microRNA-935 is reduced in non-small cell lung cancer tissue, is linked to poor outcome, and acts on signal transduction mediator E2F7 and the AKT pathway

Wang, C; Xu, Jihua; Niu, Wenbo; Li, S

doi:10.1080/09674845.2018.1520066

Cited by 32 publications

(32 citation statements)

References 30 publications

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“…There are eight genes in this family (E2F1–E2F8), among which E2F1–E2F3 played the role of activators for transcription while E2F4–E2F8 work contrastingly. E2F7 was found to be upregulated in many types of neoplasms, like endometrial cancer (Q. Li et al, 2015) and non‐small‐cell lung cancer (Wang, Li, Xu, Niu, & Li, 2019). But the roles it plays are controversial in different cancer types, for example, it may serve as a protective factor in cutaneous squamous cell carcinoma (Thurlings et al, 2017), or risk factor in hepatocellular carcinoma (HCC; Ma et al, 2018) and lung adenocarcinoma (LUAD; Liang et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

miR‐129‐5p inhibits proliferation, migration, and invasion in rectal adenocarcinoma cells through targeting E2F7

Wan

Bai

Yang

et al. 2020

Journal Cellular Physiology

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microRNAs (miRNAs), a kind of small noncoding RNAs, are considered able to regulate expression of genes and mediate RNA silencing. miR‐129‐5p was shown to be a cancer‐related miRNA. However, the influence of miR‐129‐5p in rectal adenocarcinoma (READ) development remains to be determined. Based on the TCGA data, downregulation of miR‐129‐5p in READ samples was observed. Manual restoration of the miR‐129‐5p in SW1463 and SW480 cell lines significantly inhibited invasion, migration, and proliferation of READ cell lines, while the apoptosis ability was enhanced. Meanwhile, we found E2F7 acted as a potential target of miR‐129‐5p and was upregulated in READ samples. E2F7 upregulation reversed the repression of miR‐129‐5p on READ development. Finally, in vivo experiments showed that inhibition of tumor growth in nude mice was achieved through upregulating miR‐129‐5p. Overall, our findings suggest increasing of miR‐129‐5p leads to the suppression of READ progression through regulating the expression of E2F7, which may provide novel insights into the treatment of READ.

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Section: Introductionmentioning

confidence: 99%

miR‐129‐5p inhibits proliferation, migration, and invasion in rectal adenocarcinoma cells through targeting E2F7

Wan

Bai

Yang

et al. 2020

Journal Cellular Physiology

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“…For instance, the aberrant expression of miR-935 in colorectal carcinoma tissues has been documented to serve a biomarker to predict the prognosis of cancer patients (13). Similarly, the decreased expression of miR-935 in non-small cell lung cancer also indicated a poor prognosis in cancer patients (14). In this study, the serum miR-935 was found to be downregulated in BCa patients.…”

Section: Discussionmentioning

confidence: 54%

“…By the prediction with bioinformatics analysis, a binding site of miR-935 was found at the sequences of KCNQ1OT1. miR-935 has been investigated in renal cell carcinoma (12), colorectal carcinoma (13) and non-small cell lung cancer (14), but little is known about its role in BCa.…”

Section: Discussionmentioning

confidence: 99%

“…Our study predicted a binding site of KCNQ1OT1 at the seed sequence of miR-935. The role of miR-935 has been investigated in some human malignancies, including renal cell carcinoma (12), colorectal carcinoma (13) and non-small cell lung cancer (14). In an in silico study by Zhu et al, the BCa cells with chemotherapy resistance had signi cantly lower miR-935 expression than normal cells (15), which may imply that miR-935 might be involved in the progression of BCa.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-935 mediates the regulatory effect of lncRNA KCNQ1OT1 on tumor progression of breast cancer

