scholarly journals IL‑8 is upregulated in cervical cancer tissues and is associated with the proliferation and migration of HeLa cervical cancer cells

2017 ◽  
Author(s):  
Linlin Jia ◽  
Fengying Li ◽  
Mingliang Shao ◽  
Wei Zhang ◽  
Chunbin Zhang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

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 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.

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.

miR-375 Affects the Proliferation, Invasion, and Apoptosis of HPV16-Positive Human Cervical Cancer Cells by Targeting IGF-1R

2016 ◽  
Vol 26 (5) ◽  
pp. 851-858 ◽  
Author(s):  
Xiao Yu ◽  
Weihong Zhao ◽  
Xin Yang ◽  
Zhilian Wang ◽  
Min Hao
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Target Gene ◽  
Negative Control ◽  
Expression Level ◽  
Cell Proliferation And Migration ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

ObjectiveThe aim of this study was to examine the relationship between miR-375 expression and the proliferation, apoptosis, and migration of cervical cancer cells. To further explore the potential target gene of miR-375, insulin-like growth factor 1 receptor (IGF-1R) was detected in miR-375 overexpressed and inhibited cervical cancer cells, which clarified the potential mechanism of miR-375 in the growth and development of cervical cancer.MethodsIn a cervical cancer cell line (Caski), miR-375 overexpression and knockdown were achieved by transfection with a synthetic miR-375 mimic or miR-375–targeting inhibitor oligonucleotides, respectively, using siRNA-Mate transfection reagents. Real-time Polymerase Chain Reaction was performed to detect the expression level of miR-375. The functional effects of miR-375 on cell proliferation, migration, and apoptosis were evaluated using a Cell Counting Kit (CCK-8) and through scratch wound tests and apoptosis assays, respectively. Western blotting was performed to detect the expression level of the IGF-1R protein.ResultTransfection with the miR-375 mimic significantly upregulated the expression of miR-375 by approximately 7.76-fold (P< 0.05), reduced cell proliferation and migration (P< 0.05), increased apoptosis (P< 0.05), and decreased the expression of the IGF-1R protein by 24.73% (P< 0.05) compared with the negative control. In contrast, transfection of the miR-375 inhibitor decreased the expression of miR-375 by 14.39% (P< 0.05), significantly increased cell proliferation and migration (P< 0.05), significantly reduced the cell apoptosis (P< 0.05), and upregulated the expression of the IGF-1R protein by 2.29-fold (P< 0.05). The cells transfected with the negative control showed no significant changes compared with the blank control for each parameter (P> 0.05).ConclusionsmiR-375 plays an important role in the tumorigenesis and development of cervical cancer. IGF-1R might represent a target gene of miR-375 in cervical cancer.

Long noncoding RNA NEAT1 promotes the growth of cervical cancer cells via sponging miR-9-5p

2019 ◽  
Vol 97 (2) ◽  
pp. 100-108 ◽  
Author(s):  
Qiuxian Xie ◽  
Shanna Lin ◽  
Manjia Zheng ◽  
Qiutao Cai ◽  
Ya Tu
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Noncoding Rna ◽  
Inhibitory Effect ◽  
Micro Rna ◽  
Cancer Cell Growth ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Cancer Tissues ◽  
Competitive Endogenous Rna

Evidence has accumulated demonstrating that long noncoding RNAs (lncRNAs) participate in the initiation and progression of cancers. In this study, we found that the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) is significantly increased in both cervical cancer tissues and cell lines. Overexpression of NEAT1 promoted the proliferation and migration of cervical cancer cells. Molecular studies uncovered that NEAT1 functions as competitive endogenous RNA (ceRNA), binding the micro-RNA miR-9-5p and suppressing its expression. However, we consistently found that when NEAT1 was highly expressed, it attenuated the inhibitory effect of miR-9-5p on the expression of PTEN and POU2F1, which are the targets of miR-9-5p. Consistent with the negative regulation of NEAT1 on miR-9-5p, restoration of miR-9-5p inhibited the growth-promoting effects of NEAT1 on cervical cancer cells. Taken together, these results indicated that NEAT1 plays an important role in the regulation cervical cancer cell growth by targeting miR-9-5p. Our findings characterized the possible mechanism of NEAT1 in cervical cancer.

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