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SOX17 restrains proliferation and tumor formation by down-regulating activity of the Wnt/ss-catenin signaling pathway via trans-suppressing ss-catenin in cervical cancer SCIE PubMed Scopus
期刊论文 | 2018 , 9 | CELL DEATH & DISEASE
SCOPUS Cited Count: 1
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Abstract :

The SRY-box containing gene 17 (SOX17) is considered as a regulator in stemness maintenance and a suppressor in some malignant tumors. However, the biological function and molecular mechanism of SOX17 in the process of initiation and progression of cervical cancer remain obscure. In this study, immunohistochemistry showed that the expression of SOX17 was high in the normal cervix, moderate in the high-grade squamous intraepithelial lesion, and low in the cervical cancer. SOX17 inhibited the proliferation and viability of cervical cancer cells in vitro as well as tumor formation in vivo. Additionally, SOX17 induced the cell cycle arrest at the transition from the G(0)/G(1) phase to the S phase. The TOP/FOP-Flash reporter assay and Western blotting showed SOX17 inhibited the activity of the Wnt/ss-catenin signaling pathway in cervical cancer. Further, firefly luciferase reporter assay and quantitative chromatin immunoprecipitation (qChIP) assays confirmed that SOX17 trans-suppressed the expression of ss-catenin by directly binding to the specific region of the ss-catenin promoter. Together, our data demonstrated that SOX17 restrained the proliferation and tumor formation by down-regulating the activity of the Wnt/ss-catenin signaling pathway via trans-suppression of ss-catenin in cervical cancer.

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GB/T 7714 Li, Lu , Yang, Wen-Ting , Zheng, Peng-Sheng et al. SOX17 restrains proliferation and tumor formation by down-regulating activity of the Wnt/ss-catenin signaling pathway via trans-suppressing ss-catenin in cervical cancer [J]. | CELL DEATH & DISEASE , 2018 , 9 .
MLA Li, Lu et al. "SOX17 restrains proliferation and tumor formation by down-regulating activity of the Wnt/ss-catenin signaling pathway via trans-suppressing ss-catenin in cervical cancer" . | CELL DEATH & DISEASE 9 (2018) .
APA Li, Lu , Yang, Wen-Ting , Zheng, Peng-Sheng , Liu, Xiao-Fang . SOX17 restrains proliferation and tumor formation by down-regulating activity of the Wnt/ss-catenin signaling pathway via trans-suppressing ss-catenin in cervical cancer . | CELL DEATH & DISEASE , 2018 , 9 .
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GDF15 promotes the proliferation of cervical cancer cells by phosphorylating AKT1 and Erk1/2 through the receptor ErbB2 SCIE PubMed Scopus
期刊论文 | 2018 , 37 | JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
WoS CC Cited Count: 13 SCOPUS Cited Count: 14
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Background: Growth differentiation factor 15 (GDF15) is a member of the TGF-beta superfamily, and evidence suggests that a substantial amount of GDF15 is secreted in various human cancers, such as ovarian cancer, prostate cancer, and breast cancer, among others. However, the function of GDF15 in cervical cancer has not yet been reported. Methods: Immunohistochemistry was used to detect GDF15 expression in normal cervix and in different cervical cancer lesions. Cell growth curves, MTT, tumor formation assays and flow cytometry were utilized to observe the effects of ectopic GDF15 expression on the proliferation and cell cycle of cervical cancer cells. Real-time PCR, western blotting and immunoprecipitation assays were conducted to measure the expression of genes related to the cell cycle and the PI3K/AKT and MAPK/ERK signaling pathways. A chromatin immunoprecipitation assay was performed to confirm whether C-myc bound to a specific region of the GDF15 promoter. Inhibitor treatment and immunoprecipitation assays were employed to identify the association between GDF15 and ErbB2. Results: GDF15 expression gradually increased during the progression of cervical carcinogenesis. GDF15 promoted cervical cancer cell proliferation via exogenous rhGDF15 treatment or the use of gene editing technology in vitro and in vivo and significantly accelerated the cell cycle transition from G0/G1 to S phase. The expression of p-ErbB2, p-AKT1, p-Erk1/2, CyclinD1 and CyclinE1 was up-regulated and the expression of p21 was down-regulated in GDF15-overexpressing and rhGDF15-treated cervical cancer cells. C-myc trans-activated GDF15 expression by binding to the E-box motifs in the promoter of GDF15 and contributed to the positive feedback of GDF15/C-myc/GDF15. Furthermore, GDF15 bound to ErbB2 in a protein complex in cervical cancer cells. Conclusions: Our data demonstrated that GDF15 promoted the proliferation of cervical cancer cells via the up-regulation of CyclinD1 and CyclinE1 and the down-regulation of p21 through both the PI3K/AKT and MAPK/ERK signaling pathways in a complex with ErbB2.

