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Screening of Therapeutic Candidate Genes of Quercetin for Cervical Cancer and Analysis of Their Regulatory Network SCIE PubMed
期刊论文 | 2021 , 14 , 857-866 | ONCOTARGETS AND THERAPY
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Abstract :

Purpose: To explore the therapeutic targets and regulatory mechanisms of the antitumor drug quercetin in the treatment of cervical cancer. Methods: Cervical cancer (HeLa) cells were treated with quercetin and subjected to RNA sequencing using the BGISEQ-500 platform. By combined analysis of GEO database and RNA-seq results, the differentially expressed genes (DEGs) (namely, the genes in the GEO database that were upregulated/downregulated in cervical cancer compared with normal cervix and downregulated/upregulated after quercetin treatment) were identified. Functional enrichment and protein-protein interaction analyses were carried out for the DEGs. The candidate genes were identified using the Gentiscape2.2 and MCODE plug-ins for Cytoscape software, and the upstream miRNAs, lncRNAs, and circRNAs of the candidate genes were predicted using the online tools MirDIP, TarBase, and ENCORI. Finally, the regulatory network was constructed using Cytoscape software. Results: Quercetin significantly inhibited the proliferation of cervical cancer cells. The combined analyses of the GEO database and RNA-seq results obtained 74 DEGs, and the functional enrichment analysis of the DEGs identified 861 biological processes, 32 cellular components, 50 molecular functions, and 56 KEGG pathways. Five therapeutic candidate genes, including EGFR, JUN, AR, CD44, and MUC1, were selected, and 10 miRNAs, 1 lncRNA, and 71 circRNAs upstream of these genes were identified. Finally, a lncRNA/circRNA-miRNA-mRNA-pathway regulatory network was constructed. Conclusion: In this study, data mining was used to identify candidate genes and their regulatory network for the treatment of cervical cancer to provide a theoretical basis for targeted therapy of cervical cancer.

Keyword :

quercetin candidate genes RNA-seq analysis regulatory network cervical cancer GEO DEGs

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GB/T 7714 Li, Yuanyuan , Kou, Jiushe , Wu, Tao et al. Screening of Therapeutic Candidate Genes of Quercetin for Cervical Cancer and Analysis of Their Regulatory Network [J]. | ONCOTARGETS AND THERAPY , 2021 , 14 : 857-866 .
MLA Li, Yuanyuan et al. "Screening of Therapeutic Candidate Genes of Quercetin for Cervical Cancer and Analysis of Their Regulatory Network" . | ONCOTARGETS AND THERAPY 14 (2021) : 857-866 .
APA Li, Yuanyuan , Kou, Jiushe , Wu, Tao , Zheng, Pengsheng , Chao, Xu . Screening of Therapeutic Candidate Genes of Quercetin for Cervical Cancer and Analysis of Their Regulatory Network . | ONCOTARGETS AND THERAPY , 2021 , 14 , 857-866 .
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Msi1 inhibits cervical cancer cell apoptosis by downregulating BAK through AKT signaling SCIE PubMed
期刊论文 | 2021 , 12 (8) , 2422-2429 | JOURNAL OF CANCER
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Musashi-1 (Msi1) is an RNA binding protein that functions as a regulator in multiple carcinomas. Our previous study demonstrated that Msi1 could promote the proliferation of cervical cancer cells by targeting the cell cycle proteins P21, P27 and P53. However, the mechanisms by which Msi1 affects the survival of cervical cancer cells, such as apoptosis, are still unclear. In this study, we found that the expression of Msi1 inhibited cervical cancer cell apoptosis in vitro and in vivo. Furthermore, the expression of Msi1 downregulated the expression of PTEN, while AKT signaling was activated, which resulted in a reduction in the proapoptotic protein BAK. In addition, rescue the expression of BAK in Msi1 expressing cervical cancer cells induced the increase of apoptosis cells. These findings indicate that Msi1 regulates cervical cancer cell apoptosis by inhibiting PTEN and activating AKT signaling, which leads to the downregulation of BAK.

