miR-671-5p inhibits epithelial-to-mesenchymal transition by downregulating FOXM1 expression in breast cancer

Tan, Xiaohui; Fu, Yebo; Chen, Liang; Lee, Woojin; Lai, Yinglei; Rezaei, M. Katayoon; Tabbara, Sana O.; Latham, Patricia S.; Teal, Christine B.; Man, Yan‐gao; Siegel, Robert S.; Brem, Rachel F.; Fu, Sidney W.

doi:10.18632/oncotarget.6344

Cited by 89 publications

(71 citation statements)

References 50 publications

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“…MiR-671-5p has been found to be a tumour suppressor in several types of cancers [16,17]. Downregulation of miR-671-5p expression has been found in breast cancer tissues compared with their adjacent tissues [18]. Overexpression of miR-671-5p inhibits breast cancer cell proliferation and invasion, as well results in a shift from epithelial-to-mesenchymal transition (EMT) to mesenchymal-to-epithelial transition (MET) phenotypes.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA DLEU1 aggravates osteosarcoma carcinogenesis via regulating the miR-671-5p/DDX5 axis

Chen

Zhang

Wang

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Long non-coding RNAs (LncRNAs) have been proven to be involved in the progression of osteosarcoma. LncRNA DLEU1 was found to act as an oncogene in various types of cancer. In this study, we aimed to explore the biological functions of DLEU1 in osteosarcoma and the specific mechanism. Our results showed that DLEU1 was highly expressed in osteosarcoma tissue specimens and cells. Downregulation of DLEU1 in osteosarcoma cells inhibited the cell proliferation, migration and invasion. Further mechanistic analysis and functional assays demonstrated that DLEU1 exerted its role by sponging microRNA (miR)-671-5p in osteosarcoma cells. Moreover, DEAD-box helicase 5 (DDX5) was confirmed as the target of miR-671-5p. Furthermore, rescue assays indicated that miR-671-5p inhibitor significantly reversed the effects of DLEU1 knockdown on osteosarcoma cell proliferation and invasion while restoration of DDX5 rescued the proliferation and invasion of osteosarcoma cells transfected with miR-671-5p mimics. In conclusion, DLEU1 acted as an oncogene in osteosarcoma by directly sponging miR-671-5p and regulating the expression of DDX5. These findings suggested that DLEU1 might be a novel therapeutic target in the treatment of osteosarcoma. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA DLEU1 aggravates osteosarcoma carcinogenesis via regulating the miR-671-5p/DDX5 axis

Chen

Zhang

Wang

2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…The epithelial to mesenchymal transition (EMT), where in epithelial cells lose epithelial phenotypic markers and gain mesenchymal phenotypic markers, is a potential mechanism by which tumor cells gain metastatic features [25]. FOXM1 has been previously identified a master EMT regulator in cancer progression [26][27][28][29][30]. Our results showed that overexpression of miR-361-5p decreased the expression of EMT-related transcription factors and suppressed the TGF-β-induced EMT, suggesting that miR-361-5p inhibits the lung cancer progression through suppression the EMT-like phenotype by down-regulation of FOXM1…”

Section: Discussionmentioning

confidence: 99%

miR-361-5p suppresses lung cancer cell lines progression by targeting FOXM1

Hou¹,

Sun²,

Yu³

et al. 2017

neo

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Lung cancer is the most common type of cancer and the leading cause of death in worldwide. MicroRNAs are known to be key players in a variety of biological processes, including tumorigenesis. In present study, we investigated the effect of miR-361-5p on lung cancer progression. We found that miR-361-5p was down-regulated in lung cancer. Overexpression of miR-361-5p suppressed lung cancer proliferation and invasion. Mechanistically, FOXM1 was identified as a direct target of miR-361-5p. Furthermore, miR-361-5p inhibits EMT-like phenotype through down-regulation of FOXM1 expression in lung cancer cells. In conclusion, our results indicated that miR-361-5p acts as a tumor suppressor in lung cancer.

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“…We observed higher expression of PHLPP1 in AGS cells treated with the hp0175 knockout strain compared with wild type H. pylori (Figures 6b and S6a Expression of miR-29b-1-5p was quantitated by quantitative reverse transcription polymerase chain reaction. (Forkhead box M1) and inhibits epithelial to mesenchymal transition in breast cancer (Tan et al, 2015), and miR-3646 contributes to breast cancer cell proliferation, migration, and invasion by modulating G 2 /M transition. Data represent means ± SD (n = 3).…”

Section: Role Of Hp0175 In Mir-29b-1-5p/phlpp1dependent Mmp Inductimentioning

confidence: 99%

“…GAPDH = glyceraldehyde 3-phosphate dehydrogenase wound healing assays also supported a role of HP0175 in cell migration (Figure 6f). (Forkhead box M1) and inhibits epithelial to mesenchymal transition in breast cancer (Tan et al, 2015), and miR-3646 contributes to breast cancer cell proliferation, migration, and invasion by modulating G 2 /M transition. (Tao et al, 2016).…”

Section: Role Of Hp0175 In Mir-29b-1-5p/phlpp1dependent Mmp Inductimentioning

confidence: 99%

Genome-wide mRNA-miRNA profiling uncovers a role of the microRNA miR-29b-1-5p/PHLPP1 signalling pathway inHelicobacter pylori-driven matrix metalloproteinase production in gastric epithelial cells

Datta

Subuddhi

Kumar

et al. 2018

Cellular Microbiology

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Aberrant expression of microRNAs (miRNAs) is associated with tumour progression, extracellular matrix remodelling, and cell proliferation. miRNAs modulate host gene expression during infection by pathogens such as Helicobacter pylori, which is associated with varying degrees of gastric pathology. In order to gain insight into the regulation of gene expression by miRNAs during H. pylori infection of gastric epithelial cells and its likely downstream consequences, we analysed the transcriptomes and miRnomes of AGS cells infected with H. pylori. In silico analysis of miRNA-mRNA interactions suggested that miR-29b-1-5p was a likely regulator of pathways associated with gastric epithelial cell pathology. We validated PH domain leucine rich phosphatase 1 (PHLPP1), a negative regulator of the Akt signalling pathway, as a target of miR-29b-1-5p. In an in vivo mouse model, we observed that infection with H. pylori was associated with upregulation of miR-29b-1-5p and downregulation of PHLPP1. Transfection with either a mimic or an inhibitor of miR-29b-1-5p confirmed that downregulation of PHLPP1 upregulates Akt-dependent NF-κB signalling leading to activation of matrix metalloproteinases 2 and 9, players in the degradation of extracellular matrix during H. pylori infection. The secreted antigen HP0175 was associated with upregulation of miR-29b-1-5p, regulation of metalloproteinase activity, and migration of AGS cells. Our study suggests that targeting the miR-29b-1-5p/PHLPP1 signalling axis could be a potential host-directed approach for regulating the outcome of H. pylori infection.

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miR-671-5p inhibits epithelial-to-mesenchymal transition by downregulating FOXM1 expression in breast cancer

Cited by 89 publications

References 50 publications

Long noncoding RNA DLEU1 aggravates osteosarcoma carcinogenesis via regulating the miR-671-5p/DDX5 axis

Long noncoding RNA DLEU1 aggravates osteosarcoma carcinogenesis via regulating the miR-671-5p/DDX5 axis

miR-361-5p suppresses lung cancer cell lines progression by targeting FOXM1

Genome-wide mRNA-miRNA profiling uncovers a role of the microRNA miR-29b-1-5p/PHLPP1 signalling pathway inHelicobacter pylori-driven matrix metalloproteinase production in gastric epithelial cells

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