scholarly journals Essential role of autophagy in fucoxanthin-induced cytotoxicity to human epithelial cervical cancer HeLa cells

2013 ◽  
Vol 34 (11) ◽  
pp. 1403-1410 ◽  
Author(s):  
Li-li Hou ◽  
Chao Gao ◽  
Liang Chen ◽  
Guo-qiang Hu ◽  
Song-qiang Xie
Keyword(s):  
Cervical Cancer ◽  
Hela Cells ◽  
Essential Role

scholarly journals An essential role of Cdc42-like GTPases in mitosis of HeLa cells

FEBS Letters ◽  
2006 ◽  
Vol 580 (14) ◽  
pp. 3375-3380 ◽  
Author(s):  
Shingo Yasuda ◽  
Hiroyuki Taniguchi ◽  
Fabian Oceguera-Yanez ◽  
Yoshikazu Ando ◽  
Sadanori Watanabe ◽  
...  
Keyword(s):  
Hela Cells ◽  
Essential Role

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 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

scholarly journals miR-145 Contributes to the Progression of Cervical Carcinoma by Directly Regulating FSCN1

2019 ◽  
Vol 28 (9-10) ◽  
pp. 1299-1305 ◽  
Author(s):  
Li Ma ◽  
Ling-Ling Li
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cervical Carcinoma ◽  
Hela Cells ◽  
Underlying Mechanism ◽  
Luciferase Assay ◽  
Cancer Cell Proliferation ◽  
Expression Levels ◽  
Direct Target

The purpose of our study was to investigate the underlying mechanism and functional role of microRNA-145 (miR-145) in cervical cancer. In this study, quantitative real-time PCR (qRT-PCR) was used to detect miR-145 and FSCN1 expression levels in tissues and HeLa cells. Western blotting was performed to determine the protein level of FSCN1. The luciferase assay was used to verify the direct target of miR-145. The CCK-8 assay and 2D colony formation assays were performed to determine the effects of miR-145 mimics or FSCN1 silencing on cell proliferation. miR-145 expression levels were significantly down-regulated, while FSCN1 expression levels were significantly up-regulated in the cervical carcinoma tissues compared with their matched non-cancerous tissues. In addition, FSCN1 expression levels were negatively correlated to miR-145 in tissues. Next, FSCN1 was verified as the direct target of miR-145 in HeLa cells. Moreover, overexpression of miR-145 dramatically inhibited the proliferation of HeLa cells. The silencing of FSCN1 exhibited the similar patterns on cell proliferation as miR-145 overexpression. The miR-145/ FSCN1 axis contributes to the progression of cervical cancer by inhibition of cervical cancer cell proliferation.

scholarly journals The Role of Apollon Gene Silencing on Viablity and Radiosensitivity of Cervical Cancer Hela Cells

2016 ◽  
Vol 59 (0) ◽  
Author(s):  
Saeideh Milani ◽  
Mojgan Bandehpour ◽  
Zohreh Sharifi ◽  
Bahram Kazemi
Keyword(s):  
Cervical Cancer ◽  
Gene Silencing ◽  
Hela Cells

scholarly journals Comprehensive circular RNA expression profile in radiation-treated HeLa cells and analysis of radioresistance-related circRNAs

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5011 ◽  
Author(s):  
Duo Yu ◽  
Yunfeng Li ◽  
Zhihui Ming ◽  
Hongyong Wang ◽  
Zhuo Dong ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
High Throughput ◽  
Protein Interaction ◽  
Hela Cells ◽  
High Throughput Sequencing ◽  
Interaction Network ◽  
Circular Rna ◽  
Protein Protein Interaction ◽  
Hub Proteins