Keyword :

AKT signaling cervical cancer Msi1 apoptosis

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GB/T 7714 Liu, Xian , Zhang, Yanru , Zheng, PengSheng et al. Msi1 inhibits cervical cancer cell apoptosis by downregulating BAK through AKT signaling [J]. | JOURNAL OF CANCER , 2021 , 12 (8) : 2422-2429 .
MLA Liu, Xian et al. "Msi1 inhibits cervical cancer cell apoptosis by downregulating BAK through AKT signaling" . | JOURNAL OF CANCER 12 . 8 (2021) : 2422-2429 .
APA Liu, Xian , Zhang, Yanru , Zheng, PengSheng , Cui, Nan . Msi1 inhibits cervical cancer cell apoptosis by downregulating BAK through AKT signaling . | JOURNAL OF CANCER , 2021 , 12 (8) , 2422-2429 .
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Absence of EpCAM in cervical cancer cells is involved in sluginduced epithelial-mesenchymal transition SCIE PubMed
期刊论文 | 2021 , 21 (1) | CANCER CELL INTERNATIONAL
WoS CC Cited Count: 1
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Background Slug (Snai2) is a pivotal player in initiating epithelial-mesenchymal transition (EMT) through its trans-suppression effect on E-cadherin in various normal and malignant cells. In this study, the positive effect of Slug on promoting cell motility and metastasis in cervical cancer was further confirmed in this study. Methods RNA-Seq was performed to explore the potential molecules that participate in Slug-mediated EMT in cervical cancer cells. The negative correlation between Slug and EpCAM expression in cervical cancer cells was detected in this study, and linked them with in vitro migration and invasion assay, in vivo metastasis experiments, luciferase reporter assay and Chromatin immunoprecipitation. Results Transcriptome sequencing analysis revealed that epithelial cell adhesion molecule (EpCAM) was significantly decreased in Slug-overexpressing SiHa cells. Simultaneously, an absence of EpCAM expression was observed in Slug-overexpressing cells. Further studies revealed the trans-suppression effect of Slug on EpCAM through its binding to the E-boxes in the proximal promoter region of EpCAM in cervical cancer cells. Restoring EpCAM in Slug-overexpressing cells by transiently transfecting an EpCAM recombinant plasmid attenuated cell motility and promoted cell growth. Moreover, the negative correlation between Slug and EpCAM expression in human squamous cervical carcinoma (SCC) samples was verified by using Pearson correlation analysis. Conclusions These results demonstrated that the absence of EpCAM under Slug expression in cervical cancer cells probably participated in Slug-regulated EMT and further promoted tumor metastasis. Additionally, this study supports a potential way for Slug to initiate EMT progression in cervical cancer cells in addition to inhibiting E-cadherin.

Keyword :

Slug Cervical cancer EpCAM Metastasis EMT

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GB/T 7714 Liu, Xian , Feng, Qian , Zhang, Yanru et al. Absence of EpCAM in cervical cancer cells is involved in sluginduced epithelial-mesenchymal transition [J]. | CANCER CELL INTERNATIONAL , 2021 , 21 (1) .
MLA Liu, Xian et al. "Absence of EpCAM in cervical cancer cells is involved in sluginduced epithelial-mesenchymal transition" . | CANCER CELL INTERNATIONAL 21 . 1 (2021) .
APA Liu, Xian , Feng, Qian , Zhang, Yanru , Zheng, PengSheng , Cui, Nan . Absence of EpCAM in cervical cancer cells is involved in sluginduced epithelial-mesenchymal transition . | CANCER CELL INTERNATIONAL , 2021 , 21 (1) .
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PRDM4 inhibits cell proliferation and tumorigenesis by inactivating the PI3K/AKT signaling pathway through targeting of PTEN in cervical carcinoma SCIE PubMed
期刊论文 | 2021 , 40 (18) , 3318-3330 | ONCOGENE
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PR domain zinc finger protein 4 (PRDM4) is a transcription factor that plays key roles in stem cell self-renewal and tumorigenesis. However, its biological role and exact mechanism in cervical cancer remain unknown. Here, both immunohistochemistry (IHC) and Western blot assays demonstrated that the expression of PRDM4 in cervical cancer tissues was much lower than that in the normal cervix. A xenograft assay showed that PRDM4 overexpression in the cervical cancer cell lines SiHa and HeLa dramatically inhibited cell proliferation and tumorigenic potential in vivo. Conversely, the silencing of PRDM4 promoted cervical cancer cell proliferation and tumorigenic potential. Mechanistically, PRDM4 induced cell cycle arrest at the transition from G0/G1 phase to S phase by upregulating p27 and p21 expression and downregulating Cyclin D1 and CDK4 expression. Furthermore, the PI3K/AKT signaling pathway was inactivated in PRDM4-overexpressing cells, which decreased the levels of p-AKT and upregulated the expression of PTEN, an inhibitor of the PI3K/AKT signaling pathway, at both the transcriptional and translational levels. Dual-luciferase reporter assays and qChIP assays confirmed that PRDM4 transactivated the expression of PTEN by binding to two specific regions in the PTEN promoter. Furthermore, PTEN silencing or a PTEN inhibitor rescued the cell defects induced by PRDM4 overexpression. Therefore, our data suggest that PRDM4 inhibits cell proliferation and tumorigenesis by downregulating the activity of the PI3K/AKT signaling pathway by directly transactivating PTEN expression in cervical cancer.

