scholarly journals MicroRNA-300 Inhibits the Proliferation and Metastasis of Cervical Cancer Cells via Posttranscriptional Suppression of G Protein-Coupled Receptor 34 (GPR34)

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Mei Wang ◽  
Ying Tian ◽  
Lin Miao ◽  
Wenxia Zhao
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
G Protein ◽  
Migration And Invasion ◽  
G Protein Coupled Receptor ◽  
Gynecological Disorders ◽  
Cervical Cancer Cells ◽  
G Protein Coupled

Cervical cancer is one of the dominant gynecological disorders which has poor prognosis and often diagnosed at advanced stages where it becomes nearly impossible to effectively manage this disorder. MicroRNA-300 (miR-300) has dual role in human tumorogenesis. However, characterization of its regulatory action has not been made in cervical cancer. The molecular role of miR-300 in cervical cancer was thus explored in the present study with prime focus on elucidating its mechanism of action. The results showed significant (P < 0.05) downregulation of miR-300 in cervical cancer. Overexpression of miR-300 in cervical cancer cells inhibited their proliferation in vitro by inducing apoptosis. Cervical cancer cells overexpressing miR-300 also showed decreased rates of migration and invasion. G protein-coupled receptor 34 (GPR34) was found to be the functional regulatory target of miR-300 in cervical cancer. GPR34 was found to be significantly (P < 0.05) overexpressed in cervical cancer tissues and cell lines. Silencing of GPR34 inhibited the growth of the cervical cancer cells. However, overexpression of GPR34 could prevent the tumor-suppressive effects of miR-300 on cervical cancer cells. Collectively, the results of the current study are indicative of the tumor-suppressive regulatory role of miR-300 in cervical cancer and suggestive of the potential therapeutic value of miR-300/GPR34 molecular axis.

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 Upregulation of Long Non-Coding RNA Small Nucleolar RNA Host Gene 12 Contributes to Cell Growth and Invasion in Cervical Cancer by Acting as a Sponge for MiR-424-5p

2018 ◽  
Vol 45 (5) ◽  
pp. 2086-2094 ◽  
Author(s):  
Jing Dong ◽  
Qing Wang ◽  
Li Li ◽  
Zhang Xiao-jin
Keyword(s):  
Cervical Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Host Gene ◽  
Migration And Invasion ◽  
Small Nucleolar Rna ◽  
Cervical Cancer Cells ◽  
Cancer Tissues ◽  
Nucleolar Rna

Background/Aims: Cervical cancer, which is one of the most aggressive cancers affecting females, has high rates of recurrence and mortality. Small nucleolar RNA host gene 12 (SNHG12) is known to promote the progression of several cancers; however, its exact effects and molecular mechanisms in cervical cancer remain unknown. Methods: Real-time quantitative PCR was used to determine the expression level of SNHG12 in cervical cancer tissues and cell lines. Loss-of-function assays were performed to examine the effect of SNHG12 on the proliferation, apoptosis, migration and invasion of cervical cancer cells in vitro and tumor growth in vivo. Luciferase experiments were employed to explore the interactions between SNHG12 and miR-424-5p. Results: SNHG12 was found to be abnormally elevated in human cervical cancer tissues compared with paired adjacent normal tissues. Moreover, high SNHG12 expression in tumor tissues was significantly correlated with vascular involvement, lymph node metastasis, advanced FIGO stage and poor prognosis. Furthermore, the knockdown of SNHG12 was found to inhibit proliferation, migration and invasion of cervical cancer cells in vitro, and silencing SNHG12 was shown to suppress tumor growth in a nude mouse model. Mechanistic studies showed that SNHG12 functioned as an endogenous sponge for miR-424-5p, thereby downregulating the expression of miR-424-5p in cervical cancer. Furthermore, the inhibition of miR-424-5p in SNHG12-depleted cells partially reversed the effects on cervical cancer cell apoptosis, adhesion and invasion. Conclusion: In summary, our findings suggest that the tumor-promoting role of SNHG12 is to function as a molecular sponge, which negatively regulates miR-424-5p. These findings may provide a potent therapeutic target for cervical cancer.

