scholarly journals CircZNF652 accelerates the proliferation and migration of primary lung carcinoma cells by downregulating miR-766

2021 ◽  
Vol 20 (11) ◽  
pp. 2255-2260
Author(s):  
Xiaobing Hong ◽  
Yongqing Chen ◽  
Danzhen Zhang
Keyword(s):  
Lung Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Biological Functions ◽  
Mesenchymal Transition ◽  
Lung Carcinoma Cells ◽  
Kaplan Meier ◽  
Primary Lung Carcinoma ◽  
Knockdown Effect ◽  
And Migration

Purpose: To explore the biological functions and molecular mechanism of circZNF652 involvement in primary lung carcinoma.Methods: CircZNF652 levels in primary lung carcinoma cases and controls were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Its prognostic value in primary lung carcinoma was examined by depicting it with Kaplan-Meier curves. The biological functions of circZNF652 in regulating proliferative and migratory capacities in A549 and SPC-A-1 cells were analyzed from the curves. Interaction between circZNF652 and its downstream gene, miR-766, wasassessed, and their co-regulation on primary lung carcinoma was determined by rescue experiments.Results: CircZNF652 was abnormally and significantly upregulated in primary lung carcinoma cases (p< 0.05), resulting in a poor prognosis. The knockdown effect of circZNF652 attenuated the proliferative and migratory capacities of A549 and SPC-A-1 cells, and downregulated epithelial-mesenchymal transition (EMT)-associated genes. CircZNF652 bound and negatively regulated miR-766, a keydownstream gene involved in circZNF652-induced aggravation of primary lung carcinoma.Conclusion: CircZNF652 serves as an oncogene, triggering the aggravation of primary lung carcinoma by negatively regulating miR-766. The results of this study may provide new insights into the treatment of lung carcinoma.

scholarly journals The crosstalk between p38 and Akt signaling pathways orchestrates EMT by regulating SATB2 expression in NSCLC cells

Tumor Biology ◽  
2017 ◽  
Vol 39 (9) ◽  
pp. 101042831770621 ◽  
Author(s):  
Hakan Kucuksayan ◽  
Hakan Akca
Keyword(s):  
Lung Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Binding Protein ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Carcinoma Cells ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Mesenchymal Transition ◽  
Lung Carcinoma Cells

Epithelial–mesenchymal transition is a crucial event for metastasis and could be mediated by several pathways such as phosphoinositide 3-kinase/Akt, mitogen-activated protein kinases, as well as many epigenetic regulators. Special AT-rich sequence-binding protein 2 is an epigenetic regulator involved in epithelial–mesenchymal transition and osteoblastic differentiation. It has been reported that the crosstalk between several pathways is responsible for the regulation of epithelial–mesenchymal transition in cancer cells. However, crosstalks between p38 and Akt pathways involved in epithelial–mesenchymal transition are still unknown. We recently reported that there is a crosstalk between p38 and Akt pathways in non-small-cell lung carcinoma cells, and this crosstalk is associated with E-cadherin and special AT-rich sequence-binding protein 2 expressions. Therefore, we aimed to determine whether this crosstalk has a mediator role in the regulation of epithelial–mesenchymal transition in non-small-cell lung carcinoma. Our results showed that inhibition of p38 leads to the disruption of this crosstalk via decreased expression of phosphatase and tensin homolog (PTEN) and subsequently increased activation of Akt in non-small-cell lung carcinoma cells. Then, we found that p38 inhibition upregulated special AT-rich sequence-binding protein 2 expression and reversed epithelial–mesenchymal transition in non-small-cell lung carcinoma cells. Furthermore, special AT-rich sequence-binding protein 2 knockdown abolished the effect of p38 inhibition on epithelial–mesenchymal transition in non-small-cell lung carcinoma cells. In conclusion, our results strongly indicate that the crosstalk between p38 and Akt pathways can determine special AT-rich sequence-binding protein 2 expression and epithelial character of non-small-cell lung carcinoma cells, and special AT-rich sequence-binding protein 2 is a critical epigenetic regulator for epithelial–mesenchymal transition mediated by p38 pathway in non-small-cell lung carcinoma. Our findings will contribute to illuminate the molecular mechanisms of the epithelial–mesenchymal transition process that has a critical significance for lung cancer metastasis.

MiR-32 Suppresses the Development of Lung Cancer via Modulating PI3K/Akt

2021 ◽  
Vol 11 (7) ◽  
pp. 1271-1276
Author(s):  
Qing-Feng Liu ◽  
Ye Zhang ◽  
Lei Deng ◽  
Tao Zhang ◽  
Jian-Ping Xiao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Carcinoma ◽  
Target Gene ◽  
A549 Cells ◽  
Carcinoma Cells ◽  
Lung Carcinoma Cells ◽  
Kaplan Meier ◽  
Primary Lung Carcinoma ◽  
Apoptosis Assay ◽  
The Impact

Our team utilized qRT-PCR for prospecting miR-32 expression level in primary lung carcinoma tissues and cell lines, as well as Kaplan–Meier method for dissecting the relation of miR-32 expression with the prognosis of lung carcinoma. We transfected lung cancer A549 cells with miR-32 mimic/inhibitor and mimic/inhibitor NC, and appraised the influences of miR-32 on the phenotype changes of lung carcinoma cells via MTT assay, wound healing assay and cell apoptosis assay, separately. Then the target gene of miR-32 was predicted via bioinformatics. Finally, Western blotting was adopted for analyzing the impact of alteration of miR-32 expression on the PI3K/Akt axis in A549 cells. In lung carcinoma tissues as well as cells, miR-32 expression is down-regulated, and miR-32 partakes in the progress of lung carcinoma via PI3K/Akt pathway.

