RETRACTED: miR‐655 suppresses epithelial‐to‐mesenchymal transition by targeting Prrx1 in triple‐negative breast cancer

Lv, Zhi‐Dong; Kong, Bin; Liu, Xiangping; Jin, Lina; Dong, Qi; Li, Fu‐Nian; Wang, Haibo

doi:10.1111/jcmm.12770

Cited by 74 publications

(63 citation statements)

References 34 publications

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“…Harazono et al (2013) [47] reported that the overexpression of miR-655, which is an EMT-suppressive miRNA that targets TGFBR2 and ZEB1, not only induced the up-regulation of E-cadherin and the downregulation of typical EMT inducers but also inhibited the invasion and migration of mesenchymal-like cancer cells. Furthermore, the upregulation of miR-655 inhibits cell invasion in esophageal squamous cell carcinoma [48], triple-negative breast cancer [49], and hepatocellular carcinoma [50]. MiRNA-455 (miR-455) is recognized as a broadly conserved noncoding RNA that has been implicated in various cancers.…”

Section: Discussionmentioning

confidence: 99%

Identification of novel genes associated with a poor prognosis in pancreatic ductal adenocarcinoma via a bioinformatics analysis

et al. 2019

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Pancreatic ductal adenocarcinoma (PDAC) is a class of the commonest malignant carcinomas. The present study aimed to elucidate the potential biomarker and prognostic targets in PDAC. The array data of GSE41368, GSE43795, GSE55643, and GSE41369 were downloaded from Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) and differentially expressed microRNAs (DEmiRNAs) in PDAC were obtained by using GEO2R, and overlapped DEGs were acquired with Venn Diagrams. Functional enrichment analysis of overlapped DEGs and DEmiRNAs was conducted with Metascape and FunRich, respectively. The protein–protein interaction (PPI) network of overlapped DEGs was constructed by STRING and visualized with Cytoscape. Overall survival (OS) of DEmiRNAs and hub genes were investigated by Kaplan–Meier (KM) plotter (KM plotter). Transcriptional data and correlation analyses among hub genes were verified through GEPIA and Human Protein Atlas (HPA). Additionally, miRNA targets were searched using miRTarBase, then miRNA–DEG regulatory network was visualized with Cytoscape. A total of 32 DEmiRNAs and 150 overlapped DEGs were identified, and Metascape showed that DEGs were significantly enriched in cellular chemical homeostasis and pathways in cancer, while DEmiRNAs were mainly enriched in signal transduction and Glypican pathway. Moreover, seven hub genes with a high degree, namely, V-myc avian myelocytomatosis viral oncogene homolog (MYC), solute carrier family 2 member 1 (SLC2A1), PKM, plasminogen activator, urokinase (PLAU), peroxisome proliferator activated receptor γ (PPARG), MET proto-oncogene, receptor tyrosine kinase (MET), and integrin subunit α 3 (ITGA3), were identified and found to be up-regulated between PDAC and normal tissues. miR-135b, miR-221, miR-21, miR-27a, miR-199b-5p, miR-143, miR-196a, miR-655, miR-455-3p, miR-744 and hub genes predicted poor OS of PDAC. An integrative bioinformatics analysis identified several hub genes that may serve as potential biomarkers or targets for early diagnosis and precision target treatment of PDAC.

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Section: Discussionmentioning

confidence: 99%

Identification of novel genes associated with a poor prognosis in pancreatic ductal adenocarcinoma via a bioinformatics analysis

et al. 2019

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“…Furthermore, the upregulation of miR‐183‐5p induced apoptosis and inhibited EMT, proliferation, invasion, and migration by the downregulation of ezrin in human endometrial cancer cells . Collectively, EMT is inhibited by many miRNAs, including miR‐145, miR‐497, miR‐145‐5p, miR‐138, miR‐200a, miR‐200b, miR‐655, miR‐30‐5p, and miR‐32 . In addition, EMT is also promoted by many miRNAs, including miR‐221, miR‐222, miR‐214‐3p, and miR‐181a …”

Section: Small Molecules Against Emtmentioning

confidence: 99%

“…194 Collectively, EMT is inhibited by many miRNAs, including miR-145, miR-497, miR-145-5p, miR-138, miR-200a, miR-200b, miR-655, miR-30-5p, and miR-32. [195][196][197][198][199][200][201] In addition, EMT is also promoted by many miRNAs, including miR-221, miR-222, miR-214-3p, and miR-181a. [202][203][204] The flavonoids rhamnetin from cloves, berries and cirsiliol from Cirsium lineare (Thunb.)…”