Keyword :

ErbB2 GDF15 Proliferation Cervical cancer

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GB/T 7714 Li, Shan , Ma, Yan-Min , Zheng, Peng-Sheng et al. GDF15 promotes the proliferation of cervical cancer cells by phosphorylating AKT1 and Erk1/2 through the receptor ErbB2 [J]. | JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH , 2018 , 37 .
MLA Li, Shan et al. "GDF15 promotes the proliferation of cervical cancer cells by phosphorylating AKT1 and Erk1/2 through the receptor ErbB2" . | JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH 37 (2018) .
APA Li, Shan , Ma, Yan-Min , Zheng, Peng-Sheng , Zhang, Ping . GDF15 promotes the proliferation of cervical cancer cells by phosphorylating AKT1 and Erk1/2 through the receptor ErbB2 . | JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH , 2018 , 37 .
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DAX1 promotes cervical cancer cell growth and tumorigenicity through activation of Wnt/beta-catenin pathway via GSK3 beta SCIE PubMed Scopus
期刊论文 | 2018 , 9 | CELL DEATH & DISEASE
WoS CC Cited Count: 7 SCOPUS Cited Count: 9
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DAX1 is well known for its fundamental role in several types of cancer, while its biological role in cervical cancer remains largely unexplored. The expression of DAX1 in cervical carcinoma tissue was examined using immunohistochemistry and western blot. The effects of DAX1 silencing on the cell growth, tumor formation, and CSC (cancer stem cell) characteristics were also investigated. DAX1 expressed a gradual increase from normal cervix to high-grade squamous intraepithelial lesions, and consequently to cervical cancer. Silence of DAX1 significantly inhibited the cell growth, tumorigenicity, and tumorsphere formation. Furthermore, the TOP/FOP-Flash reporter assay revealed that Wnt/beta-catenin pathway was significantly inactivated in DAX1-silenced cervical cancer cells with the downregulation of Wnt/beta-catenin targeting genes, including cyclinD1 and c-myc. Moreover, dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assay confirmed that DAX1 transcriptionally repressed glycogen synthase kinase 3 beta (GSK3 beta), an inhibitor of the Wnt/beta-catenin pathway, by physically interacting with -666 similar to-444 motif on the GSK3 beta promoter. Additionally, the blockage of GSK3 beta by CHIR-99021 resulted in a significant increase of CSC characteristics induced by the silence of DAX1. Our data demonstrated that DAX1 is overexpressed in cervical cancer, and that it promotes cell growth and tumorigenicity through activating Wnt/beta-catenin pathway mediated by GSK3 beta.

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GB/T 7714 Liu, Xiao-Fang , Li, Xue-Yuan , Zheng, Peng-Sheng et al. DAX1 promotes cervical cancer cell growth and tumorigenicity through activation of Wnt/beta-catenin pathway via GSK3 beta [J]. | CELL DEATH & DISEASE , 2018 , 9 .
MLA Liu, Xiao-Fang et al. "DAX1 promotes cervical cancer cell growth and tumorigenicity through activation of Wnt/beta-catenin pathway via GSK3 beta" . | CELL DEATH & DISEASE 9 (2018) .
APA Liu, Xiao-Fang , Li, Xue-Yuan , Zheng, Peng-Sheng , Yang, Wen-Ting . DAX1 promotes cervical cancer cell growth and tumorigenicity through activation of Wnt/beta-catenin pathway via GSK3 beta . | CELL DEATH & DISEASE , 2018 , 9 .
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Complement activation fragment C3a is a sensitive biomarker for patients with recurrent miscarriage SCIE
期刊论文 | 2017 , 10 (4) , 4566-+ | INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY | IF: 1.396
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Abstract :