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GB/T 7714 Yang, Wen-Ting , Chen, Mei , Xu, Rui et al. PRDM4 inhibits cell proliferation and tumorigenesis by inactivating the PI3K/AKT signaling pathway through targeting of PTEN in cervical carcinoma [J]. | ONCOGENE , 2021 , 40 (18) : 3318-3330 .
MLA Yang, Wen-Ting et al. "PRDM4 inhibits cell proliferation and tumorigenesis by inactivating the PI3K/AKT signaling pathway through targeting of PTEN in cervical carcinoma" . | ONCOGENE 40 . 18 (2021) : 3318-3330 .
APA Yang, Wen-Ting , Chen, Mei , Xu, Rui , Zheng, Peng-Sheng . PRDM4 inhibits cell proliferation and tumorigenesis by inactivating the PI3K/AKT signaling pathway through targeting of PTEN in cervical carcinoma . | ONCOGENE , 2021 , 40 (18) , 3318-3330 .
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HOXB4 inhibits the proliferation and tumorigenesis of cervical cancer cells by downregulating the activity of Wnt/beta-catenin signaling pathway SCIE PubMed
期刊论文 | 2021 , 12 (1) | CELL DEATH & DISEASE
WoS CC Cited Count: 4
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Homeobox B4 (HOXB4), which belongs to the homeobox (HOX) family, possesses transcription factor activity and has a crucial role in stem cell self-renewal and tumorigenesis. However, its biological function and exact mechanism in cervical cancer remain unknown. Here, we found that HOXB4 was markedly downregulated in cervical cancer. We demonstrated that HOXB4 obviously suppressed cervical cancer cell proliferation and tumorigenic potential in nude mice. Additionally, HOXB4-induced cell cycle arrest at the transition from the G0/G1 phase to the S phase. Conversely, loss of HOXB4 promoted cervical cancer cell growth both in vitro and in vivo. Bioinformatics analyses and mechanistic studies revealed that HOXB4 inhibited the activity of the Wnt/beta -catenin signaling pathway by direct transcriptional repression of beta -catenin. Furthermore, beta -catenin re-expression rescued HOXB4-induced cervical cancer cell defects. Taken together, these findings suggested that HOXB4 directly transcriptional repressed beta -catenin and subsequently inactivated the Wnt/beta -catenin signaling pathway, leading to significant inhibition of cervical cancer cell growth and tumor formation.