INHIBITION OF MALIGNANT POTENTIAL AND EXPRESSION OF PROTEINS ASSOCIATED WITH EPITHELIAL-MESENCHYMAL TRANSITION IN LEWIS LUNG CARCINOMA CELLS TRANSDUCED WITH MURINE ifn-/3 GENE IN RECOMBINANT BACULOVIRUS

2016 ◽  
Vol 38 (1) ◽  
pp. 13-21
Author(s):  
O O Lykhova ◽  
O Kovalova ◽  
N Bezdenezhnykh ◽  
I Adamenko ◽  
A Vorontsova ◽  
...  
Keyword(s):  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Recombinant Baculovirus ◽  
Malignant Potential ◽  
Carcinoma Cells ◽  
Lewis Lung ◽  
Mesenchymal Transition ◽  
Lung Carcinoma Cells ◽  
P Gene

Aim: To analyze biological characteristics, malignant potential and expression of protei.os associated with epithelial-mesenchymal transition in murine lung carcinoma cells transduced with interferon-beta (ifn-{J) gene in baculovirus vector. Materials and Meth­ ods; The study was performed on Lewis lung carcinoma (LL) ceUs transduced  with ifil-P gene in recombinant bacuJovirus vector. Biological characteristics of the LL cells were studied with the use of standard cell culture methods, cytogenetic and immunocyto­ chemical assays. Results: Recombinant baculovirus-mediated transduction ofLLcells with ifn-P gene resulted i.o significant decrease of cell growth rate and density both io compJete and serum-free medium.Also, LL ceUs transduction with ifn-P gene significantly inhibited ceU migration  in vitro.Transduction of LL cells by baculovirus vector with or without ifn-{J gene caused significant geno­ tox.ic effect  in these ceUs. Furthermore, ifn-{J gene transfer to lung carcinoma cells resulted in significant increase of nuclear ex­ pression ofpl(p       < 0.01), p21w.IJ'e (p < 0.001),cytoplasmlc expression ofE-cadherin (p < 0.005) and inhibition oftranscrlption factors of epithelial-mesenchymal transition (EMn Twist (p <0.005) and Slug (p < 0.00 I) expression.Condusions: Transduction with ij11-{J gene of LL cells in recombinant baculovirus resulted in acquirement of less malignant phenotype i11 vitro and suppressed expression of proteins associated with EMT.

scholarly journals Benzotriazole Enhances Cell Invasive Potency in Endometrial Carcinoma Through CTBP1-Mediated Epithelial-Mesenchymal Transition

2017 ◽  
Vol 44 (6) ◽  
pp. 2357-2367 ◽  
Author(s):  
Yiquan Wang ◽  
Chencheng Dai ◽  
Cheng Zhou ◽  
Wenqu Li ◽  
Yujia Qian ◽  
...  
Keyword(s):  
Endometrial Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Expression Patterns ◽  
Underlying Mechanism ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Female Reproductive Health ◽  
Gene Microarray Analysis ◽  
And Migration

Background/Aims: Benzotriazole (BTR) and its derivatives, such as intermediates and UV stabilizers, are important man-made organic chemicals found in everyday life that have been recently identified as environmental toxins and a threat to female reproductive health. Previous studies have shown that BTR could act as a carcinogen by mimicking estrogen. Environmental estrogen mimics could promote the initiation and development of female cancers, such as endometrial carcinoma, a type of estrogenic-sensitive malignancy. However, there is little information on the relationship between BTR and endometrial carcinoma. In this study, we aimed to demonstrate the biological function of BTR in endometrial carcinoma and explored the underlying mechanism. Methods: The CCK-8 assay was performed to detect cell viability; transwell-filter assay was used to assess cell invasion; gene microarray analysis was employed to determine gene expression patterns in response to BTR treatment; western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were carried out to detect the expression levels of BTR-related genes. Results: Our data showed that BTR could induce the invasion and migration of endometrial carcinoma cells (Ishikawa and HEC-1-B). In addition, BTR increased the expression level of CTBP1, which could enhance the epithelial-mesenchymal transition (EMT) in cancer cells. Moreover, CTBP1 silencing reversed the effect of BTR on EMT progression in endometrial carcinoma cells. Conclusion: This study indicates that BTR could act as a carcinogen to promote the development of endometrial carcinoma mainly through CTBP1-mediated EMT, which deserves more attention.

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