Purpose: This study aimed to investigate complement activation in recurrent miscarriage (RM) and to identify biomarkers for RM. Methods: A total of 108 female patients who were diagnosed with RM and 120 control female volunteers for reproductive health screening were included in this study. ELISA was used to measure plasma levels of the complement activation fragments C3a, C4a, C5a, and serum levels of anticardiolipin antibodies and anti-beta 2 glycoprotein I. Nephelometric immunoassays were used to measure serum C3 and C4 levels. Results: All complement activation fragment (C3a, C4a and C5a) levels were significantly higher in RM patients than in controls (P < 0.05). Only C3a levels were significantly higher in RM patients with normal C3 or C4 levels than in controls (P < 0.05). C3a levels were significantly higher in RM patients with or without antiphospholipid antibodies than in controls (P < 0.05). Conclusion: Complement activation is a common event that occurs in RM patients. Additionally, the complement activation fragment C3a is a sensitive biomarker for RM patients.

Keyword :

C3a antiphospholipid antibodies Recurrent miscarriage antiphospholipid syndrome complements activation

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GB/T 7714 Chen, Mei , Wang, Li-Ting , Zheng, Peng-Sheng . Complement activation fragment C3a is a sensitive biomarker for patients with recurrent miscarriage [J]. | INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY , 2017 , 10 (4) : 4566-+ .
MLA Chen, Mei et al. "Complement activation fragment C3a is a sensitive biomarker for patients with recurrent miscarriage" . | INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY 10 . 4 (2017) : 4566-+ .
APA Chen, Mei , Wang, Li-Ting , Zheng, Peng-Sheng . Complement activation fragment C3a is a sensitive biomarker for patients with recurrent miscarriage . | INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY , 2017 , 10 (4) , 4566-+ .
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LGR5 promotes cancer stem cell traits and chemoresistance in cervical cancer SCIE PubMed
期刊论文 | 2017 , 8 | CELL DEATH & DISEASE | IF: 5.638
WoS CC Cited Count: 13
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Cancer stem cells (CSCs), also known as tumor-initiating cells, contribute to tumorigenesis, resistance to chemoradiotherapy and recurrence in human cancers, suggesting targeting CSCs may represent a potential therapeutic strategy. Leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5) has recently been found to be a bona fide marker of colorectal CSCs. Our previous study showed that LGR5 functions as a tumor promoter in cervical cancer by activating the Wnt/beta-catenin pathway. However, very little is known about the function or contribution of LGR5 to cervical CSCs. Here, we have modulated the expression of LGR5 using an overexpression vector or short hairpin RNA in cervical cancer cell lines. We demonstrated that elevated LGR5 expression in cervical cancer cells increased tumorsphere-forming efficiency; conferred chemoresistance to cisplatin treatment; augmented cell migration, invasion and clonogenicity; and elevated the levels of stem cell-related transcription factors in vitro. Furthermore, modulated LGR5(+) cells, unlike LGR5-cells, were highly tumorigenic in vivo. In addition, the modulated LGR5+ cells could give rise to both LGR5(+) and LGR5-cells in vitro and in vivo, thereby establishing a cellular hierarchy. Finally, we found that the increased tumorsphere-forming efficiency induced by LGR5 could be regulated through the inhibition or activation of the Wnt/beta-catenin pathway in cervical cancer cells. Taken together, these results indicate that LGR5 has a vital oncogenic role by promoting cervical CSC traits and may represent a potential clinical target.

