The Experts below are selected from a list of 26046 Experts worldwide ranked by ideXlab platform
Lianmei Zhao - One of the best experts on this subject based on the ideXlab platform.
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MTA2 promotes the metastasis of esophageal squamous cell carcinoma via eif4e twist feedback loop
Cancer Science, 2021Co-Authors: Su Li Dai, Lianmei Zhao, Si Si Wei, Cong Zhang, Yue Ping Liu, Zhenzhen Zhang, Baoen ShanAbstract:Metastasis-associated protein 2 (MTA2) is frequently amplified in many types of cancers, however, the role and underlying molecular mechanism of MTA2 in esophageal squamous cell carcinoma (ESCC)remain unknown. Here, we reported that MTA2 is highly expressed in ESCC tissue and cells, and is closely related to the malignant characteristics and poor prognosis of ESCC patients. Through in vitro and in vivo experiments, we demonstrated that MTA2 significantly promoted ESCC growth, metastasis and epithelial-mesenchymal transition (EMT) progression. The integrative analysis combined with expression microarray showed that MTA2 could interact with eukaryotic initiation factor 4E (EIF4E), which positively regulates the expression of Twist, known as a master regulator of EMT. Moreover, the result of Chromatin Immunoprecipitation (ChIP) revealed that MTA2 was recruited to the promoter of E-cadherin by Twist,which reduced the acetylation level of the promoter region and thus inhibited the expression of E-cadherin and subsequently promoted the aggressive progression of ESCC. Collectively, our study provided novel evidence that MTA2 plays an aggressive role in ESCC metastasis by a novel EIF4E-Twist positive feedback loop, which may provide a potential therapeutic target for the management of ESCC.
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snhg5 inhibits the progression of emt through the ubiquitin degradation of MTA2 in oesophageal cancer
Carcinogenesis, 2021Co-Authors: Si Si Wei, Lianmei Zhao, Su Li Dai, Cong Zhang, Shiping Sun, Xinliang Zhou, Yaojie Wang, Baoen ShanAbstract:A substantial fraction of transcripts are known as long noncoding RNAs (lncRNAs), and these transcripts play pivotal roles in the development of cancer. However, little information has been published regarding the functions of lncRNAs in oesophageal squamous cell carcinoma (ESCC) and the underlying mechanisms. In our previous studies, we demonstrated that small nucleolar RNA host gene 5 (SNHG5), a known lncRNA, is dysregulated in gastric cancer (GC). In this study, we explored the expression and function of SNHG5 in development of ESCC. SNHG5 was found to be downregulated in human ESCC tissues and cell lines, and this downregulation was associated with cancer progression, clinical outcomes and survival rates of ESCC patients. Furthermore, we also found that overexpression of SNHG5 significantly inhibited the proliferation, migration and invasion of ESCC cells in vivo and in vitro. Notably, we found that metastasis-associated protein 2 (MTA2) was pulled down by SNHG5 in ESCC cells using RNA pulldown assay. We also found that SNHG5 reversed the epithelial-mesenchymal transition by interacting with MTA2. In addition, overexpression of SNHG5 downregulated the transcription of MTA2 and caused its ubiquitin-mediated degradation. Thus, overexpression of MTA2 partially abrogated the effect of SNHG5 in ESCC cell lines. Furthermore, we found that MTA2 mRNA expression was significantly elevated in ESCC specimens, and a negative correlation between SNHG5 and MTA2 expression was detected. Overall, this study demonstrated, for the first time, that SNHG5-regulated MTA2 functions as an important player in the progression of ESCC and provide a new potential therapeutic strategy for ESCC.
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long non coding rna snhg5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
Oncogene, 2016Co-Authors: Lianmei Zhao, B Zhou, J Feng, Yexiong Li, Li Li, Shang Zhang, Dexian ZhengAbstract:Long non-coding RNA SNHG5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
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long non coding rna snhg5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
Oncogene, 2016Co-Authors: Lianmei Zhao, B Zhou, J Feng, Huiqin Guo, Tao Han, L Liu, Shuyang Zhang, Yongshuo Liu, Juan ShiAbstract:Recently, intriguing new roles for some small nucleolar RNA host genes (SNHGs) in cancer have emerged. In the present study, a panel of SNHGs was profiled to detect aberrantly expressed SNHGs in gastric cancer (GC). The expression of SNHG5 was significantly downregulated in GC and was significantly associated with the formation of a tumor embolus and with the tumor, node and metastasis stage. SNHG5 was a long non-coding RNA, which was a class of non-coding RNA transcripts longer than 200 nucleotides. SNHG5 suppressed GC cell proliferation and metastasis in vitro and in vivo. Furthermore, SNHG5 exerted its function through interacting with MTA2, preventing the translocation of MTA2 from the cytoplasm into the nucleus. SNHG5 overexpression led to significant increases in the acetylation levels of histone H3 and p53, indicating that SNHG5 might affect acetylation by trapping MTA2 in the cytosol, thereby interfering with the formation of the nucleosome remodeling and histone deacetylation complex. This study is the first to demonstrate that SNHG5 is a critical and powerful regulator that is involved in GC progression through trapping MTA2 in the cytosol. These results imply that SNHG5 may be a novel therapeutic target for the treatment of GC.
