Effects of Down-regulation of HDAC6 Expression on Proliferation, Cell Cycling and Migration of Esophageal Squamous Cell Carcinoma Cells and Related Molecular Mechanisms

Li, Ning; Xiaojing, Tie; Liu, Peijie; Zhang, Yan; Ren, Hongzheng; Gào, Xin

doi:10.7314/apjcp.2013.14.2.685

Cited by 13 publications

(9 citation statements)

References 22 publications

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“…Our results are consistent with the functions of other HDACs in other cancer types. For example, Hrzenjak at al reported that HDAC2 down-regulation results in increased p21 expression [ 35 ]; Wilson et al showed that up-regulation of HDAC3 leads to inhibition of p21 expression, and that HDAC3 silencing enhances the expression of p21 in colon cancer cells [ 36 ]; Li et al found that HDAC6 down-regulation increases p21 expression and cell cycle arrest in EC9706 cells [ 37 ]. Our results further show that down-regulation of HDAC4 elevates p27 expression in EC cell, indicating that p27 is also involved in HDAC4-mediated cell cycle arrest, which has not been previously reported.…”

Section: Discussionmentioning

confidence: 99%

“…Our results are consistent with previous reports on other HDACs in cancer cells. In 2013, Li et al reported that down-regulation of HDAC6 reduces the migration of ESCC cells by inhibiting EMT [ 37 ]. Hsieh et al found that HDAC6 is required for phthalate-induced cell migration and invasion during EMT in vitro and metastasis into the lungs in nude mice [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

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Overexpressed HDAC4 is associated with poor survival and promotes tumor progression in esophageal carcinoma

Zeng¹,

Yang²,

Wen

et al. 2016

Aging

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Histone deacetylases (HDACs) mediate histone deacetylation, leading to transcriptional repression, which is involved in many diseases, including age-related tissue degeneration, heart failure and cancer. In this study, we were aimed to investigate the expression, clinical significance and biological function of HDAC4 in esophageal carcinoma (EC). We found that HDAC4 mRNA and protein are overexpressed in esophageal squamous cell carcinoma (ESCC) tissues and cell lines. HDAC4 overexpression is associated with higher tumor grade, advanced clinical stage and poor survival. Mechanistically, HDAC4 promotes proliferation and G1/S cell cycle progression in EC cells by inhibiting cyclin-dependent kinase (CDK) inhibitors p21 and p27 and up-regulating CDK2/4 and CDK-dependent Rb phosphorylation. HDAC4 also enhances ESCC cell migration. Furthermore, HDAC4 positively regulates epithelial-mesenchymal transition (EMT) by increasing the expression of Vimentin and decreasing the expression of E-Cadherin/α-Catenin. Together, our study shows that HDAC4 overexpression is important for the oncogenesis of EC, which may serve as a useful prognostic biomarker and therapeutic target for this malignancy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Overexpressed HDAC4 is associated with poor survival and promotes tumor progression in esophageal carcinoma

Zeng¹,

Yang²,

Wen

et al. 2016

Aging

View full text Add to dashboard Cite

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“…Li (Li et al, 2013) found that HDAC6 siRNA can effectively downregulate the expression of HDAC6 mRNA and protein in EC9706 cells. Down-regulation of HDAC6 expression can obviously inhibit cell proliferation, arrest cell cycling in the G0/G1 phase and reduce cell migration.…”

Section: Discussionmentioning

confidence: 99%

Effects of PLCE1 Gene Silencing by RNA Interference on Cell Cycling and Apoptosis in Esophageal Carcinoma Cells

Zhao¹,

Wei²,

Yang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Esophageal squamous cell carcinoma (ESCC) is one of the most malignancies with a poor prognosis. The phospholipase Cε gene (PLCE1) encodes a novel ras-related protein effector mediating the effects of R-Ras on the actin cytoskeleton and membrane protrusion. However, molecular mechanisms pertinent to ESCC are unclear. We therefore designed PLCE1-special small interfering RNA and transfected to esophageal squamous cell (EC) 9706 cells to investigat the effects of PLCE1 gene silencing on the cell cycle and apoptosis of ESCC and indicate its important role in the development of ESCC. Esophageal cancer tissue specimens and normal esophageal mucosa were obtained and assayed by immunohistochemical staining to confirm overexpression of PLCE1 in neoplasias. Fluorescence microscopy was used to examine transfection efficiency, while the result of PLCE1 silencing was examined by reverse transcription (RT-PCR). Flow cytometry and annexin V apoptosis assays were used to assess the cell cycle and apoptosis, respectively. Expression of cyclin D1 and caspase-3 was detected by Western-blotting. The level of PLCE1 protein in esophageal cancer tissue was significantly higher than that in normal tissue. After transfection, the expression of PLCE1 mRNA in EC 9706 was significantly reduced, compared with the control group. Furthermore, flow cytometry results suggested that the PLCE1 gene silencing arrested the cell cycle in the G0/G1 phase; apoptosis was significantly higher than in the negative control group and mock group. PLCE1 gene silencing by RNAi resulted in decreased expression of cyclin D1 and increased expression of caspase-3. Our study suggests that PLCE1 may be an oncogene and play an important role in esophageal carcinogenesis through regulating proteins which control cell cycling and apoptosis.

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“…Thus we assume that matrine may prove to be a valuable tool for inducing cell cycle arrest at G0/G1 phase. In the repression of gene transcription expression, histone deacetylases (HDACs) play a significant role by changing chromatin structure (Thiagalingam et al, 2003) and affecting proliferation, cell cycling, apoptosis, differentiation, DNA replication, DNA damage response and migration of cancer cells (Langer et al, 2010;Li et al, 2013a). It has been reported that over-expression of HDACs has been detected in lung cancer tissues (Sasaki et al, 2004;Krusche et al, 2005;Nakagawa et al, 2007;Fritzsche et al, 2008;Weichert et al, 2008a;Weichert et al, 2008b;Kallsen et al, 2012) and that the expression of HDAC promotes the progress of lung cancer (Zhang et al, 2012b).…”

Section: Discussionmentioning

confidence: 99%

Matrine Reduces Proliferation of Human Lung Cancer Cells by Inducing Apoptosis and Changing miRNA Expression Profiles

Liu

Li²,

Qin³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Effects of Down-regulation of HDAC6 Expression on Proliferation, Cell Cycling and Migration of Esophageal Squamous Cell Carcinoma Cells and Related Molecular Mechanisms

Cited by 13 publications

References 22 publications

Overexpressed HDAC4 is associated with poor survival and promotes tumor progression in esophageal carcinoma

Overexpressed HDAC4 is associated with poor survival and promotes tumor progression in esophageal carcinoma

Effects of PLCE1 Gene Silencing by RNA Interference on Cell Cycling and Apoptosis in Esophageal Carcinoma Cells

Matrine Reduces Proliferation of Human Lung Cancer Cells by Inducing Apoptosis and Changing miRNA Expression Profiles

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