Silencing Anti-Silencing Function 1B Inhibited Proliferation and Migration of Cervical Cancer Cells and Promoted Apoptosis by Down-Regulating Chromatin Assembly Factor 1, Subunit B

2021 ◽  
Vol 11 (1) ◽  
pp. 28-37
Author(s):  
Linxia Li ◽  
Kaihan Yang ◽  
Jun Wan ◽  
Yi Xu ◽  
Xiahui Li ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Hela Cells ◽  
Chromatin Assembly ◽  
Migration And Invasion ◽  
Cervical Cancer Cells ◽  
Assembly Factor ◽  
And Migration ◽  
Subunit B ◽  
Proliferation And Migration

The expression of anti-silencing function 1B (ASF1B) in cervical cancer patients were previously reported, indicating its implications as a new candidate gene related to the development of cervical lesions and cancer. In this study, we investigated the possible role of ASF1B in cervical carcinogenesis. ASF1B messenger RNA and protein expression was assessed in five cervical cancer cell line models, Hela, C-33A, SiHa, CaSKi, HCC-94 and normal cervical epithelium cell Ect. Gene silencing approach was employed to investigate the potential role of ASF1B in cellular growth, proliferation, colony-forming ability, migration and invasion in Hela cells. Our data indicated that ASF1B was expressed in all cervical cancer cells at the gene and protein level. Gene silencing of ASF1B caused significant inhibition in cellular proliferation, colony-forming ability, migration and invasion ability, and promote apoptosis of Hela cells. However, the biological effects of ASF1B silencing on Hela cells were reversing after down-regulating recombinant chromatin assembly factor 1, subunit B (CHAF1B). Collectively, our findings concluded that silencing ASF1B inhibits proliferation and migration of Hela cells and promotes apoptosis by down-regulating CHAF1B.

scholarly journals Up-regulation of miRNA-148a inhibits proliferation, invasion, and migration while promoting apoptosis of cervical cancer cells by down-regulating RRS1

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Ying Zhang ◽  
Bingmei Sun ◽  
Lianbin Zhao ◽  
Zhengling Liu ◽  
Zonglan Xu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Hela Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Cervical Cancer Cells ◽  
And Migration

Abstract The purpose of the present study is to figure out the role of miRNA-148a (miR-148a) in growth, apoptosis, invasion, and migration of cervical cancer cells by binding to regulator of ribosome synthesis 1 (RRS1). Cervical cancer and adjacent normal tissues, as well as cervical cancer cell line Caski, HeLa, C-33A, and normal cervical epithelial cell line H8 were obtained to detect the expression of miR-148a and RRS1. Relationship between miR-148a and RRS1 expression with clinicopathological characteristics was assessed. The selected Caski and HeLa cells were then transfected with miR-148a mimics, miR-148a inhibitors or RRS1 siRNA to investigate the role of miR-148a and RRS1 on proliferation, apoptosis, colony formation, invasion, and migration abilities of cervical cancer cells. Bioinformatics information and dual luciferase reporter gene assay was for used to detect the targetting relationship between miR-148a and RRS1. Down-regulated miR-148a and up-regulated RRS1 were found in cervical cancer tissues and cells. Down-regulated miR-148a and up-regulated RRS1 are closely related with prognostic factors of cervical cancer. RRS1 was determined as a target gene of miR-148a and miR-148a inhibited RRS1 expression in cervical cancer cells. Up-regulation of miR-148a inhibited cell proliferation, migration, and invasion while promoting apoptosis in Caski and HeLa cells. Our study suggests that miR-148a down-regulates RRS1 expression, thereby inhibiting the proliferation, migration, and invasion while promoting cell apoptosis of cervical cancer cells.

scholarly journals MicroRNA-222 promotes the proliferation and migration of cervical cancer cells

2014 ◽  
Vol 37 (3) ◽  
pp. 131 ◽  
Author(s):  
Yi Sun ◽  
Bo Zhang ◽  
Jiajing Cheng ◽  
Yi Wu ◽  
Fing Xing ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Phosphatase And Tensin Homolog ◽  
Migration Assay ◽  
Tensin Homolog ◽  
Siha Cells ◽  
Non Coding Rna ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

Purpose: This study aimed to investigate the role of small non-coding RNA-222 (microRNA-222; miR-222) in the development of cervical cancer (CC). Methods: Normal and CC specimens were obtained from 18 patients. HeLa and SiHa cells were grown in Dulbecco’s modified Eagle’s medium. RT–PCR, Western blot, migration assay, flow cytometry and immunofluorescence microscopy were used for analyses. Results: When compared with normal cervical tissues, miR-222 was upregulated in human CC, and the extent of up-regulation was associated with the extent and depth of CC invasion. Expression of miR-222 was inversely related to the expression of phosphatase and tensin homolog (PTEN) and p27. The reduced the expression of PTEN and p27 by miR-222 in HeLa cells and SiHa cells was associated with increased proliferation and migration of CC cells. The expression of proteins (E-cadherin and paxillin) related to the proliferation and migration was also elevated. Conclusion: MiR-222 plays an important role in the tumorigenesis of CC, possibly by specifically down-regulating p27Kip1 and PTEN. Our findings suggest that miR-222 may serve as a new therapeutic target in CC.