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GB/T 7714 Cao, Hao-Zhe , Liu, Xiao-Fang , Yang, Wen-Ting et al. LGR5 promotes cancer stem cell traits and chemoresistance in cervical cancer [J]. | CELL DEATH & DISEASE , 2017 , 8 .
MLA Cao, Hao-Zhe et al. "LGR5 promotes cancer stem cell traits and chemoresistance in cervical cancer" . | CELL DEATH & DISEASE 8 (2017) .
APA Cao, Hao-Zhe , Liu, Xiao-Fang , Yang, Wen-Ting , Chen, Qing , Zheng, Peng-Sheng . LGR5 promotes cancer stem cell traits and chemoresistance in cervical cancer . | CELL DEATH & DISEASE , 2017 , 8 .
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BMX/Etk promotes cell proliferation and tumorigenicity of cervical cancer cells through PI3K/AKT/mTOR and STAT3 pathways SCIE PubMed Scopus
期刊论文 | 2017 , 8 (30) , 49238-49252 | ONCOTARGET
WoS CC Cited Count: 8 SCOPUS Cited Count: 7
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Bone marrow X-linked kinase (BMX, also known as Etk) has been reported to be involved in cell proliferation, differentiation, apoptosis, migration and invasion in several types of tumors, but its role in cervical carcinoma remains poorly understood. In this study, we showed that BMX expression exhibits a gradually increasing trend from normal cervical tissue to cervical cancer in situ and then to invasive cervical cancer tissue. Through BMX-IN-1, a potent and irreversible BMX kinase inhibitor, inhibited the expression of BMX, the cell proliferation was significantly decreased. Knockdown of BMX in HeLa and SiHa cervical cancer cell lines using two different silencing technologies, TALEN and shRNA, inhibited cell growth in vitro and suppressed xenograft tumor formation in vivo, whereas overexpression of BMX in the cell line C-33A significantly increased cell proliferation. Furthermore, a mechanism study showed that silencing BMX blocked cell cycle transit from G0/G1 to S or G2/M phase, and knockdown of BMX inhibited the expression of p-AKT and p-STAT3. These results suggested that BMX can promote cell proliferation through PI3K/AKT/mTOR and STAT3 signaling pathways in cervical cancer cells.

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cell proliferation STAT3 BMX cervical carcinoma AKT

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GB/T 7714 Li, Yuanyuan , Cui, Nan , Zheng, Peng-Sheng et al. BMX/Etk promotes cell proliferation and tumorigenicity of cervical cancer cells through PI3K/AKT/mTOR and STAT3 pathways [J]. | ONCOTARGET , 2017 , 8 (30) : 49238-49252 .
MLA Li, Yuanyuan et al. "BMX/Etk promotes cell proliferation and tumorigenicity of cervical cancer cells through PI3K/AKT/mTOR and STAT3 pathways" . | ONCOTARGET 8 . 30 (2017) : 49238-49252 .
APA Li, Yuanyuan , Cui, Nan , Zheng, Peng-Sheng , Yang, Wen-Ting . BMX/Etk promotes cell proliferation and tumorigenicity of cervical cancer cells through PI3K/AKT/mTOR and STAT3 pathways . | ONCOTARGET , 2017 , 8 (30) , 49238-49252 .
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Tafazzin (TAZ) promotes the tumorigenicity of cervical cancer cells and inhibits apoptosis SCIE PubMed Scopus
期刊论文 | 2017 , 12 (5) | PLOS ONE | IF: 2.766
WoS CC Cited Count: 6 SCOPUS Cited Count: 3
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Tafazzin (TAZ) is often aberrantly expressed in some cancers, including rectal cancer and thyroid neoplasms. However, the function of TAZ in cervical cancer cells remains unknown. This study aims to explore the expression and function of TAZ in cervical cancer cells. Here, we determined the expression of TAZ protein in normal cervical tissue (NC, n = 27), high-grade squamous intraepithelial lesions (HSIL, n = 26) and squamous cervical carcinoma (SCC, n = 41) by immunohistochemistry, the expression of TAZ protein gradually increased from NC to HSIL to SCC. TAZ was overexpressed or down-regulated in cervical cancer cells by stably transfecting a TAZ-expressing plasmid or a shRNA plasmid targeting TAZ. In vitro, the cell growth curves and MTT assays showed that TAZ may promote the growth and viability of cervical cancer cells. In vivo, xenografts experiment showed that TAZ may increase tumor-forming ability. The percentage of apoptosis cells analyzed by FACS and TUNEL assays consistently showed that TAZ inhibits apoptosis in cervical cancer cells. Furthermore, the Cleaved Caspase 9 and Cleaved Caspase 3 were down-regulated by TAZ in cervical cancer cells. Taken together, this study demonstrated that TAZ is overexpressed in cervical cancer and may promote tumorigenicity of cervical cancer cells and inhibit apoptosis.