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up regulation of MTA2 in esophageal squamous carcinoma tissues and its association with the proliferation and migration of esophageal carcinoma kyse510 cells
Tumori, 2015Co-Authors: Su Li Dai, Lianmei Zhao, Wenxuan Cui, Kenan Peng, Juan Shi, Baoen ShanAbstract:Objective: To investigate the expression level of metastasis-associated gene 2 (MTA2) in esophageal cancer tissues and the effect of MTA2 on the proliferation and migration of esophageal cancer KYSE510 cells.Methods: Fifty specimens of esophageal cancer tissues and adjacent para-cancerous tissues were obtained from patients who underwent surgery in Fourth Hospital, Herbei Medical University in 2014. The expression levels of MTA2 and transcription factor specificity protein 1 (Sp1) mRNAs were examined by real-time fluorescent quantitative PCR. After KYSE510 cells transfection with MTA2-siRNA and negative control siRNA, the abilities of proliferation, migration and invasion were detected by MTS and Transwell assay, and the expressions of epithelial-mesenchymal transition (EMT)-related proteins in KYSE510 cells were detected by Western blotting.Results: The expression level of MTA2 mRNA in esophageal cancer tissues was significantly higher than that in adjacent para-cancerous tissues (P < 0.05), and it was corrected with TNM staging, lymph node metastasis and blood vessel invasion (all P < 0.01). The expression level of Sp1 mRNA in esophageal cancer tissues was significantly higher than that in adjacent para-cancerous tissues (P < 0.05), and the expression level of Sp1 mRNA was positively correlated with MTA2 mRNA (r = 0.407, P = 0.028). The capacities of proliferation, migration and invasion of KYSE510 cells in MTA2-siRNA transfection group were lower than those in negative control group (KYSE510 cells transfected with negative control-siRNA) and in blank control group (KYSE510 cells without any transfection) (all P < 0.05). The expression level of E-cadherin protein in KYSE510 cells after transfection with MTA2-siRNA was up-regulated (P < 0.05), and the expression level of N-cadherin, vimentin and CD24 proteins were down-regulated (P < 0.05, P < 0.01 and P < 0.05).Conclusion: The expression level of MTA2 mRNA in esophageal cancer tissues is significantly increased, and it may be related to the higher expression of Sp1. MTA2-siRNA can inhibit the proliferation, migration and invasion of esophageal cancer KYSE510 cells, and this effect may be related to EMT. DOI:10.3781/j.issn.1000-7431.2015.33.533
Dexian Zheng - One of the best experts on this subject based on the ideXlab platform.
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long non coding rna snhg5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
Oncogene, 2016Co-Authors: Lianmei Zhao, B Zhou, J Feng, Yexiong Li, Li Li, Shang Zhang, Dexian ZhengAbstract:Long non-coding RNA SNHG5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
Jun Zhang - One of the best experts on this subject based on the ideXlab platform.
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atypical gata transcription factor trps1 represses gene expression by recruiting chd4 nurd MTA2 and suppresses cell migration and invasion by repressing tp63 expression
Oncogenesis, 2018Co-Authors: Weiguang Liu, Xue Gong, Xue Lin, Yuzhi Wang, Jun Zhang, Liming ChenAbstract:Transcriptional repressor GATA binding 1 (TRPS1), an atypical GATA transcription factor, functions as a transcriptional repressor and is also implicated in human cancers. However, the underlying mechanism of TRPS1 contributing to malignancy remains obscure. In the current study, we report that TRPS1 recognizes both gene proximal and distal transcription start site (TSS) sequences to repress gene expression. Co-IP mass spectrometry and biochemical studies showed that TRPS1 binds to CHD4/NuRD(MTA2). Genome-wide and molecular studies revealed that CHD4/NuRD(MTA2) is required for TRPS1 transcriptional repression. Mechanically, TRPS1 and CHD4/NuRD(MTA2) form precision-guided transcriptional repression machinery in which TRPS1 guides the machinery to specific target sites by recognizing GATA elements, and CHD4/NuRD(MTA2) represses the transcription of target genes. Furthermore, TP63 was identified and validated to be a direct target of TRPS1-CHD4/NuRD(MTA2) complex, which represses TP63 expression by involving decommission of TP63 enhancer in the described precision-guided manner, leading to a reduction of the ΔNp63 level and contributing to migration and invasion of cancer cells.