Section: Ras Signaling Pathwaymentioning

confidence: 99%

Small molecule inhibitors of epithelial‐mesenchymal transition for the treatment of cancer and fibrosis

Feng

Chen

Vaziri

et al. 2019

Medicinal Research Reviews

102

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Tissue fibrosis and cancer both lead to high morbidity and mortality worldwide; thus, effective therapeutic strategies are urgently needed. Because drug resistance has been widely reported in fibrotic tissue and cancer, developing a strategy to discover novel targets for targeted drug intervention is necessary for the effective treatment of fibrosis and cancer. Although many factors lead to fibrosis and cancer, pathophysiological analysis has demonstrated that tissue fibrosis and cancer share a common process of epithelial‐mesenchymal transition (EMT). EMT is associated with many mediators, including transcription factors (Snail, zinc‐finger E‐box‐binding protein and signal transducer and activator of transcription 3), signaling pathways (transforming growth factor‐β1, RAC‐α serine/threonine‐protein kinase, Wnt, nuclear factor‐kappa B, peroxisome proliferator‐activated receptor, Notch, and RAS), RNA‐binding proteins (ESRP1 and ESRP2) and microRNAs. Therefore, drugs targeting EMT may be a promising therapy against both fibrosis and tumors. A large number of compounds that are synthesized or derived from natural products and their derivatives suppress the EMT by targeting these mediators in fibrosis and cancer. By targeting EMT, these compounds exhibited anticancer effects in multiple cancer types, and some of them also showed antifibrotic effects. Therefore, drugs targeting EMT not only have both antifibrotic and anticancer effects but also exert effective therapeutic effects on multiorgan fibrosis and cancer, which provides effective therapy against fibrosis and cancer. Taken together, the results highlighted in this review provide new concepts for discovering new antifibrotic and antitumor drugs.

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“…carcinoma (19,20), triple-negative breast cancer (21) and esophageal squamous cell carcinoma (22). However, the expression, role and molecular mechanisms of miR-655 in OSCC have not yet been elucidated.…”

Section: Microrna-655 Suppresses Cell Proliferation and Invasion In Omentioning

confidence: 99%

MicroRNA‑655 suppresses cell proliferation and invasion in oral squamous cell carcinoma by directly targeting metadherin and regulating the PTEN/AKT pathway

Wang

et al. 2018

Mol Med Report

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MicroRNAs (miRNAs) are important regulators of a variety of biological processes and their dysregulation is closely related to cancer formation and progression. Therefore, examination of aberrantly expressed miRNAs in oral squamous cell carcinoma (OSCC) may provide important clues for the diagnosis and treatment of patients with OSCC. The aim of the present study was to determine miRNA (miR)‑655‑3p expression in OSCC tissues and cell lines, and to investigate the biological roles and mechanisms of miR‑655‑3p associated with OSCC. Data from the present study indicated that miR‑655 expression was significantly downregulated in human OSCC tissues and cell lines. Overexpression of miR‑655 attenuated cell proliferation and invasion in OSCC in vitro. Metadherin (MTDH) mRNA was predicted as a potential target of miR‑655 by bioinformatics analysis, and this was confirmed by luciferase reporter assay, reverse transcription‑quantitative polymerase chain reaction and western blot analysis. In OSCC tissues, MTDH was highly expressed and inversely correlated with miR‑655 expression levels. MTDH overexpression reversed the inhibitory effects of miR‑655 mimics in OSCC cells. Notably, the upregulation of miR‑655 expression inhibited the activation of the phosphatase and tensin homolog (PTEN)/RAC‑α serine/threonine‑protein kinase (AKT) pathway in OSCC cells. Therefore, these results may provide the first evidence that miR‑655 targets MTDH to inhibit proliferation and invasion of OSCC by inhibiting PTEN/AKT signaling. Thus, the restoration of miR‑655 expression may be a novel therapeutic strategy for patients with OSCC.

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RETRACTED: miR‐655 suppresses epithelial‐to‐mesenchymal transition by targeting Prrx1 in triple‐negative breast cancer

Cited by 74 publications

References 34 publications

Identification of novel genes associated with a poor prognosis in pancreatic ductal adenocarcinoma via a bioinformatics analysis

Identification of novel genes associated with a poor prognosis in pancreatic ductal adenocarcinoma via a bioinformatics analysis

Small molecule inhibitors of epithelial‐mesenchymal transition for the treatment of cancer and fibrosis

MicroRNA‑655 suppresses cell proliferation and invasion in oral squamous cell carcinoma by directly targeting metadherin and regulating the PTEN/AKT pathway

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