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 Knockdown of Ezrin inhibited migration and invasion of cervical cancer cells in vitro

2020 ◽  
Vol 34 ◽  
pp. 205873842093089
Author(s):  
Meili Xi ◽  
Wenbin Tang
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Messenger Rna ◽  
Migration And Invasion ◽  
Protein Levels ◽  
Sulforhodamine B ◽  
Ezrin Expression ◽  
Cervical Cancer Cells ◽  
Polymerase Chain

Cervical cancer is the fourth most common malignancy in women. The aim of this study was to investigate the functions of Ezrin in cervical cancer cells. Two cervical cancer cell lines, SiHa and CaSki, were cultured in vitro. Following the knockdown of Ezrin using siRNA, real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis were applied to analyze Ezrin expression at the messenger RNA (mRNA) and protein levels. Subsequently, wound healing assay, transwell assay, and sulforhodamine B (SRB) assay were used to detect the migration, invasion, and viability of cervical cancer cells, respectively. Results revealed that Ezrin siRNA can notably inhibit the migration and invasion of SiHa and CaSki cells ( P  < 0.05). However, knockdown of Ezrin shows no effects on the viability of SiHa and CaSki cells ( P  < 0.05). It is indicated that Ezrin plays a possible role in promoting the migration and invasion of cervical cancer cells and may be a therapeutic target to prevent metastasis of cervical cancer.

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 YTHDF1 Aggravates the Progression of Cervical Cancer Through m6A-Mediated Up-Regulation of RANBP2

2021 ◽  
Vol 11 ◽  
Author(s):  
Haocheng Wang ◽  
Qingya Luo ◽  
Jianyi Kang ◽  
Qinglv Wei ◽  
Yu Yang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
The Poor ◽  
Cervical Cancer Cells ◽  
On Line ◽  
Induced Apoptosis

N6-methyladenosine (m6A) is the most common post-transcriptional modification of RNA in eukaryotes, which has been demonstrated to play important roles in various cancers. YTHDF1 acts as a crucial m6A “reader” and regulates the fate of m6A modified mRNA. However, its role in cervical cancer remains unknown. In this study, we showed that YTHDF1 was highly expressed in cervical cancer, and was closely associated with the poor prognosis of cervical cancer patients. YTHDF1 knockdown suppressed the growth, migration and invasion, and induced apoptosis of cervical cancer cells. Moreover, YTHDF1 knockdown inhibited tumorigenesis of cervical cancer cells in vivo. Through combined on-line data analysis of RIP-seq, meRIP-seq and Ribo-seq upon YTHDF1 knockdown, RANBP2 was identified as the key target of YTHDF1 in cervical cancer cells. YTHDF1 regulated RANBP2 translation in an m6A-dependent manner without effect on its mRNA expression. RANBP2 potentiated the growth, migration and invasion of cervical cancer cells. Our study demonstrated the oncogenic role of YTHDF1 in cervical cancer by regulating RANBP2 expression and YTHDF1 represents a potential target for cervical cancer therapy.

Identification of miR-885-5p as a tumor biomarker: regulation of cellular function in cervical cancer

2021 ◽  
Author(s):  
Yuanqi Zu ◽  
Qianqian Wang ◽  
Hong Wang
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Clinical Significance ◽  
Migration And Invasion ◽  
Rank Test ◽  
Tumor Biomarker ◽  
Cancer Tissue ◽  
Cervical Cancer Cells ◽  
Tissue Specimens

Objectives: MicroRNAs were revealed as biomarkers for early detection or prognosis predictors of cancer and were involved in the progression of cancer. The present study investigated the expression pattern, potential clinical, and functional role of miR-885-5p in cervical cancer. Design: A total of 115 pairs of cervical cancer tissue specimens and adjacent non-tumor paracancerous tissue specimens were collected from the cervical cancer patients who underwent surgical resection or biopsy without preoperative systemic therapy at Maternity and Child Health Care of Zaozhuang from 2012 to 2014. Participants/Materials, Setting, Methods: The expression levels of miR-885-5p in cervical cancer were measured using the qRT-PCR assay. A follow-up study was conducted and the Kaplan-Meier method with log-rank test was used to analyze the potential clinical significance of miR-885-5p in cervical cancer. The functional experiments including CCK-8, Transwell migration, and invasion assays were used to investigate the biological function of miR-885-5p in cervical cancer cells. Results: miR-885-5p expression was decreased in tumor tissues and tumor cell lines compared to normal control. Low expression of miR-885-5p was related to lymph node metastasis, late FIGO stage, and shorter overall survival outcome. Ascending expression of miR-885-5p inhibited the proliferative, migratory, and invasive abilities of cervical cancer cells, while downregulation of miR-885-5p promoted these cellular abilities of cervical cancer cells in vitro. Limitations: The patient population size was limited, thus the clinical significance of miR-885-5p requires further verification. Secondly, the precise mechanism of miR-885-5p in cervical cancer still exclusive. In future studies, a larger sample size will be required to confirm the prognostic value of miR-885-5p in cervical cancer, and the possible targets, as well as the detailed mechanism of miR-885-5p, will be investigated. Conclusions: miR-885-5p expression was decreased in cervical cancer and downregulation of miR-885-5p promoted the progression of cervical cancer cells. miR-885-5p may be an independent prognostic predictor and therapeutic target for treating cervical cancer.

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