scholarly journals HPV16 E6-178G/E7-647G Promotes Proliferation and Inhibits Apoptosis in Cervical Cancer C33A Cells

2021 ◽  
Author(s):  
Xiangyi Zhe ◽  
Huizhen Xin ◽  
Chunhe Zhang ◽  
Zhenzhen Pan ◽  
Dongmei Li ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Flow Cytometry ◽  
Cell Proliferation ◽  
Cell Cloning ◽  
Proliferation Assay ◽  
Hpv16 E6 ◽  
Proliferation And Apoptosis ◽  
Cervical Cancer Cells ◽  
Cloning Assay

Abstract Background：HPV16 is the main cause of cervical cancer. In our study, we aimed to investigate the role of HPV mutants HPV16 E6-178G/E7-647G in the proliferation and apoptosis of cervical cancer C33A cells. Methods：Plasmids encoding the HPV16 E7 prototype (E7-647A)-GV144, E7 mutant (E7-647G)-GV144, HPV16 E6/E7 prototype (E6-178T/E7-647A)-GV144, and E6/E7 mutant (E6-178G/E7-647G)-GV144 were stably transfected into cervical cancer C33A cells. Western blot analysis, CCK8 proliferation assay, cell cloning assay and flow cytometry were used to detect the effects of the different polymorphism sites in HPV16 on cell proliferation and apoptosis. Results：HPV16 mutations promoted the proliferation and inhibited the apoptosis of cervical cancer C33A cells, and the effect of the E6-178G/E7-647G co-mutation was significantly greater than that of the single E7-647G mutant (P<0.05). Conclusions：HPV16 E6-178G/E7-647G can thus promote the proliferation and inhibit the apoptosis of cervical cancer cells.

scholarly journals HPV16 E6-178G/E7-647G Promotes Proliferation and Inhibits Apoptosis in Cervical Cancer C33A Cells

2021 ◽  
Author(s):  
Xiangyi Zhe ◽  
Chunhe Zhang ◽  
Huizhen Xin ◽  
Zhenzhen Pan ◽  
Dongmei Li ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Tumor Development ◽  
Hpv16 E6 ◽  
Hpv16 Variant ◽  
Carcinogenic Potential ◽  
Proliferation And Apoptosis ◽  
Cervical Cancer Cells ◽  
Cloning Assay ◽  
And Behavior

Abstract BackgroundHPV16 is the main cause of cervical cancer. In our study, we aimed to investigate the role of HPV mutants HPV16 E6-178G/E7-647G in the proliferation and apoptosis of cervical cancer C33A cells. MethodsPlasmids encoding the HPV16 E7 prototype (E7-647A)-GV144, E7 mutant (E7-647G)-GV144, HPV16 E6/E7 prototype (E6-178T/E7-647A)-GV144, and E6/E7 mutant (E6-178G/E7-647G)-GV144 were stably transfected into cervical cancer C33A cells. Western blot analysis, CCK8 proliferation assay, cell cloning assay and flow cytometry were used to detect the effects of the different polymorphism sites in HPV16 on cell proliferation and apoptosis. ResultsHPV16 mutations promoted the proliferation and inhibited the apoptosis of cervical cancer C33A cells, and the effect of the E6-178G/E7-647G co-mutation was significantly greater than that of the single E7-647G mutant (P<0.05). ConclusionsHPV16 E6-178G/E7-647G can thus promote the proliferation and inhibit the apoptosis of cervical cancer cells. Importance: HPV16 is the most common type and the main cause of cervical cancer. It is a fatal threat to the health of millions of women. The genetic differences among HPV16 sub-types may be related to their carcinogenic potential. HPV mutations can differ in biology and etiology, leading to differences in tumor development and behavior. However, little is known about the carcinogenic potential of the HPV16 variant in Asian women compared to many studies in European and American populations.

scholarly journals The potential oncogenic and MLN4924-resistant effects of CSN5 on cervical cancer cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Huilin Zhang ◽  
Ping He ◽  
Qing Zhou ◽  
Yan Lu ◽  
Bingjian Lu
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Cervical Cancers ◽  
Cervical Cancer Cells

