Histone deacetylase 1 is required for transforming growth factor-β1-induced epithelial–mesenchymal transition

Lei, Weiwei; Zhang, Kehua; Pan, Xiaowei; Ying, Hanjie; Wang, Dongmei; Yuan, Xinwang; Gao, Shu; Song, Jianguo

doi:10.1016/j.biocel.2010.05.006

Cited by 75 publications

(60 citation statements)

References 51 publications

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“…7d-f). These results are consistent with our previous observation that HDAC1 knockdown in AML12 cells led to a significant increase of HDAC2 level 37 . Further investigation showed that the knockdown of HDAC1 significantly increased the binding of HDAC2 to Smad2 and Smad3 promoters (Fig.…”

Section: Hdac1 Is a Target Of Pfn2 In Regulating The Smad Expressionsupporting

confidence: 94%

Epigenetic regulation of Smad2 and Smad3 by profilin-2 promotes lung cancer growth and metastasis

et al. 2015

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Altered transforming growth factor-b (TGF-b) signalling has been implicated in tumour development and progression. However, the molecular mechanism behind this alteration is poorly understood. Here we show that profilin-2 (Pfn2) increases Smad2 and Smad3 expression via an epigenetic mechanism, and that profilin-2 and Smad expression correlate with an unfavourable prognosis of lung cancer patients. Profilin-2 overexpression promotes, whereas profilin-2 knockdown drastically reduces, lung cancer growth and metastasis. We show that profilin-2 suppresses the recruitment of HDAC1 to Smad2 and Smad3 promoters by preventing nuclear translocation of HDAC1 through protein-protein interaction at the C terminus of both proteins, leading to the transcriptional activation of Smad2 and Smad3. Increased Smad2 and Smad3 expression enhances TGF-b1-induced EMT and production of the angiogenic factors VEGF and CTGF. These findings reveal a new regulatory mechanism of TGF-b1/Smad signalling, and suggest a potential molecular target for the development of anticancer drugs.

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Section: Hdac1 Is a Target Of Pfn2 In Regulating The Smad Expressionsupporting

confidence: 94%

Epigenetic regulation of Smad2 and Smad3 by profilin-2 promotes lung cancer growth and metastasis

et al. 2015

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“…Besides, the up-regulated expression of p16INK4α by Q/B and further by Q+B in immunoblotting was associated with the local hypermethylation of p16INK4α gene promoter attenuated by Q/B and further by Q+B in MS-PCR. The NF-κBp65 activity and HDAC are important inducers of epithelial-mesenchymal transition (EMT), cell metastasis and invasiveness (Strippoli et al, 2010;Lei et al, 2010). In this experiment the E-cadherin expression was increased, suggesting that the reversal EMT may be contributed to inhibiting migration/invasive potency of Eca9706 cells mediated via HD1 or inactivation of NF-κBp65 induced by Q/B, especially by Q+B.…”

Section: Discussionmentioning

confidence: 71%

Aberrant Epigenetic Alteration in Eca9706 Cells Modulated by Nanoliposomal Quercetin Combined with Butyrate Mediated via Epigenetic-NF-κB Signaling

Naigang¹,

Wang²,

Yang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Asian Pac J Cancer Prev, 15 (11), 4539-4543 IntroductionThere is close relationship between neoplasia and inflammation. Many cancers arise from sites of chronic inflammation or irritation, and an oncogenic change always induces an inflammatory microenvironment to promote development of tumors. Inflammatory conditions in selected organs increase the risk of cancer, and in the tumor microenvironment smoldering inflammation contributes to proliferation and cancer progression. Natural bioactive compounds exhibit anti-inflammatory modulation (Pan et al., 2009;Gupta et al., 2011). The dietary flavonoid quercetin and resveratrol have nonsteroidal anti-inflammatory activity that may have applications for anti-inflammation treatment (Donnelly et al., 2004;Tuñón et al., 2009). Our other experiment indicates that the pro-inflammatory cytokine IP-10 in co-cultured human esophageal cancer 9706 cells can be inhibited by the polyphenol quercetin. Prevention of cancer has to be associated with prevention of inflammation, especially chronic inflammation.Flavonoid quercetin is one kind of yellowish powdered crystalline compound, (C15H10O7 in structure with five OH groups), widespread in vegetables, fruits and some

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“…As reported, HDAC1 is required for TGF-b-induced EMT in mouse hepatocytes [33]. Inhibition of HDAC1, by pan-HDAC inhibitors (TSA, NaB) or a HDAC1-selective inhibitor (MS-275) or HDAC1 RNA interfere plasmid, can block TGF-b-induced EMT as examined by cell morphological changes and the levels of ZO-1, Ecadherin, and fibronectin [33].…”

Section: The Expression and Functional Roles Of Hdacsmentioning

confidence: 86%

Epigenetic modifications by histone deacetylases: Biological implications and therapeutic potential in liver fibrosis

et al. 2015

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Histone deacetylase 1 is required for transforming growth factor-β1-induced epithelial–mesenchymal transition

Cited by 75 publications

References 51 publications

Epigenetic regulation of Smad2 and Smad3 by profilin-2 promotes lung cancer growth and metastasis

Epigenetic regulation of Smad2 and Smad3 by profilin-2 promotes lung cancer growth and metastasis

Aberrant Epigenetic Alteration in Eca9706 Cells Modulated by Nanoliposomal Quercetin Combined with Butyrate Mediated via Epigenetic-NF-κB Signaling

Epigenetic modifications by histone deacetylases: Biological implications and therapeutic potential in liver fibrosis

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