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MTA2 enhances colony formation and tumor growth of gastric cancer cells through il 11
BMC Cancer, 2015Co-Authors: Chenfei Zhou, Qu Cai, Min Shi, Xuehua Chen, Zhenggang Zhu, Jun ZhangAbstract:We have preliminarily reported MTA2 expression in gastric cancer and its biological functions by using knockdown cell models, while the molecular mechanisms of MTA2 in regulating malignant behaviors are still unclear. MTA2 overexpression models were established by transfection assay in gastric cancer cells BGC-823 and MKN28. Cell proliferation assay, colony formation in soft agar, wound-healing assay and transwell migration assay were performed with MTA2 overexpression and negative control (NC) cells. Subcutaneous xenografts and pulmonary metastasis models by BGC-823/MTA2 and BGC-823/NC cells were used to observe the capacity of growth and metastasis in vivo. Differential gene expression in MTA2 knockdown and overexpression cells was analyzed by microarrays. IL-11, which demonstrated as differential expression in microarray, was detected by real-time PCR, western blot, ELISA and immunohistochemistry staining. Recombinant human IL-11 (rhIL-11) was administrated in cell proliferation and colony formation as rescue assay. The numbers of colonies in soft agar were significantly more in BGC-823/MTA2 and MKN28/MTA2 cells, comparing with those in their NC cells. Capabilities of cell proliferation, wound-healing and cell migration were not significantly changed in MTA2 overexpression cells. The sizes of subcutaneous xenografts and pulmonary metastases of BGC-832/MTA2 cells were significantly larger than those in BGC-823/NC group. Differential expression of IL-11 was identified by genome expression microarray both in MTA2 knockdown and overexpression cells. IL-11 expression was elevated in BGC-823/MTA2 cells, whereas reduced in SGC-7901/shMTA2 cells. Administration of rhIL-11 recovered colony formation capacity of SGC-7901/shMTA2 cells. MTA2 overexpression enhances colony formation and tumor growth of gastric cancer cells, but not plays important role in cancer cell migration and metastasis. IL-11 is one of the downstream effectors of MTA2 in regulating gastric cancer cells growth.
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MTA2 promotes gastric cancer cells invasion and is transcriptionally regulated by sp1
Molecular Cancer, 2013Co-Authors: Chenfei Zhou, Qu Cai, Min Shi, Xuehua Chen, Zhenggang Zhu, Bingya Liu, Jun ZhangAbstract:Background MTA2 gene belongs to metastasis associated family, and is highly expressed in some solid tumors, including gastric cancer. Its biological function in gastric cancer is currently undefined.
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expression of metastasis associated 1 family member 2 MTA2 in gastric cancer and its relationship with transcription factor sp1
Chinese journal of oncology, 2012Co-Authors: Chenfei Zhou, Jun Zhang, Fei Yuan, Bingya Liu, Zhenggang ZhuAbstract:Objective To determine the expression patterns of metastasis associated 1 family member 2 （MTA2） in gastric cancer and non-cancerous gastric mucosa, and analyze its relationship with nuclear transcription factor Sp1 expression. Methods Tissue samples and clinicopathological information from 83 gastric cancer patients, who underwent surgery, were collected from Shanghai Rui Jin Hospital. All samples included cancer tissue and non-cancerous mucosa which was 5 cm away from the tumor lesion. The expression of MTA2 and Sp1 were detected by immunohistochemistry （IHC） staining. The mRNA of MTA2 was also detected by reverse transcription-polymerase chain reaction （RT-PCR）. SPSS software was used for statistical analysis. Results The expression of MTA2 protein was significantly higher in primary lesions of the gastric cancer than that in non-cancerous mucosa by IHC （31.3% vs 12.0% , P 〈 0.01 ）. MTA2 expression was closely reiated with tumor invasion or T staging （X^2 = 5. 677, P 〈 0.05 ）. Yet, no significant relationship was observed between MTA2 expression and other chnieopathological parameters, including the age, sex, tumor differentiation, Lanren classification, lymph node metastasis, distant metastasis, as well as pathological staging. Furthermore, MTA2 expression was concomitant with Sp1 expression （r = 0.320, P 〈 0.05）. Elevated MTA2 expression was observed in Sp1 positive cancer tissues （Xz = 9. 565, P 〈 0.01 ）. RT-PCR results also demonstrated that MTA2 mRNA was also highly expressed in the tissue samples with Sp1 expression. Conclnsions MTA2 is highly expressed in the primary lesions of gastric cancer than that in adjacent non-cancerous tissues, and is closely related with tumor invasion. MTA2 expression is elevated in Sp1 positive gastric cancer. Key words: Gastric neoplasms; Metastasis associated 1 family member 2; Nuclear transcription factor Sp1
B Zhou - One of the best experts on this subject based on the ideXlab platform.