Abstract Background CSN5, a member of Cop9 signalosome, is essential for protein neddylation. It has been supposed to serve as an oncogene in some cancers. However, the role of CSN5 has not been investigated in cervical cancer yet. Methods Data from TCGA cohorts and GEO dataset was analyzed to examine the expression profile of CSN5 and clinical relevance in cervical cancers. The role of CSN5 on cervical cancer cell proliferation was investigated in cervical cancer cell lines, Siha and Hela, through CSN5 knockdown via CRISPR–CAS9. Western blot was used to detect the effect of CSN5 knockdown and overexpression. The biological behaviors were analyzed by CCK8, clone formation assay, 3-D spheroid generation assay and cell cycle assay. Besides, the role CSN5 knockdown in vivo was evaluated by xenograft tumor model. MLN4924 was given in Siha and Hela with CSN5 overexpression. Results We found that downregulation of CSN5 in Siha and Hela cells inhibited cell proliferation in vitro and in vivo, and the inhibitory effects were largely rescued by CSN5 overexpression. Moreover, deletion of CSN5 caused cell cycle arrest rather than inducing apoptosis. Importantly, CSN5 overexpression confers resistance to the anti-cancer effects of MLN4924 (pevonedistat) in cervical cancer cells. Conclusions Our findings demonstrated that CSN5 functions as an oncogene in cervical cancers and may serve as a potential indicator for predicting the effects of MLN4924 treatment in the future.

The Potential Oncogenic and MLN4924-Resistant Effects of CSN5 on Cervical Cancer Cells

2021 ◽  
Author(s):  
Huilin Zhang ◽  
Ping He ◽  
Qing Zhou ◽  
Yan Lu ◽  
Bingjian Lu
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Cervical Cancers ◽  
Cervical Cancer Cells

Abstract BackgroundsCSN5, a member of Cop9 signalosome, is essential for protein neddylation. It has been supposed to serve as an oncogene in some cancers. However, the role of CSN5 has not been investigated in cervical cancer yet.MethodsData from TCGA cohorts and GEO dataset was analyzed to examine the expression profile of CSN5 in cervical cancers. The role of CSN5 on cervical cancer cell proliferation was investigated in cervical cancer cell lines, Siha and Hela, through CSN5 knockdown via CRISPR-CAS9. Western blot was used to detect the effect of CSN5 knockdown and overexpression. CCK8, clone formation assay and cell cycle assay were also employed. Besides, the role CSN5 knockdown in vivo was evaluated by xenograft tumor model. Moreover, MLN4924 was applied in Siha and Hela with CSN5 overexpression.ResultsWe found that downregulation of CSN5 in Siha and Hela cells inhibited cell proliferation in vitro and in vivo, and the inhibitory effects were largely rescued by CSN5 overexpression. Moreover, deletion of CSN5 caused cell cycle arrest rather than inducing apoptosis. Importantly, CSN5 overexpression confers resistance to the anti-cancer effects of MLN4924 (pevonedistat) in cervical cancer cells.ConclusionsOur findings demonstrated that CSN5 functions as an oncogene in cervical cancers and may serve as a potential indicator for predicting the effects of MLN4924 treatment in the future.

scholarly journals E2F1/2/7/8 as independent indicators of survival in patients with cervical squamous cell carcinoma

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Chang Yang ◽  
Zhao-Cong Zhang ◽  
Tian -Bo Liu ◽  
Ye Xu ◽  
Bai-Rong Xia ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Proliferation ◽  
Transcription Factors ◽  
Prognostic Factors ◽  
Cancer Cells ◽  
In Vitro Experiments ◽  
Cervical Cancer Cells