scholarly journals Retraction: RNA-sequencing identified miR-3681 as a negative regulator in the proliferation and migration of cervical cancer cells via the posttranscriptional suppression of HGFR

RSC Advances ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 5230-5230
Author(s):  
Laura Fisher
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Rna Sequencing ◽  
Negative Regulator ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

Retraction of ‘RNA-sequencing identified miR-3681 as a negative regulator in the proliferation and migration of cervical cancer cells via the posttranscriptional suppression of HGFR’ by Fan Shi et al., RSC Adv., 2019, 9, 22376–22383, DOI: 10.1039/C9RA01785B.

scholarly journals RNA-sequencing identified miR-3681 as a negative regulator in the proliferation and migration of cervical cancer cells via the posttranscriptional suppression of HGFR

RSC Advances ◽  
2019 ◽  
Vol 9 (39) ◽  
pp. 22376-22383 ◽  
Author(s):  
Fan Shi ◽  
Yingbing Zhang ◽  
Juan Wang ◽  
Jin Su ◽  
Zi Liu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Rna Sequencing ◽  
Negative Regulator ◽  
Tumor Tissues ◽  
Differentially Expressed Mirnas ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

In this study, RNA-sequencing was used to investigate the differentially expressed miRNAs between cervical cancer tissues and matched adjacent non-tumor tissues.

scholarly journals Swertiamarin exerts anticancer effects on human cervical cancer cells via induction of apoptosis, inhibition of cell migration and targeting of MEK-ERK pathway

2021 ◽  
Vol 20 (1) ◽  
pp. 75-81
Author(s):  
Xinxiang Wang ◽  
Tao Wang
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Western Blotting ◽  
Hela Cells ◽  
Migration And Invasion ◽  
Inhibition Of Proliferation ◽  
Anticancer Effects ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer

Purpose: To investigate the anticancer effects of swertiamarin against taxol- resistant human cervical cancer cells.Method: Cell viability was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5–diphenyl tetrazolium bromide (MTT) assay while colony survival was evaluated by clonogenic assay. Apoptotic cell death was assessed by AO/ETBR staining and western blotting techniques. The levels of reactive oxygen species (ROS) were measured using 2,7, dicholoro dihydrofluoresceindiacetate (H2DCFDA) staining.Cell migration and invasion were monitored with Transwell chamber assay. Western blotting assay was used to determine the expression levels of proteins of the MEK/ERK signaling pathway.Results: Swertiamarin induced dose- and time-dependent inhibition of proliferation of HeLa cervical cancer cells (p < 0.05). It also suppressed the colony formation potential of HeLa cells, and induced various structural modifications in HeLa cells. Swertiamarin exposure resulted in the formation of earlyapoptotic, late-apoptotic and necrotic cells, and significant modulation of apoptosis-allied proteins. It was observed that the migration and invasion of HeLa cells were potentially suppressed in dose-reliant fashion by swertiamarin. Western blotting results showed that the expressions of p-MEK and p-ERK were markedly reduced, while those of MEK and ERK were unaffected (p < 0.05).Conclusion: Swertiamarin exerts in vitro anticancer activity against cervical cancer cells (HeLa). Thus, it is promising for use in cervical cancer chemotherapy. However, there is need for confirmation of these findings through further in vivo and in vitro investigations. Keywords: Swertiamarin, Gentianaceae, Triterpene Sapogenin, Cervical cance

scholarly journals 5p and 3p Strands of miR-34 Family Members Have Differential Effects in Cell Proliferation, Migration, and Invasion in Cervical Cancer Cells

2019 ◽  
Vol 20 (3) ◽  
pp. 545 ◽  
Author(s):  
Sergio Córdova-Rivas ◽  
Ixamail Fraire-Soto ◽  
Andrea Mercado-Casas Torres ◽  
Luis Servín-González ◽  
Angelica Granados-López ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Invasion ◽  
Family Members ◽  
Micro Rna ◽  
Migration And Invasion ◽  
Protein Inhibition ◽  
The Difference ◽  
And Migration ◽  
Proliferation And Migration