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GB/T 7714 Chen, Mei , Zhang, Yuan , Zheng, Peng-Sheng . Tafazzin (TAZ) promotes the tumorigenicity of cervical cancer cells and inhibits apoptosis [J]. | PLOS ONE , 2017 , 12 (5) .
MLA Chen, Mei et al. "Tafazzin (TAZ) promotes the tumorigenicity of cervical cancer cells and inhibits apoptosis" . | PLOS ONE 12 . 5 (2017) .
APA Chen, Mei , Zhang, Yuan , Zheng, Peng-Sheng . Tafazzin (TAZ) promotes the tumorigenicity of cervical cancer cells and inhibits apoptosis . | PLOS ONE , 2017 , 12 (5) .
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ALDH1在宫颈癌组织中的表达及临床意义
期刊论文 | 2016 , (1) , 45-48,69 | 中国妇幼健康研究
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目的:探讨乙醛脱氢酶1( ALDH1)在正常宫颈组织、宫颈上皮内瘤样病变组织及宫颈浸润癌组织中的表达及临床意义。方法采用免疫细胞化学的方法检测ALDH1蛋白在宫颈癌细胞系HeLa、SiHa、C33A、CaSki和HT-3中的表达,采用免疫组织化学法检测ALDH1蛋白在100例正常宫颈组织、100例宫颈上皮内瘤样病变组织及100例浸润性宫颈癌组织中的表达,同时分析ALDH1的表达与100例宫颈浸润癌患者临床病理特征的关系。结果免疫细胞化学结果显示,ALDH1蛋白在宫颈癌细胞系C33A中的阳性率为42.24%,在HT-3细胞系中表达的阳性率为12.39%,而在宫颈癌细胞系SiHa、HeLa和CaSki中均未检测到ALDH1蛋白的表达。随着正常宫颈、宫颈上皮内瘤样病变到宫颈浸润癌的进展,ALDH1蛋白在正常宫颈组织、宫颈上皮内瘤样病变组织及宫颈癌组织中表达的阳性率分别为28.00%、38.00%和65.00%,ALDH1蛋白的阳性率和评分均逐渐增加(χ2=29.785,P=0.000);Spearman相关性分析结果显示,ALDH1的表达与宫颈癌患者的病理分级、临床分期、盆腔淋巴结转移、肿瘤大小及患者年龄均无显著性差异(均P>0.05)。结论 ALDH1蛋白随着宫颈癌的进展表达逐渐增加,提示其可能作为癌基因参与宫颈癌的发生发展。

Keyword :

肿瘤干细胞 宫颈上皮内瘤样病变 乙醛脱氢酶1 宫颈浸润癌

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GB/T 7714 张丽 , 杨文婷 , 郑鹏生 . ALDH1在宫颈癌组织中的表达及临床意义 [J]. | 中国妇幼健康研究 , 2016 , (1) : 45-48,69 .
MLA 张丽 et al. "ALDH1在宫颈癌组织中的表达及临床意义" . | 中国妇幼健康研究 1 (2016) : 45-48,69 .
APA 张丽 , 杨文婷 , 郑鹏生 . ALDH1在宫颈癌组织中的表达及临床意义 . | 中国妇幼健康研究 , 2016 , (1) , 45-48,69 .
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EZH2-mediated repression of GSK-3 beta and TP53 promotes Wnt/beta-catenin signaling-dependent cell expansion in cervical carcinoma SCIE PubMed Scopus
期刊论文 | 2016 , 7 (24) , 36115-36129 | ONCOTARGET | IF: 5.168
WoS CC Cited Count: 13 SCOPUS Cited Count: 18
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Enhancer of zeste homolog 2 (EZH2), a catalytic core component of the Polycomb repressive complex 2 (PRC2), stimulates the silencing of target genes through histone H3 lysine 27 trimethylation (H3K27me3). Recent findings have indicated EZH2 is involved in the development and progression of various human cancers. However, the exact mechanism of EZH2 in the promotion of cervical cancer is largely unknown. Here, we show that EZH2 expression gradually increases during the progression of cervical cancer. We identified a significant positive correlation between EZH2 expression and cell proliferation in vitro and tumor formation in vivo by the up-regulation or down regulation of EZH2 using CRISPR-Cas9-mediated gene editing technology and shRNA in HeLa and SiHa cells. Further investigation indicated that EZH2 protein significantly accelerated the cell cycle transition from the G0/G1 to S phase. TOP/FOP-Flash reporter assay revealed that EZH2 significantly activated Wnt/beta-catenin signaling and the target genes of Wnt/beta-catenin pathway were up-regulated, including p-catenin, cyclin D1, and c-myc. Moreover, dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays confirmed that EZH2 inhibited the expression of glycogen synthase kinase-3 beta (GSK-3 beta) and TP53 through physically interacting with motifs in the promoters of the GSK-3 beta and TP53 genes. Additionally, blockage of the Wnt/beta-catenin pathway resulted in significant inhibition of cell proliferation, and activation of the Wnt/beta-catenin pathway resulted in significant enhancement of cell proliferation, as induced by EZH2. Taken together, our data demonstrate that EZH2 promotes cell proliferation and tumor formation in cervical cancer through activating the Wnt/beta-catenin pathway by epigenetic silencing via GSK-3 beta and TP53.