Zhang¹,

Gong²,

Li³

et al. 2020

Preprint

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Background The biological function of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have received increasing attention in the pathogenesis of various malignancies. This study aimed to evaluate the functional role and clinical significance of the KCNQ1OT1/miR-935 axis in breast cancer (BCa) progression. Methods Expression of KCNQ1OT1 and miR-935 was estimated using quantitative real-time PCR (qRT-PCR). The interaction between KCNQ1OT1 and miR-935 was confirmed by luciferase reporter assay. BCa cell proliferation, migration and invasion were evaluated using CCK-8 and Transwell assays. The clinical significance of the KCNQ1OT1/miR-935 axis in BCa diagnosis was examined by ROC analysis. Results The expression of KCNQ1OT1 was significantly elevated, but the miR-935 expression was decreased in BCa cells (all P < 0.01). KCNQ1OT1 could directly bind to miR-935, leading to the decreased miR-935 expression in BCa cells (P < 0.001). The overexpression of miR-935 could inhibit BCa cell proliferation, migration and invasion, and remarkably reversed the regulatory effect of KCNQ1OT1 on BCa cell biological processes (all P < 0.05). Serum KCNQ1OT1 levels were negatively correlated with miR-935 levels in BCa patients. The aberrant expression of KCNQ1OT1 and miR-935 had relatively high diagnostic accuracy for the screening of BCa patients. Conclusion In conclusion, miR-935 expression is downregulated in BCa cells, which can be inhibited by KCNQ1OT1 and mediates the promoting effect of KCNQ1OT1 on BCa tumor progression in vivo. Serum reduced expression of miR-935 may serve as a diagnostic biomarker of BCa, and the KCNQ1OT1/miR-935 axis provides potential therapeutic targets for BCa treatment.

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“…In our RNAseq data with miR-29a overexpressing PSCs, we found E2F1 to be one of the indirect downregulated targets. In addition, E2F7 has also been shown to be activated by Akt signaling in carcinomas [82][83][84]. Although the exact mechanisms of MYBL2 and E2F7 in PSCs is still to be understood, our results suggest that dysregulation of miR-29a in PSCs derepresses genes such as IGF-1, MYBL2 and E2F7, which may in turn disrupt stromal p53 regulation promoting PSC-mediated tumor proliferation.…”

Section: Discussionmentioning

confidence: 68%

Global targetome analysis reveals critical role of miR-29a in pancreatic stellate cell mediated regulation of PDAC tumor microenvironment

Dey

Liu

Factora

et al. 2020

Preprint

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BackgroundPancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive forms of malignancies with a nearly equal incidence and mortality rates in patients. Pancreatic stellate cells (PSCs) are critical players in PDAC microenvironment to promote the aggressiveness and pathogenesis of the disease.Dysregulation of microRNAs (miRNAs) have been shown to play a significant role in progression of PDAC. Earlier, we observed a PSC-specific downregulation of miR-29a in PDAC pancreas, however, the mechanism of action of the molecule in PSCs is still to be elucidated. The current study aims to clarify the regulation of miR-29a in PSCs and identifies functionally important downstream targets that contribute to tumorigenic activities during PDAC progression. MethodsIn this study, using RNAseq approach, we performed transcriptome analysis of paired miR-29a overexpressing hPSC cells and controls. Enrichment analysis was performed with the identified differentially expressed genes (DEGs). miR-29a targets in the dataset were identified, which were utilized to create network interactions. Western blots were performed with the top candidate miR-29a targets in hPSC cells transfected with miR-29a mimic or scramble control. ResultsRNAseq analysis identified 202 differentially expressed genes, which included 19 downregulated direct miR-29a targets. Translational repression of eight key pro-tumorigenic and -fibrotic targets namely IGF-1, COL5A3, CLDN1, E2F7, MYBL2, ITGA6 and ADAMTS2 by miR-29a was observed in PSCs.Using pathway analysis, we find that miR-29a modulates effectors of IGF-1-p53 signaling in PSCs that may hinder carcinogenesis. We further observe a regulatory role of the molecule in pathways associated with PDAC ECM remodeling and tumor-stromal crosstalk, such as INS/IGF-1, RAS/MAPK, laminin interactions and collagen biosynthesis. ConclusionsTogether, our study presents a comprehensive understanding of miR-29a regulation of PSCs, and identifies essential pathways associated with PSC-mediated PDAC pathogenesis. The findings suggest an anti-tumorigenic role of miR-29a in the context of PSC-tumor cell crosstalk and advocates for the potential of the molecule in PDAC targeted therapies. 4

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microRNA-935 is reduced in non-small cell lung cancer tissue, is linked to poor outcome, and acts on signal transduction mediator E2F7 and the AKT pathway

Cited by 32 publications

References 30 publications

miR‐129‐5p inhibits proliferation, migration, and invasion in rectal adenocarcinoma cells through targeting E2F7

miR‐129‐5p inhibits proliferation, migration, and invasion in rectal adenocarcinoma cells through targeting E2F7

MicroRNA-935 mediates the regulatory effect of lncRNA KCNQ1OT1 on tumor progression of breast cancer

Global targetome analysis reveals critical role of miR-29a in pancreatic stellate cell mediated regulation of PDAC tumor microenvironment

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