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GB/T 7714 Lei, Dan , Yang, Wen-Ting , Zheng, Peng-Sheng . HOXB4 inhibits the proliferation and tumorigenesis of cervical cancer cells by downregulating the activity of Wnt/beta-catenin signaling pathway [J]. | CELL DEATH & DISEASE , 2021 , 12 (1) .
MLA Lei, Dan et al. "HOXB4 inhibits the proliferation and tumorigenesis of cervical cancer cells by downregulating the activity of Wnt/beta-catenin signaling pathway" . | CELL DEATH & DISEASE 12 . 1 (2021) .
APA Lei, Dan , Yang, Wen-Ting , Zheng, Peng-Sheng . HOXB4 inhibits the proliferation and tumorigenesis of cervical cancer cells by downregulating the activity of Wnt/beta-catenin signaling pathway . | CELL DEATH & DISEASE , 2021 , 12 (1) .
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LGR6 activates the Wnt/beta-catenin signaling pathway and forms a beta-catenin/TCF7L2/LGR6 feedback loop in LGR6(high) cervical cancer stem cells SCIE PubMed
期刊论文 | 2021 , 40 (42) , 6103-6114 | ONCOGENE
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The leucine-rich repeat-containing G-protein-coupled receptor 6 (LGR6) is considered to be a stem cell marker in many normal tissues and promotes tissue development, regeneration, and repair. LGR6 is also related to the initiation and progression of some malignant tumors. However, the role of LGR6 in cervical cancer has not been reported. Here, immunohistochemistry and western blotting showed that LGR6 was significantly upregulated in cervical cancer, compared with the normal cervix. By analyzing The Cancer Genome Atlas database, LGR6 was found to be correlated with a poor prognosis of cervical cancer. Then, a small population of LGR6(high) cells isolated by using the fluorescence-activated cell sorting exhibited enhanced properties of cancer stem cells including self-renewal, differentiation, and tumorigenicity. Moreover, RNA sequencing revealed that LGR6 was correlated with the Wnt signaling pathway and TOP/FOP, reverse transcription-PCR, and western blotting further proved that LGR6 could activate the Wnt/beta-catenin signaling pathway. Interestingly, LGR6 upregulated the expression of TCF7L2 by activating the Wnt/beta-catenin pathway. Then, TCF7L2 combining with beta-catenin in the nucleus enhanced LGR6 transcription by binding the promoter of LGR6, which further activated the Wnt signaling to form a positive feedback loop. Thus, our study demonstrated that LGR6 activated a novel beta-catenin/TCF7L2/LGR6-positive feedback loop in LGR6(high) cervical cancer stem cells (CSCs), which provided a new therapeutic strategy for targeting cervical CSCs to improve the prognosis of cervical cancer patients.

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GB/T 7714 Feng, Qian , Li, Shan , Ma, Hong-Mei et al. LGR6 activates the Wnt/beta-catenin signaling pathway and forms a beta-catenin/TCF7L2/LGR6 feedback loop in LGR6(high) cervical cancer stem cells [J]. | ONCOGENE , 2021 , 40 (42) : 6103-6114 .
MLA Feng, Qian et al. "LGR6 activates the Wnt/beta-catenin signaling pathway and forms a beta-catenin/TCF7L2/LGR6 feedback loop in LGR6(high) cervical cancer stem cells" . | ONCOGENE 40 . 42 (2021) : 6103-6114 .
APA Feng, Qian , Li, Shan , Ma, Hong-Mei , Yang, Wen-Ting , Zheng, Peng-Sheng . LGR6 activates the Wnt/beta-catenin signaling pathway and forms a beta-catenin/TCF7L2/LGR6 feedback loop in LGR6(high) cervical cancer stem cells . | ONCOGENE , 2021 , 40 (42) , 6103-6114 .
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Hexokinases 2 promoted cell motility and distant metastasis by elevating fibronectin through Akt1/p-Akt1 in cervical cancer cells SCIE PubMed
期刊论文 | 2021 , 21 (1) | CANCER CELL INTERNATIONAL
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Background Hexokinases 2 (HK2) is a member of the hexokinases, linking with malignant tumor growth and distant metastasis. However, evidence regarding the potential role of HK2 in regulating cell motility and tumor metastasis during the cervical cancer malignant progression remains limited. Methods In vitro migration and invasion assay, in vivo metastasis experiments were performed to detect the effective of HK2 on regulating cell motility and tumor metastasis in cervical cancer cells. RNA-Seq was performed to explore the potential molecules that participate in HK2-mediated cell motility and tumor metastasis in cervical cancer cells. The correlation between HK2 and Akt1, p-Akt1, FN1 expression in cervical cancer cells and human squamous cervical carcinoma (SCC) samples was verified in this study. Results In this study, cervical cancer cells with exogenous HK2 expression exhibited enhanced cell motility and distant metastasis. Transcriptome sequencing analysis revealed that fibronectin (FN1) was significantly increased in HK2-overexpressing HeLa cells, and the PI3K/Akt signaling pathway was identified by KEGG pathway enrichment analysis. Further studies demonstrated that this promotion of cell motility by HK2 was probably a result of it inducing FN1, MMP2 and MMP9 expression by activating Akt1 in cervical cancer cells. Additionally, HK2 expression was altered with the changing of Akt1/p-Akt1 expression, implying that HK2 expression is also modulated by Akt1/p-Akt1. Moreover, the positive correlation between HK2 and Akt1, p-Akt1, FN1 expression in human squamous cervical carcinoma (SCC) samples was verified by using Pearson correlation analysis. Conclusions This study demonstrated that HK2 could activate Akt1 in cervical cancer cells, subsequently enhancing cell motility and tumor metastasis by inducing FN1, MMP2 and MMP9 expression. There likely exists an interactive regulatory mechanism between HK2 and Akt1 during the malignant process of cervical cancer.