Abstract Background Cervical cancer is the second leading cause of death in women 20–39 years old. Because coverage for cervical cancer screening is low, and the vaccination rate of human papillomavirus (HPV) is poor in some countries, potential markers to detect the disease at early stages are needed. E2F transcription factors (E2Fs) are a family of transcription factors that function in cell proliferation, differentiation, apoptosis, and tumorigenesis. As abnormal activation and regulation of E2Fs are related to tumor development and poor prognosis, we performed bioinformatic analyses and in vitro assays to evaluate the role of E2Fs in cervical cancer. Methods Transcriptional expression of E2Fs was initially evaluated in silico using ONCOMINE and Gene Expression Profiling Interactive Analysis (GEPIA), followed by evaluation of E2F1/2/7/8 protein levels using immunohistochemistry in 88 patient tissues. E2F2 and E2F7 mRNA levels were measured by RT-qPCR. LinkedOmics and Metascape were used to predict functions of E2Fs, and in vitro experiments were performed to assess the tumorigenic role of E2F2 and E2F7. Results In silico analysis showed that E2F1/2/7/8 were significantly overexpressed in cervical cancer, findings which were confirmed at the protein level using immunohistochemistry. Further, upregulation of E2F1/2/7/8 was associated with different clinicopathological prognostic factors, including positivity for lymph vessel invasion and deep invasion of cervical stroma. Increased expression of E2F1/2/7/8 was also related to shorter overall survival (OS) and disease-free survival (DFS) in patients with cervical cancer. Using multivariate analysis, we confirmed E2F1/2/7/8 as independent prognostic factors for shorter OS of patients with cervical cancer. Finally, in vitro experiments showed that E2F2 and E2F7 are involved in cell proliferation and migration and cell cycle regulation in both HPV-positive and HPV-negative cervical cancer cells. Conclusions E2F1/2/7/8 may be prognostic biomarkers for survival of patients with cervical cancer. E2F2 and E2F7 are involved in cell proliferation, migration, and cell cycle in both HPV-positive and HPV-negative cervical cancer cells.

scholarly journals The polymorphism of rs2227513 can affect the expression of IL-22 and the proliferation of FLS, which leads to the progress of rheumatoid arthritis

2021 ◽  
Author(s):  
Jinping Yi ◽  
Lijuan Quan ◽  
Chufeng Yi ◽  
Zikun Huang ◽  
Xiaowen Chen
Keyword(s):  
Rheumatoid Arthritis ◽  
Flow Cytometry ◽  
Cell Proliferation ◽  
Cellular Proliferation ◽  
Combined Effect ◽  
Luciferase Assay ◽  
Quantitative Real Time Pcr ◽  
Proliferation And Apoptosis ◽  
Elevated Expression

IntroductionMiR-101 rs7536540 may influence the expression of miR-101 and another polymorphism, rs2227513, which in turn affects the expression of IL-22, . However, studies on the combined effect of these polymorphisms are still scarce.Material and methodsQuantitative real-time PCR was performed to analyze the expression of miR-101 and IL-22 mRNA. ELISA and Western blot were carried out to examine the expression of IL-22 protein. MTT assay and flow cytometry were used to assess the cellular proliferation and apoptosis . Immunofluorescence was performed to measure the expression of p-STAT3. Luciferase assay was carried out to explore the inhibitory role of miR-101 in the expression of IL-22.ResultsThe severity of RA was progressively increased in patients with rs7536540 GG + rs2227513 AA, rs7536540 GG + rs2227513 AG, rs7536540 CC/CG + rs2227513 AA and rs7536540 CC/CG + rs2227513 AG genotypes. The CC/CG alleles at rs7536540 were correlated with up-regulated miR-101 expression in the serum and SF of RA patients, whereas both CC/CG alleles at rs7536540 and AG alleles at rs2227513 were correlated with elevated expression of IL-22. Incubation of FLS with SF isolated from RA patients carrying the CC/CG alleles at rs7536540 and AG alleles at rs2227513 remarkably increased the cell proliferation and inhibited the apoptosis of FLS. Luciferase assay demonstrated that the expression of IL-22 was notably suppressed by miR-101 in THP-1 cells.ConclusionsOur study revealed the combined effect of polymorphisms rs7536540 and rs2227513 on the expression of IL-22 and the proliferation of FLS as well as their association with the severity of RA

scholarly journals MiR-17-5p targets TP53INP1 and regulates cell proliferation and apoptosis of cervical cancer cells

