Uc.206 regulates cell proliferation and apoptosis by targeting P53 in 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.

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

Cancer Cell International ◽

10.1186/s12935-021-02078-5 ◽

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.

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Arsenic trioxide inhibits cell proliferation and human papillomavirus oncogene expression in cervical cancer cells

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2014.08.014 ◽

2014 ◽

Vol 451 (4) ◽

pp. 556-561 ◽

Cited By ~ 16

Author(s):

Hongtao Wang ◽

Peng Gao ◽

Jie Zheng

Keyword(s):

Cervical Cancer ◽

Cell Proliferation ◽

Human Papillomavirus ◽

Cancer Cells ◽

Arsenic Trioxide ◽

Oncogene Expression ◽

Cervical Cancer Cells

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miR-181b promotes cell proliferation and reduces apoptosis by repressing the expression of adenylyl cyclase 9 (AC9) in cervical cancer cells

FEBS Letters ◽

10.1016/j.febslet.2013.11.019 ◽

2013 ◽

Vol 588 (1) ◽

pp. 124-130 ◽

Cited By ~ 41

Author(s):

Lei Yang ◽

Yan-Li Wang ◽

Shang Liu ◽

Pei-Pei Zhang ◽

Zheng Chen ◽

...

Keyword(s):

Cervical Cancer ◽

Cell Proliferation ◽

Adenylyl Cyclase ◽

Cancer Cells ◽

Cervical Cancer Cells

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

10.21203/rs.3.rs-550782/v1 ◽

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.

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High expression of TMEM33 predicts poor prognosis and promotes cell proliferation in cervical cancer

10.21203/rs.3.rs-1252853/v1 ◽

2022 ◽

Author(s):

Hanxiang Chen ◽

Yongqing Li ◽

Shaoming Zhang ◽

Yunshan Wang ◽

Lili Wang ◽

...

Keyword(s):

Cervical Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Gene Networks ◽

Cox Regression ◽

Interaction Analysis ◽

Transmembrane Protein ◽

Functional Enrichment ◽

High Expression ◽

Cervical Cancer Cells

Abstract Background As one of the most common cancer among women worldwide, the prognosis of patients with advanced cervical cancer remains unsatisfactory. A study indicated that transmembrane protein 33 (TMEM33) was implicated in tumor recurrence, while its role in cervical cancer has not been elucidated. Methods TMEM33 expression in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) was primarily screened in The Cancer Genome Altas (TCGA), and further validated in Gene Expression Omnibus (GEO) database. The Kaplan–Meier plotter analysis and Cox regression were constructed to evaluate the prognostic value of TMEM33 in CESC. Functional enrichment analysis was performed with GO, KEGG and GSEA tools. Protein-protein interaction analysis and correlated gene networks were conducted using STING and GEPIA2 websites, respectively. The expression of TMEM33 in cervical cancer cells were examined by immunoblotting and RT-qPCR. Finally, CCK-8 assay and colony formation assay were performed to investigate the role of TMEM33 in cervical cancer cell proliferation. Results TMEM33 expression was significantly elevated in CESC compared with normal tissues. High expression of TMEM33 was associated with poor prognostic clinical characteristics in CESC patients. KM-plotter analysis revealed that patients with increased TMEM33 had shorter overall survival (OS), progress free interval (PFI), and disease specific survival (DSS). Moreover, Multivariate Cox analysis further confirmed that high TMEM33 expression was an independent risk factor for OS in patients with CESC. TMEM33 was associated with immune cell infiltration, and its expression was correlated with tumorigenesis-related genes RNF4, OCIAD1, TMED5, DHX15, MED28 and LETM1. More importantly, knockdown of TMEM33 in cervical cancer cells decreased the expression of those genes and inhibited cell proliferation. Conclusions Increased TMEM33 in cervical cancer can serve as an independent prognostic marker and might play a role in tumorigenesis by promoting cell proliferation.

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LncRNA HOXD-AS1 affects proliferation and apoptosis of cervical cancer cells by promoting FRRS1 expression via transcription factor ELF1

Cell Cycle ◽

10.1080/15384101.2021.2020962 ◽

2022 ◽

pp. 1-11

Author(s):

Huan Liu ◽

Li Liu ◽

Qiong Liu ◽

Fengjiao He ◽

Hong Zhu

Keyword(s):

Cervical Cancer ◽

Transcription Factor ◽

Cancer Cells ◽

Proliferation And Apoptosis ◽

Cervical Cancer Cells

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LncRNA SNHG1 enhances cell proliferation, migration, and invasion in cervical cancer

Biochemistry and Cell Biology ◽

10.1139/bcb-2017-0188 ◽

2018 ◽

Vol 96 (1) ◽

pp. 38-43 ◽

Cited By ~ 34

Author(s):

Yang Liu ◽

Yanling Yang ◽

Lei Li ◽

Yuan Liu ◽

Peng Geng ◽

...

Keyword(s):

Cervical Cancer ◽

Cell Proliferation ◽

Cell Migration ◽

Cancer Cells ◽

Cell Lines ◽

Cancer Cell ◽

Cancer Cell Lines ◽

Cervical Cancer Cell ◽

Knock Down ◽

Cervical Cancer Cells

Objective: This study investigated the effects of lncRNA SNHG1 on the proliferation, migration, and invasiveness of cervical cancer cells. Methods: Three pairs of cervical cancer tissue samples and their corresponding adjacent samples were analyzed using Human LncRNA Microarray V3.0 chip for differential analysis. The expression of SNHG1 in cervical cancer cell lines was verified by qRT–PCR. CCK8 assays and colony formation assays were used to study the changes in cell proliferation. Cell migration and Transwell assays were used to study changes in cell migration and invasiveness. Results: SNHG1 was highly expressed in cervical cancer tissues and cervical cancer cell lines. SNHG1 siRNA could knock-down the expression level of SNHG1 in cervical cancer cell lines HeLa and C33-A. After knock-down of SNHG1, cell proliferation and migration as well as invasiveness in HeLa and C-33A cells decreased. Conclusion: LncRNA SNHG1 promotes the development of cervical cancer cells.

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