Epigenetic regulation of epithelial-mesenchymal transition: focusing on hypoxia and TGF-β signaling

Lin, Yueh-Te; Wu, Kou-Juey

doi:10.1186/s12929-020-00632-3

Cited by 140 publications

(114 citation statements)

References 64 publications

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“…The complexes translocate into the nucleus, and regulate EMT target genes through interacting with various transcription factors [30]. Smad2/3, an intracellular signaling molecule, activates different EMT transcription factors [31]. In the present study, we found that the protein level of P-Smad2/3 was inhibited by HCK knockdown in GBM cells, suggesting HCK is involved in EMT via TGFβ/Smad signaling pathway.…”

Section: Discussionsupporting

confidence: 55%

HCK promotes glioblastoma progression by TGFβ signaling

et al. 2020

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The hematopoietic cell kinase (HCK), a member of the Src family protein-tyrosine kinases (SFKs), is primarily expressed in cells of the myeloid and B lymphocyte lineages. Nevertheless, the roles of HCK in glioblastoma (GBM) remain to be examined. Thus, we aimed to investigate the effects of HCK on GBM development both in vitro and in vivo, as well as the underlying mechanism. The present study found that HCK was highly expressed in both tumor tissues from patients with GBM and cancer cell lines. HCK enhanced cell viability, proliferation, and migration, and induced cell apoptosis in vitro. Tumor xenografts results also demonstrated that HCK knockdown significantly inhibited tumor growth. Interestingly, gene set enrichment analysis (GSEA) showed HCK was closed associated with epithelial mesenchymal transition (EMT) and TGFβ signaling in GBM. In addition, we also found that HCK accentuates TGFβ-induced EMT, suggesting silencing HCK inhibited EMT through the inactivation of Smad signaling pathway. In conclusion, our findings indicated that HCK is involved in GBM progression via mediating EMT process, and may be served as a promising therapeutic target for GBM.

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Section: Discussionsupporting

confidence: 55%

HCK promotes glioblastoma progression by TGFβ signaling

et al. 2020

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“…Small changes may lead to major consequences and result in cellular dysfunction or malignant outgrowth (Sun and Fang, 2016). Growing evidence suggests the epigenetic regulation of pro-inflammatory and pro-fibrotic gene expression, mediated by DNA methylation, histone modifications or microRNAs, is important in EMT and renal fibrogenesis (Wing et al, 2013;Rodriguez-Romo et al, 2015;Wanner and Bechtel-Walz, 2017;Lin and Wu, 2020).…”

Section: Epigenetic Regulation Of Pemt In the Kidneymentioning

confidence: 99%

New Insights Into the Role and Mechanism of Partial Epithelial-Mesenchymal Transition in Kidney Fibrosis

2020

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Epithelial-mesenchymal transition (EMT) is described as the process in which injured renal tubular epithelial cells undergo a phenotype change, acquiring mesenchymal characteristics and morphing into fibroblasts. Initially, it was widely thought of as a critical mechanism of fibrogenesis underlying chronic kidney disease. However, evidence that renal tubular epithelial cells can cross the basement membrane and become fibroblasts in the renal interstitium is rare, leading to debate about the existence of EMT. Recent research has demonstrated that after injury, renal tubular epithelial cells acquire mesenchymal characteristics and the ability to produce a variety of profibrotic factors and cytokines, but remain attached to the basement membrane. On this basis, a new concept of "partial epithelial-mesenchymal transition (pEMT)" was proposed to explain the contribution of renal epithelial cells to renal fibrogenesis. In this review, we discuss the concept of pEMT and the most recent findings related to this process, including cell cycle arrest, metabolic alternation of epithelial cells, infiltration of immune cells, epigenetic regulation as well as the novel signaling pathways that mediate this disturbed epithelial-mesenchymal communication. A deeper understanding of the role and the mechanism of pEMT may help in developing novel therapies to prevent and halt fibrosis in kidney disease.

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“…Gene amplification/deletion/mutation or chromosomal translocation is abnormal genetic changes that lead to tumorigenesis and tumor development [5,6]. Recently, there has been increasing evidence that epigenetic regulation plays a major role in cancer [7,8]. Epigenetic modifications are heritable and reversible and can regulate gene expression and cancer progression without DNA sequence changes [1,5].…”

Section: Introductionmentioning

confidence: 99%

Emerging role of RNA methyltransferase METTL3 in gastrointestinal cancer

et al. 2020

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Gastrointestinal cancer, the most common solid tumor, has a poor prognosis. With the development of highthroughput sequencing and detection technology, recent studies have suggested that many chemical modifications of human RNA are involved in the development of human diseases, including cancer. m 6 A, the most abundant modification, was revealed to participate in a series of aspects of cancer progression. Recent evidence has shown that methyltransferase-like 3 (METTL3), the first identified and a critical methyltransferase, catalyzes m 6 A methylation on mRNA or non-coding RNA in mammals, affecting RNA metabolism. Abnormal m 6 A levels caused by METTL3 have been reported to be involved in different aspects of cancer development, including proliferation, apoptosis, and metastasis. In this review, we will shed light on recent findings regarding the biological function of METTL3 in gastrointestinal cancer and discuss future research directions and potential clinical applications of METTL3 for gastrointestinal cancer.

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Epigenetic regulation of epithelial-mesenchymal transition: focusing on hypoxia and TGF-β signaling

Cited by 140 publications

References 64 publications

HCK promotes glioblastoma progression by TGFβ signaling

HCK promotes glioblastoma progression by TGFβ signaling

New Insights Into the Role and Mechanism of Partial Epithelial-Mesenchymal Transition in Kidney Fibrosis

Emerging role of RNA methyltransferase METTL3 in gastrointestinal cancer

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