IUBMB Life ◽  
2012 ◽  
Vol 64 (8) ◽  
pp. 697-704 ◽  
Author(s):  
Qian Wei ◽  
Yi-Xuan Li ◽  
Min Liu ◽  
Xin Li ◽  
Hua Tang
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Proliferation And Apoptosis ◽  
Cervical Cancer Cells

Antiproliferative and Proapoptotic Effects of Astemizole on Cervical Cancer Cells

2014 ◽  
Vol 24 (5) ◽  
pp. 824-828 ◽  
Author(s):  
María de Guadalupe Chávez-López ◽  
Elizabeth Hernández-Gallegos ◽  
Alma Y. Vázquez-Sánchez ◽  
Patricio Gariglio ◽  
Javier Camacho
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Cancer Cells ◽  
Cell Lines ◽  
Anticancer Agent ◽  
Mtt Method ◽  
Proliferation And Apoptosis ◽  
Different Types ◽  
Cervical Cancer Cells

ObjectiveCervical cancer is a major cause of mortality among women in developing countries. Thus, it is necessary to offer novel therapies to treat this malignancy. Astemizole has been suggested as a novel and interesting anticancer agent because it targets several proteins involved in cancer including Eag1 (ether à-go-go-1) potassium channels. Eag1 has been proposed as a tumor marker for different types of cancer. Actually, we previously suggested Eag1 channels as cervical cancer and dysplasia markers. Besides, Eag1 has been proposed as a therapeutic target for different malignancies. However, the effect of astemizole in cervical cancer cells is unknown. Therefore, we investigated the effect of astemizole on the proliferation and apoptosis of cervical cancer cells.MethodsFive cervical cancer cell lines (HeLa, SiHa, CaSki, INBL, and C-33A) were cultured according to manufacturer’s instructions. Eag1 protein expression was studied by immunocytochemistry. Cell proliferation was assayed with the MTT method, and apoptosis was investigated by flow cytometry.ResultsEag1 protein expression was observed in different cell lines. Astemizole decreased cell proliferation in up to 40% and increased apoptosis severalfold in all the cell lines studied.ConclusionsOur results suggest astemizole as a potential therapy for cervical cancer.

LncRNA LINC00858 enhances cervical cancer cell growth through miR-3064-5p/ VMA21 axis

2021 ◽  
pp. 1-11
Author(s):  
Min Wei ◽  
Youguo Chen ◽  
Wensheng Du
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Luciferase Reporter ◽  
Cancer Cell Growth ◽  
Protein Coding ◽  
Gynecological Malignancy ◽  
Promising Therapeutic Target ◽  
Proliferation And Apoptosis ◽  
Reporter Assays

BACKGROUND: Cervical cancer (CC) is the most common form of gynecological malignancy. Long intergenic non-protein coding RNA 858 (LINC00858) has been identified to participate in multiple cancers. However, the role and mechanism of LINC00858 in CC cells are still elusive. AIM: The aim of this study is to explore the biological functions and mechanisms of LINC00858 in CC cells. METHODS: RT-qPCR analysis was used to examine the expression of LINC00858 in CC cells. EdU and colony formation assay were utilized to assess cell proliferation. TUNEL assay and flow cytometry assay were conducted to assess cell apoptosis. The mechanism regarding LINC00858 was certified through RNA pull down, RIP and luciferase reporter assays. RESULTS: The up-regulated LINC00858 was detected in CC cells. Reduction of LINC00858 effectively subdued CC cells proliferation and stimulated cell apoptosis. LINC00858 was determined to bind with miR-3064-5p and up-regulate VMA21 in CC cells. In rescue assays, miR-3064-5p down-regulation and VMA21 up-regulation were able to counteract the effect caused by LINC00858 decrease on CC cell proliferation and apoptosis. CONCLUSION: LINC00858 enhances cell proliferation, while restraining cell apoptosis in CC through targeting miR-3064-5p/VMA21 axis, implying that LINC00858 may serve as a promising therapeutic target for CC.

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