and there is a negative correlation between miR-339 and ZNF689 expression in the HCC tissues. Overexpression of ZNF689 in miR-339-overexpressing HCC cells partially antagonized the inhibitory effects of miR-339. Conclusion: Our study revealed that miR-339 inhibits HCC growth through targeting oncoprotein ZNF689 and restoration of miR-339 might be feasible therapeutic strategy for HCC treatment.

show abstract

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

Cited by 18 publications

References 39 publications

Ultrasound‑targeted microbubble destruction‑mediated miR‑767 inhibition suppresses tumor progression of non‑small cell lung cancer

Ultrasound‑targeted microbubble destruction‑mediated miR‑767 inhibition suppresses tumor progression of non‑small cell lung cancer

Circulating microRNAs in Early Breast Cancer Patients and Its Association With Lymph Node Metastases

<p>MicroRNA-339 inhibits human hepatocellular carcinoma proliferation and invasion via targeting ZNF689</p>

Contact Info

Product

Resources

About