Erratum: ESRP1 is overexpressed in ovarian cancer and promotes switching from mesenchymal to epithelial phenotype in ovarian cancer cells

Jeong, Han Mo; Han, Jinil; Lee, S. H.; Park, H.-J.; Lee, H. J.; Choi, Janghoon; Lee, Y. M.; Choi, Young Don; Shin, Young Kee; Kwon, Mi

doi:10.1038/oncsis.2017.89

Cited by 56 publications

(52 citation statements)

References 35 publications

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“…increased ESRP1 levels effectively). Finally, similar to the prognostic ability of GRHL2 and OVOL [27,39] -factors that can stabilize a hybrid E/M phenotype [25,27,37,38] -higher levels of ESRP1 have been associated with (a) poor OS in breast cancer, (b) poor 5-year progression-free survival (PFS) and OS in epithelial ovarian cancer samples [55,56], and (c) poor prognosis of distant metastasis in breast cancer samples [57]. Put together, these observations support a case for ESRP1 to be referred to as 'phenotypic stability factor' (PSF).…”

Section: Discussionmentioning

confidence: 89%

Interconnected feedback loops among ESRP1, HAS2, and CD44 regulate epithelial-mesenchymal plasticity in cancer

Jolly

Preca

Tripathi

et al. 2018

Preprint

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Aberrant activation of epithelial-mesenchymal transition (EMT) in carcinoma cells contributes to increased migration and invasion, metastasis, drug resistance, and tumor-initiating capacity. EMT is not always a binary process, rather cells may exhibit a hybrid epithelial/mesenchymal (E/M) phenotype. ZEB1 -a key transcription factor driving EMT -can both induce and maintain a mesenchymal phenotype. Recent studies have identified two novel autocrine feedback loops utilizing ESRP1, HAS2, and CD44 that maintain high levels of ZEB1. However, how the crosstalk between these feedback loops alters the dynamics of epithelial-hybrid-mesenchymal transition remains elusive. Here, using an integrated theoretical-experimental framework, we identify that these feedback loops can enable cells to stably maintain a hybrid E/M phenotype. Moreover, computational analysis identifies the regulation of ESRP1 as a crucial node, a prediction that is validated by two complementary experiments showing that (a) overexpression of ESRP1 reverts EMT in MCF10A cells treated with TGFβ for 21 days, and (b) knockdown of ESRP1 in stable hybrid E/M H1975 cells drives EMT. Finally, in multiple breast cancer datasets, high levels of ESRP1, ESRP1/HAS2, and ESRP1/ZEB1 correlates with poor prognosis, supporting the relevance of ZEB1/ESRP1 and ZEB1/HAS2 axes in tumor progression. Together, our results unravel how these interconnected feedback loops act in concert to regulate ZEB1 levels and to drive the dynamics of epithelial-hybrid-mesenchymal transition.

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Section: Discussionmentioning

confidence: 89%

Interconnected feedback loops among ESRP1, HAS2, and CD44 regulate epithelial-mesenchymal plasticity in cancer

Jolly

Preca

Tripathi

et al. 2018

Preprint

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“…In fact, a report show that altered expression and splicing of ESRP1 in malignant melanoma correlates with epithelial-mesenchymal status [34]. Importantly, Jeong et al report that overexpression of ESRP1 can inhibit EMT in ovarian cancer [35]. In addition, our previous study shows that BLM inhibited ESRP1 expression, resulting in enhanced alternative splicing of FGFR2 to the mesenchymal isoform IIIc, thereby induces EMT in the lung fibrosis [26].…”

Section: Esrps Are Indispensable Regulators Of Emt and Pulmonary Fibrmentioning

confidence: 94%

Bleomycin induces epithelial-to-mesenchymal transition via bFGF/PI3K/ESRP1 signaling in pulmonary fibrosis

Weng

Chen

et al. 2020

Bioscience Reports

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Idiopathic pulmonary fibrosis (IPF) is a fatal and chronic disease with a high rate of infection and mortality; however, its etiology and pathogenesis remain unclear. Studies have revealed that epithelial-mesenchymal transition (EMT) is a crucial cellular event in IPF. Here, we identified that the pulmonary fibrosis inducer bleomycin simultaneously increased the expression of bFGF and TGF-β1 and inhibited epithelial-specific regulatory protein (ESRP1) expression in vivo and in vitro. In addition, in vitro experiments showed that bFGF and TGF-β1 down-regulated the expression of ESRP1 and that silencing ESRP1 promoted EMT in A549 cells. Notably, we determined that bFGF activates PI3K/Akt signaling, and treatment with the PI3K/Akt inhibitor LY294002 inhibited bleomycin-induced cell morphology changes and EMT. In addition, the effects of LY294002 on bleomycin-induced EMT were inhibited by ESRP1 silencing in A549 cells. Taken together, these findings suggest that bleomycin induced EMT through down-regulating ESRP1 by simultaneously increasing bFGF and TGF-β1 in pulmonary fibrosis. Additionally, our findings indicated that bFGF inhibits ESRP1 by activating PI3K/Akt signaling.

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“…For example, bleomycin inhibited ESRP1 expression, leading to the increased alternative splicing of FGFR2 to its mesenchymal isoform IIIc, which induced EMT in lung fibrosis . In addition, overexpressed ESRP1 contributed to EMT in ovarian cancer, inducing a cell‐specific variant of CD44 and a protein‐enabled homologue . Moreover, Rbfox2 was upregulated during the EMT, and the depletion of Rbfox2 suppressed the expression of mesenchymal marker genes …”

Section: Small Molecules Against Emtmentioning

confidence: 97%

“…205 In addition, overexpressed ESRP1 contributed to EMT in ovarian cancer, inducing a cell-specific variant of CD44 and a protein-enabled homologue. 206 Moreover, Rbfox2 was upregulated during the EMT, and the depletion of Rbfox2 suppressed the expression of mesenchymal marker genes. 207 Several studies have revealed that small molecules regulate the expression of RNA-binding proteins to mediate EMT.…”

Section: Ras Signaling Pathwaymentioning

confidence: 98%

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

Feng

Chen

Vaziri

et al. 2019

Medicinal Research Reviews

109

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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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Erratum: ESRP1 is overexpressed in ovarian cancer and promotes switching from mesenchymal to epithelial phenotype in ovarian cancer cells

Abstract: The legend of Figure 5 was published incorrectly. The correct legend should read as follows: This error has now been rectified and the corrected article appears in this issue together with this corrigendum.The publishers wish to apologise for any inconvenience caused.

Cited by 56 publications

References 35 publications

Interconnected feedback loops among ESRP1, HAS2, and CD44 regulate epithelial-mesenchymal plasticity in cancer

Interconnected feedback loops among ESRP1, HAS2, and CD44 regulate epithelial-mesenchymal plasticity in cancer

Bleomycin induces epithelial-to-mesenchymal transition via bFGF/PI3K/ESRP1 signaling in pulmonary fibrosis

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

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