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long non coding rna snhg5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
Oncogene, 2016Co-Authors: Lianmei Zhao, B Zhou, J Feng, Yexiong Li, Li Li, Shang Zhang, Dexian ZhengAbstract:Long non-coding RNA SNHG5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
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long non coding rna snhg5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
Oncogene, 2016Co-Authors: Lianmei Zhao, B Zhou, J Feng, Huiqin Guo, Tao Han, L Liu, Shuyang Zhang, Yongshuo Liu, Juan ShiAbstract:Recently, intriguing new roles for some small nucleolar RNA host genes (SNHGs) in cancer have emerged. In the present study, a panel of SNHGs was profiled to detect aberrantly expressed SNHGs in gastric cancer (GC). The expression of SNHG5 was significantly downregulated in GC and was significantly associated with the formation of a tumor embolus and with the tumor, node and metastasis stage. SNHG5 was a long non-coding RNA, which was a class of non-coding RNA transcripts longer than 200 nucleotides. SNHG5 suppressed GC cell proliferation and metastasis in vitro and in vivo. Furthermore, SNHG5 exerted its function through interacting with MTA2, preventing the translocation of MTA2 from the cytoplasm into the nucleus. SNHG5 overexpression led to significant increases in the acetylation levels of histone H3 and p53, indicating that SNHG5 might affect acetylation by trapping MTA2 in the cytosol, thereby interfering with the formation of the nucleosome remodeling and histone deacetylation complex. This study is the first to demonstrate that SNHG5 is a critical and powerful regulator that is involved in GC progression through trapping MTA2 in the cytosol. These results imply that SNHG5 may be a novel therapeutic target for the treatment of GC.
J Feng - One of the best experts on this subject based on the ideXlab platform.
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long non coding rna snhg5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
Oncogene, 2016Co-Authors: Lianmei Zhao, B Zhou, J Feng, Yexiong Li, Li Li, Shang Zhang, Dexian ZhengAbstract:Long non-coding RNA SNHG5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
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long non coding rna snhg5 suppresses gastric cancer progression by trapping MTA2 in the cytosol
Oncogene, 2016Co-Authors: Lianmei Zhao, B Zhou, J Feng, Huiqin Guo, Tao Han, L Liu, Shuyang Zhang, Yongshuo Liu, Juan ShiAbstract:Recently, intriguing new roles for some small nucleolar RNA host genes (SNHGs) in cancer have emerged. In the present study, a panel of SNHGs was profiled to detect aberrantly expressed SNHGs in gastric cancer (GC). The expression of SNHG5 was significantly downregulated in GC and was significantly associated with the formation of a tumor embolus and with the tumor, node and metastasis stage. SNHG5 was a long non-coding RNA, which was a class of non-coding RNA transcripts longer than 200 nucleotides. SNHG5 suppressed GC cell proliferation and metastasis in vitro and in vivo. Furthermore, SNHG5 exerted its function through interacting with MTA2, preventing the translocation of MTA2 from the cytoplasm into the nucleus. SNHG5 overexpression led to significant increases in the acetylation levels of histone H3 and p53, indicating that SNHG5 might affect acetylation by trapping MTA2 in the cytosol, thereby interfering with the formation of the nucleosome remodeling and histone deacetylation complex. This study is the first to demonstrate that SNHG5 is a critical and powerful regulator that is involved in GC progression through trapping MTA2 in the cytosol. These results imply that SNHG5 may be a novel therapeutic target for the treatment of GC.