Background Cervical cancer is one of the most common cancers in women worldwide. Malignant tumors develop resistance mechanisms and are less sensitive to or do not respond to irradiation. With the development of high-throughput sequencing technologies, circular RNA (circRNA) has been identified in an increasing number of diseases, especially cancers. It has been reported that circRNA can compete with microRNAs (miRNAs) to change the stability or translation of target RNAs, thus regulating gene expression at the transcriptional level. However, the role of circRNAs in cervical cancer and the radioresistance mechanisms of HeLa cells are unknown. The objective of this study is to investigate the role of circRNAs in radioresistance in HeLa cells. Methods High-throughput sequencing and bioinformatics analysis of irradiated and sham-irradiated HeLa cells. The reliability of high-throughput RNA sequencing was validated using quantitative real-time polymerase chain reaction. The most significant circRNA functions and pathways were selected by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. A circRNA–miRNA–target gene interaction network was used to find circRNAs associated with radioresistance. Moreover, a protein–protein interaction network was constructed to identify radioresistance-related hub proteins. Results High-throughput sequencing allowed the identification of 16,893 circRNAs involved in the response of HeLa cells to radiation. Compared with the control group, there were 153 differentially expressed circRNAs, of which 76 were up-regulated and 77 were down-regulated. GO covered three domains: biological process (BP), cellular component (CC) and molecular function (MF). The terms assigned to the BP domain were peptidyl-tyrosine dephosphorylation and regulation of cell migration. The identified CC terms were cell–cell adherens junction, nucleoplasm and cytosol, and the identified MF terms were protein binding and protein tyrosine phosphatase activity. The top five KEGG pathways were MAPK signaling pathway, endocytosis, axon guidance, neurotrophin signaling pathway, and SNARE interactions in vesicular transport. The protein–protein interaction analysis indicated that 19 proteins might be hub proteins. Conclusions CircRNAs may play a major role in the response to radiation. These findings may improve our understanding of the role of circRNAs in radioresistance in HeLa cells and allow the development of novel therapeutic approaches.

TXNIP induced by MondoA, rather than ChREBP, suppresses cervical cancer cell proliferation, migration and invasion

2019 ◽  
Vol 167 (4) ◽  
pp. 371-377 ◽  
Author(s):  
Junhua Zhang ◽  
Xingbo Tian ◽  
Huifang Yin ◽  
Songshu Xiao ◽  
Shuijing Yi ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Hela Cells ◽  
Cervical Cancer Cell ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Cancer Cell Proliferation ◽  
Interacting Protein

Abstract Evidence has indicated the associations between thioredoxin-interacting protein (TXNIP) and cancers. However, the role of TXNIP in cervical cancer remains unclear. Hence, this study aims to investigate the role of TXNIP in regulating cervical cancer cell proliferation, migration and invasion. TXNIP expression can be regulated by either MondoA or ChREBP in a cell- or tissue- dependent manner. Thus, we also explored whether TXNIP expression in cervical cancer can be regulated by MondoA or ChREBP. Our results showed that TXNIP expression was decreased in cervical cancer cells (HeLa, SiHa, CaSki, MS751, C-33A). Furthermore, TXNIP overexpression inhibited cell proliferation, migration and invasion in HeLa cells, whereas TXNIP silencing exerted the opposite effect in C-33A cells. Moreover, TXNIP expression could be induced by MondoA, rather than ChREBP in HeLa cells. Additionally, MondoA overexpression inhibited cell proliferation, migration and invasion through upregulating TXNIP in HeLa cells. In summary, TXNIP induced by MondoA, rather than ChREBP, suppresses cervical cancer cell proliferation, migration and invasion. Our findings provide new ideas for the prevention and treatment of cervical cancer.

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 SOX2 Regulates lncRNA CCAT1/MicroRNA-185-3p/FOXP3 Axis to Affect the Proliferation and Self-Renewal of Cervical Cancer Stem Cells

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Li Zhang ◽  
Chunjie Guo ◽  
Tiefeng Ji ◽  
Xin Chen
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Hela Cells ◽  
Self Renewal ◽  
Inhibition Of Proliferation ◽  
Forkhead Box ◽  
Gynecology And Obstetrics ◽  
Non Coding Rnas ◽  
The Relationship

AbstractIt has been presented the role of long non-coding RNAs (lncRNAs) in cervical cancer (CC). We aim to discuss the effect of sex-determining region Y-box 2 (SOX2)/lncRNA colon cancer-associated transcript-1 (CCAT1)/microRNA-185-3p (miR-185-3p)/forkhead box protein 3 (FOXP3) on the proliferation and self-renewal ability of CC stem cells. MiR-185-3p, SOX2, CCAT1 and FOXP3 expressions were tested in CC tissues and cells. The relationship between SOX2/CCAT1 expression and clinicopathological features in CC patients was verified. Loss- and gain-of-function investigations were conducted in CD44+HeLa cells to discuss biological functions and self-renewal capacity. Finally, the relationships among SOX2, CCAT1, FOXP3 and miR-185-3p were verified. miR-185-3p expression was decreased, while SOX2, CCAT1 and FOXP3 expressions were increased in CC tissues and cells. SOX2 and CCAT1 expressions were linked to tumor size, lymph node metastasis and international federation of gynecology and obstetrics stage of CC. Down-regulating SOX2 or CCAT1 and up-regulating miR-185-3p resulted in inhibition of proliferation, invasion, migration and cell sphere number as well as apoptosis acceleration of CD44+HeLa cells. SOX2 could bind to CCAT1 which affected miR-185-3p expression, and FOXP3 was targeted by miR-185-3p.

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