Keyword :

Cervical cancer Fibronectin (FN1) Metastasis Akt1 HK2

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GB/T 7714 Chen, Qian , Li, Lu , Liu, Xian et al. Hexokinases 2 promoted cell motility and distant metastasis by elevating fibronectin through Akt1/p-Akt1 in cervical cancer cells [J]. | CANCER CELL INTERNATIONAL , 2021 , 21 (1) .
MLA Chen, Qian et al. "Hexokinases 2 promoted cell motility and distant metastasis by elevating fibronectin through Akt1/p-Akt1 in cervical cancer cells" . | CANCER CELL INTERNATIONAL 21 . 1 (2021) .
APA Chen, Qian , Li, Lu , Liu, Xian , Feng, Qian , Zhang, Yanru , Zheng, Pengsheng et al. Hexokinases 2 promoted cell motility and distant metastasis by elevating fibronectin through Akt1/p-Akt1 in cervical cancer cells . | CANCER CELL INTERNATIONAL , 2021 , 21 (1) .
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Analysis of parental abnormal chromosomal karyotype and subsequent live births in Chinese couples with recurrent pregnancy loss SCIE PubMed
期刊论文 | 2021 , 11 (1) | SCIENTIFIC REPORTS
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The frequency and distribution of chromosomal abnormalities and the impact of parental chromosomal aberration on the pregnancy outcomes of couples with recurrent pregnancy loss remains controversial. 3235 RPL couples who experienced two or more miscarriages before 20 weeks were diagnosed in our tertiary referral hospital during 2008-2018 and included in the single-center retrospective cohort study covering a 10-year period. Chromosome aberration was detected in 121 (3.74%) among 3235 RPL couples which included 75 female and 46 male cases at an individual level. 101 cases were structural aberrations including balanced translocations in 46(38.0%) cases, Robertsonian translocations in 13(10.7%) cases, inversions in 42(34.7%) cases and 20(16.5%) cases were numerical aberrations. 121 carriers and 428 non-carriers were followed up for two years, 55 carriers and 229 non-carriers were subsequent pregnant after diagnosis by natural conception or intrauterine insemination. The frequency of carriers to have a health newborn was not significantly different with non-carriers (72.7% vs. 71.2%, adjusted P = 0.968). This study described the majority of carriers were balanced translocations and chromosome aberrations had a limited influence on live birth rate from the present data. The results of the study also remind us that natural conception may be also a good alternative rather than PGD (Pre-implantation Genetic Diagnosis) which is common in many other reproductive centers for such patients.

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GB/T 7714 Li, Shan , Chen, Mei , Zheng, Peng-Sheng . Analysis of parental abnormal chromosomal karyotype and subsequent live births in Chinese couples with recurrent pregnancy loss [J]. | SCIENTIFIC REPORTS , 2021 , 11 (1) .
MLA Li, Shan et al. "Analysis of parental abnormal chromosomal karyotype and subsequent live births in Chinese couples with recurrent pregnancy loss" . | SCIENTIFIC REPORTS 11 . 1 (2021) .
APA Li, Shan , Chen, Mei , Zheng, Peng-Sheng . Analysis of parental abnormal chromosomal karyotype and subsequent live births in Chinese couples with recurrent pregnancy loss . | SCIENTIFIC REPORTS , 2021 , 11 (1) .
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外源性过表达SALL4B对SiHa细胞增殖及凋亡的影响
期刊论文 | 2020 , 51 (12) , 1295-1300 | 山西医科大学学报
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目的 探讨SALL4B对SiHa细胞增殖和凋亡的影响及其可能分子机制.方法 采用分子克隆技术构建SALL4B过表达质粒pCAG-IRES2-AcGFP1-Neo-SALL4B,分别将空质粒pCAG-IRES2-AcGFP1-Neo和SALL4B过表达质粒转染至SiHa细胞,通过G418筛选稳定过表达SALL4B的SiHa细胞株.转染空质粒的SiHa细胞命名为SiHa-GFP组,转染SALL4B过表达质粒的SiHa细胞命名为SiHa-SALL4B组.采用细胞计数和CCK-8实验观察SALL4B对SiHa细胞增殖能力的影响.应用流式细胞仪分析SiHa细胞中SALL4B对细胞周期和细胞凋亡的影响.应用Western blot检测在SiHa-SALL4B及SiHa-GFP细胞中β-catenin蛋白的表达情况.结果 成功构建了SALL4B过表达的SiHa细胞株.与SiHa-GFP组相比,SiHa-SALL4B组细胞增殖能力和细胞活力均显著提高(P<0.05).SiHa-SALL4B组细胞处于G0/G1期的细胞比例明显低于SiHa-GFP组(59.13%±3.59%vs 65.31%±2.88%,P<0.05),而处于S期的细胞比例明显高于SiHa-GFP组(31.15%±5.78%vs 23.07%±4.96%,P<0.01).SiHa-SALL4B组凋亡细胞的比例显著低于SiHa-GFP组(8.06%±1.37%vs 13.77%±1.72%,P<0.01).与SiHa-GFP组比较,SiHa-SALL4B组细胞中β-catenin蛋白的表达水平显著上调(P<0.01).结论 SALL4B基因在SiHa细胞的增殖和凋亡中发挥重要作用,该作用可能与Wnt/β-catenin信号通路有关.

