miR‑339‑5p inhibits lung adenocarcinoma invasion and migration by directly targeting BCL6

Li, Peng; Hua-qing, Liu; Li, Yanmeng; Wang, Yan; Zhao, Lin; Wang, Hui

doi:10.3892/ol.2018.9376

Cited by 19 publications

(19 citation statements)

References 30 publications

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“…Bioinformatics tool revealed that miR-339-5p interacted with both STAT5A and SNHG17. Formerly, miR-339-5p was identified to hinder the development of multiple cancers through impairing cell proliferation and metastasis [30][31][32][33] . We firstly proved that miR-339-5p was downregulated in PC and negatively correlated with SNHG17 and STAT5A.…”

Section: Discussionmentioning

confidence: 99%

“…5d, only miR-339-5p was in the intersection of the prediction results. Several studies have revealed that miR-339-5p was a tumor-repressing gene in multiple cancers, such as ovarian cancer 30 , lung adenocarcinoma 31 , breast cancer 32 , and colorectal cancer 33 . Thus, we deduced that miR-339-5p was involved in the regulation of SNHG17 on STAT5A in PC.…”

Section: Snhg17/mir-339-5p/stat5a Positive Feedback Loop Positively Rmentioning

confidence: 99%

“…In PC, the ceRNA module is largely revealed as well 10 . MiR-339-5p has been recognized as a tumor-suppressor miRNA in myriads of cancers such as ovarian cancer 30 , lung adenocarcinoma 31 , breast cancer 32 , and colorectal cancer 33 . However, there is no report about the involvement of miR-339-3p in PC and its interaction with SNHG17.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA SNHG17 aggravated prostate cancer progression through regulating its homolog SNORA71B via a positive feedback loop

Hao

et al. 2020

Cell Death Dis

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Prostate cancer (PC) is a prevalent male malignancy with high occurrence rate. Recent studies have showed that small nucleolar host genes (SNHGs) and their homolog small nucleolar RNAs (snoRNAs) elicit regulatory functions in carcinogenesis. Present study aimed to investigate the role of SNHG17 and its homolog SNORA71B in PC. Function of SNHG17 and SNORA71B in PC is detected by CCK-8, colony formation, flow cytometry analysis of apoptosis, and transwell migration assay. The mechanism whereby SNHG17 regulated SNORA71B was detected by RIP, pulldown, ChIP, and luciferase reporter assays. Results depicted that transcript 6 of SNHG17 and SNORA71B were upregulated in PC. Knockdown of SNHG17 or SNORA71B weakened proliferation, invasion, migration, and epithelial-to-mesenchymal transition (EMT) and strengthened apoptosis. Mechanistically, SNHG17 and SNORA71B were transcriptionally activated by signal transducer and activator of transcription 5A (STAT5A). SNHG17 positively regulated SNORA71B in PC cell lines and other cell lines. SNHG17 sponged miR-339-5p to upregulate STAT5A and therefore to cause transactivation of SNORA71B. Rescue experiments delineated that SNORA71B was required for the regulation of SNHG17 on PC. Moreover, SNHG17 silence hindered tumorigenesis of PC in vivo. In conclusion, current study first revealed that lncRNA SNHG17 aggravated prostate cancer progression through regulating its homolog SNORA71B via a positive feedback loop, which might do help to the pursuit of better PC treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Snhg17/mir-339-5p/stat5a Positive Feedback Loop Positively Rmentioning

confidence: 99%

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LncRNA SNHG17 aggravated prostate cancer progression through regulating its homolog SNORA71B via a positive feedback loop

Hao

et al. 2020

Cell Death Dis

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“…elevated plasma mir-339-5p levels have previously been identified as a biomarker of lung adenocarcinoma (39) and linked to increased activation of the protein B-cell lymphoma 6 (41), whereas upregulation of the resulting protein suppresses PRCP expression (42,43). Consistent with these findings, the present study revealed that mir-339-5p was upregulated in Fc, fold-change; mirna, microrna.…”

Section: Discussionmentioning

confidence: 99%

Identification of key microRNAs and target genes for the diagnosis of bone nonunion

et al. 2020

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a number of recent studies have highlighted the causes of bone nonunion (Bn), however, the rate of Bn incidence continues to rise and available therapeutic options to treat this condition remain limited. Thus, to prevent disease progression and improve patient prognosis, it is vital that BN, or the risk thereof, be accurately identified in a timely manner. in the present study, bioinformatics analyses were used to screen for the differentially expressed genes (deGs) and differentially expressed mirnas (deMs) between patients with Bn and those with bone union, using data from the Gene expression omnibus database. Furthermore, clinical samples were collected and analyzed by reverse transcription-quantitative Pcr and western blotting. In vitro and in vivo experiments were carried out to confirm the relationship between Bn and the deGs of interest, in addition to being used to explore the underlying molecular mechanism of Bn. Functional enrichment analysis of the downregulated deGs revealed them to be enriched for genes associated with 'ecM-receptor interactions', 'focal adhesion', 'and the calcium signaling pathway'. When comparing deM target genes with these DEGs, nine DEGs were identified as putative deM targets, where hsa-microrna (mir)-1225-5p-ccnl2, hsa-mir-339-5p-PrcP, and hsa-mir-193a-3p-mitogen-activated protein kinase 10 (MaPK10) were the only three pairs which were associated with decreased gene expression levels. Furthermore, hsa-mir-193a-3p was demonstrated to induce Bn by targeting MaPK10. collectively, the results of the present study suggest that hsa-mir-193a-3p may be a viable biomarker of Bn.

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“…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

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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.

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miR‑339‑5p inhibits lung adenocarcinoma invasion and migration by directly targeting BCL6

Cited by 19 publications

References 30 publications

LncRNA SNHG17 aggravated prostate cancer progression through regulating its homolog SNORA71B via a positive feedback loop

LncRNA SNHG17 aggravated prostate cancer progression through regulating its homolog SNORA71B via a positive feedback loop

Identification of key microRNAs and target genes for the diagnosis of bone nonunion

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

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