The micro RNA (miR)-34 family is composed of 5p and 3p strands of miR-34a, miR-34b, and miR-34c. The 5p strand’s expression and function is studied in cervical cancer. The 3p strand’s function and regulation remain to be elucidated. To study the function of the passenger strands of miR-34 family members, we overexpressed 5p and 3p strands using a synthetic miRNA in cervical cell lines. Cell proliferation was evaluated using crystal violet. Migration and invasion were tested using transwell assays, Western blot, and zymography. Possible specific targets and cell signaling were investigated for each strand. We found that miR-34a-5p inhibited proliferation, migration, and cell invasion accompanied by matrix metalloproteinase 9 (MMP9) activity and microtubule-associated protein 2 (MAP2) protein reduction. We also found that miR-34b-5p and miR-34c-5p inhibit proliferation and migration, but not invasion. In contrast, miR-34c-5p inhibits MMP9 activity and MAP2 protein, while miR-34b-5p has no effect on these genes. Furthermore, miR-34a-3p and miR-34b-3p inhibit proliferation and migration, but not invasion, despite the later reducing MMP2 activity, while miR-34c-3p inhibit proliferation, migration, and cell invasion accompanied by MMP9 activity and MAP2 protein inhibition. The difference in cellular processes, MMP2 and MMP9 activity, and MAP2 protein inhibition by miR-34 family members suggests the participation of other regulated genes. This study provides insights into the roles of passenger strands (strand*) of the miR-34 family in cervical cancer.

scholarly journals Baicalein inhibits the invasion of human cervical cancer cells by inhibiting the hedgehog/Gli signaling pathway

2020 ◽  
Vol 19 (1) ◽  
pp. 115-120
Author(s):  
Hai Yang ◽  
Jiyi Xia ◽  
Yan Li ◽  
Yong Cao ◽  
Li Tang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Hela Cells ◽  
Colony Formation ◽  
Diphenyltetrazolium Bromide ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Purpose: To identify the role of baicalein in human cervical cancer and to determine whether baicalein treatment affects hedgehog/Gli signaling pathway. Methods: Cell proliferation was evaluated by MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and colony formation assays. Cell death rate was assessed by PI-staining and FACS assay. Furthermore, cell invasion was assessed by Transwell assay while the levels of the key proteins were measured by western blotting analysis. Results: Baicalein suppressed the viability and proliferation of HeLa cells. The colony formation ability and relative migration rate were significantly decreased in the HeLa cells treated with 50 μM baicalein. Furthermore, the levels of Shh, Gli1, MMP-9, and VEGF declined significantly in baicalein-treated cells. Conclusion: The results demonstrate that baicalein inhibits the growth and invasiveness of cervical cancer cells partly by suppressing the activation of hedgehog/Gli signaling pathway in a concentrationdependent manner. Keywords: Cervical cancer, baicalein, hedgehog/Gli pathway, MMP-9

Human Papillomavirus E7 Oncoprotein Promotes Proliferation and Migration through the Transcription Factor E2F1 in Cervical Cancer Cells

2020 ◽  
Vol 20 ◽  
Author(s):  
Sijuan Tian ◽  
Li Zhang ◽  
Yang Li ◽  
Di Cao ◽  
Shimin Quan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Wild Type ◽  
Migration Ability ◽  
E7 Oncoprotein ◽  
Hpv E7 ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration ◽  
Transcription Factor E2f1

Background: High-risk human papillomavirus (HR-HPV) persistent infection is the main cause of cervical cancer and its precancerous lesions. A previous study showed that HPV16 and HPV58 infections were the most common infection types in the local region. Some studies also declared that HPV58 E7 variants increased the risk of cervical cancer among Asian populations. Objective: This study aimed to determine whether the HPV58 E7 T20I (C632T) variant promotes the malignant behavior of cervical cancer cells and the underlying mechanism of the HR-HPV E7 oncoprotein involved in the development of cervical cancer. Methods: CCK-8 and clone formation assays were used to detect cell proliferation ability. Transwell assays and cell wound healing assays were used to evaluate cell migration ability. Targeted knockdown of E2F1 expression using specific siRNA, RT-qPCR and Western blot were performed to assess gene expression changes. A chromatin immunoprecipitation assay was used to verify that E2F1 interacted with the TOP2A promoter region. Results: HPV58 E7 and HPV58 E7M oncoproteins increased the proliferation and migration ability of cervical cancer cells. However, the HPV58 E7 T20I variant did not promote malignant behaviors compared with wild-type HPV58 E7. HPV E7 and E7M oncoproteins increased the expression of TOP2A, BIRC5 and E2F1, and knockdown of HPV E7 decreased their expression. Low E2F1 expression reduced the expression of TOP2A and BIRC5 and inhibited the proliferation and migration ability of cervical cancer cells. E2F1 interacted with the TOP2A gene promoter region to promote its transcriptional expression. Conclusions: The HPV58 E7 T20I variant did not promote malignant behaviors compared with wild-type HPV58 E7. The HR-HPV E7 oncoprotein enhanced the proliferation and migration of cervical cancer cells, which was considered to be due to the HPV E7 oncoprotein increasing the expression of BIRC5 and TOP2A by upregulating the transcription factor E2F1.

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