Keyword :

细胞增殖 β-连环蛋白 SiHa细胞 SALL4B 细胞凋亡

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GB/T 7714 陈梅 , 郑鹏生 . 外源性过表达SALL4B对SiHa细胞增殖及凋亡的影响 [J]. | 山西医科大学学报 , 2020 , 51 (12) : 1295-1300 .
MLA 陈梅 et al. "外源性过表达SALL4B对SiHa细胞增殖及凋亡的影响" . | 山西医科大学学报 51 . 12 (2020) : 1295-1300 .
APA 陈梅 , 郑鹏生 . 外源性过表达SALL4B对SiHa细胞增殖及凋亡的影响 . | 山西医科大学学报 , 2020 , 51 (12) , 1295-1300 .
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NF-YA promotes the cell proliferation and tumorigenic properties by transcriptional activation of SOX2 in cervical cancer SCIE PubMed
期刊论文 | 2020 , 24 (21) , 12464-12475 | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | IF: 5.31
WoS CC Cited Count: 2
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NF-YA is considered as a crucial regulator for the maintenance of cancer stem cell (CSC) and involved in various types of malignant tumours. However, the exact function and molecular mechanisms of NF-YA in the progression of cervical cancer remains poorly understood. Here, the expression of NF-YA detected by immunohistochemistry was gradually increased from normal cervical tissues, to the high-grade squamous intraepithelial lesions, and then to cervical cancer tissues. NF-YA promoted the cell proliferation and tumorigenic properties of cervical cancer cells as well as tumorsphere formation and chemoresistancein vitro. The luciferase reporter assay combined with mutagenesis analyses and Western blotting showed that NF-YA trans-activated the expression of SOX2 in cervical cancer. Furthermore, quantitative chromatin immunoprecipitation (qChIP) and electrophoretic mobility shift assay (EMSA) confirmed that NF-YA protein directly bound to the CCAAT box region located upstream of the SOX2 promoter. Together, our data demonstrated that NF-YA was highly expressed in cervical cancer and promoted the cell proliferation, tumorigenicity and CSC characteristic by trans-activating the expression of SOX2.

Keyword :

cancer stem cell cervical cancer NF-YA SOX2

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GB/T 7714 Yang, Wen-Ting , Feng, Qian , Ma, Hong-Mei et al. NF-YA promotes the cell proliferation and tumorigenic properties by transcriptional activation of SOX2 in cervical cancer [J]. | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE , 2020 , 24 (21) : 12464-12475 .
MLA Yang, Wen-Ting et al. "NF-YA promotes the cell proliferation and tumorigenic properties by transcriptional activation of SOX2 in cervical cancer" . | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 24 . 21 (2020) : 12464-12475 .
APA Yang, Wen-Ting , Feng, Qian , Ma, Hong-Mei , Lei, Dan , Zheng, Peng-Sheng . NF-YA promotes the cell proliferation and tumorigenic properties by transcriptional activation of SOX2 in cervical cancer . | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE , 2020 , 24 (21) , 12464-12475 .
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