Keyword :

GSK3 beta and TP53 EZH2 proliferation cervical cancer Wnt/beta-catenin signaling

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GB/T 7714 Chen, Qian , Zheng, Peng-Sheng , Yang, Wen-Ting . EZH2-mediated repression of GSK-3 beta and TP53 promotes Wnt/beta-catenin signaling-dependent cell expansion in cervical carcinoma [J]. | ONCOTARGET , 2016 , 7 (24) : 36115-36129 .
MLA Chen, Qian et al. "EZH2-mediated repression of GSK-3 beta and TP53 promotes Wnt/beta-catenin signaling-dependent cell expansion in cervical carcinoma" . | ONCOTARGET 7 . 24 (2016) : 36115-36129 .
APA Chen, Qian , Zheng, Peng-Sheng , Yang, Wen-Ting . EZH2-mediated repression of GSK-3 beta and TP53 promotes Wnt/beta-catenin signaling-dependent cell expansion in cervical carcinoma . | ONCOTARGET , 2016 , 7 (24) , 36115-36129 .
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Slug inhibits the proliferation and tumor formation of human cervical cancer cells by up-regulating the p21/p27 proteins and down-regulating the activity of the Wnt/beta-catenin signaling pathway via the trans-suppression Akt1/p-Akt1 expression SCIE PubMed
期刊论文 | 2016 , 7 (18) , 26152-26167 | ONCOTARGET | IF: 5.168
WoS CC Cited Count: 12
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Abstract :

Slug (Snai2) has been demonstrated to act as an oncogene or tumor suppressor in different human cancers, but the function of Slug in cervical cancer remains poorly understood. In this study, we demonstrated that Slug could suppress the proliferation of cervical cancer cells in vitro and tumor formation in vivo. Further experiments found that Slug could trans-suppress the expression of Akt1/p-Akt1 by binding to E-box motifs in the promoter of the Akt1 gene and then inhibit the cell proliferation and tumor formation of cervical cancer cells by up-regulating p21/p27 and/or downregulating the activity of the Wnt/beta-catenin signaling pathway. Therefore, Slug acts as a tumor suppressor during cervical carcinogenesis.

Keyword :

Akt1 proliferation slug cervical cancer wnt/beta-catenin

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GB/T 7714 Cui, Nan , Yang, Wen-Ting , Zheng, Peng-Sheng . Slug inhibits the proliferation and tumor formation of human cervical cancer cells by up-regulating the p21/p27 proteins and down-regulating the activity of the Wnt/beta-catenin signaling pathway via the trans-suppression Akt1/p-Akt1 expression [J]. | ONCOTARGET , 2016 , 7 (18) : 26152-26167 .
MLA Cui, Nan et al. "Slug inhibits the proliferation and tumor formation of human cervical cancer cells by up-regulating the p21/p27 proteins and down-regulating the activity of the Wnt/beta-catenin signaling pathway via the trans-suppression Akt1/p-Akt1 expression" . | ONCOTARGET 7 . 18 (2016) : 26152-26167 .
APA Cui, Nan , Yang, Wen-Ting , Zheng, Peng-Sheng . Slug inhibits the proliferation and tumor formation of human cervical cancer cells by up-regulating the p21/p27 proteins and down-regulating the activity of the Wnt/beta-catenin signaling pathway via the trans-suppression Akt1/p-Akt1 expression . | ONCOTARGET , 2016 , 7 (18) , 26152-26167 .
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