scholarly journals Cancer-testis gene PIWIL1 promotes cell proliferation, migration, and invasion in lung adenocarcinoma

2017 ◽  
Vol 7 (1) ◽  
pp. 157-166 ◽  
Author(s):  
Kaipeng Xie ◽  
Kai Zhang ◽  
Jing Kong ◽  
Cheng Wang ◽  
Yayun Gu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Migration And Invasion ◽  
Cancer Testis

scholarly journals Upregulation of SOX9 promotes cell proliferation, migration and invasion in lung adenocarcinoma

2015 ◽  
Vol 10 (2) ◽  
pp. 990-994 ◽  
Author(s):  
XIAOYING WANG ◽  
YING JU ◽  
MI ZHOU ◽  
XIAOLI LIU ◽  
CHENGJUN ZHOU
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Migration And Invasion

scholarly journals Overexpression of Long Non-Coding RNA ZXF2 Promotes Lung Adenocarcinoma Progression Through c-Myc Pathway

2015 ◽  
Vol 35 (6) ◽  
pp. 2360-2370 ◽  
Author(s):  
Ze-Tian Yang ◽  
Zhihong Li ◽  
Xian-Guo Wang ◽  
Tao Tan ◽  
Frank Yi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Tumor Progression ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Potential Interaction ◽  
Migration And Invasion ◽  
Relative Expression Level ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Objective: To investigate the expression of long non-coding RNA ZXF2 in lung adenocarcinoma tissues and its effect on cell proliferation, migration and invasion. Methods: Forty pairs of cancerous and adjacent non-cancerous lung adenocarcinoma specimens were collected for the studies. Quantitative real-time PCR was used to analyze the expression of ZXF2 in tumor tissues and adjacent normal tissues. The expression of ZXF2 was correlated with patients' clinico-pathological data. Molecular pathway controlled by ZXF2 was explored by using small interfering RNA (siRNA) technology. CCK-8 cell proliferation assay, flow cytometry analysis and transwell assays were used to evaluate cell proliferation, migration and invasion. Results: The expression of ZXF2 was 2 fold or higher in 27 out of 40 (67.5%) cases of lung adenocarcinoma specimens than that in non-cancerous tissues (P<0.05). The relative expression level of ZXF2 was positively correlated with tumor lymph node metastasis (χ2=8.485, P<0.05) and poor prognosis of the patients (p=0.0217). In order to explore the molecular mechanisms of ZXF2 mediated tumor progression, ZXF2 expression was inhibited by siRNA in A549 cells, a highly aggressive and metastatic lung adenocarcinoma cell line. We found that siRNA-ZXF2 treatment inhibited cell proliferation (P<0.01) leading to cell cycle arrest (P<0.01). The cell migration and invasion were suppressed by siRNA-ZXF2 treatment (P<0.01). Further biochemical studies revealed that the knockdown of ZXF2 led to down regulation of c-Myc signaling. Conclusion: ZXF2 was overexpressed in lung adenocarcinoma tissues and the high expression of ZXF was closely related to tumor progression through c-Myc related pathway. Given the fact that both ZXF2 and c-Myc are located in the same chromosome 8q24.2 loci, the potential interaction between ZXF2 and c-Myc might be a novel target for treatment of lung adenocarcinoma.

scholarly journals MiR-200b-3p Functions as an Oncogene by Targeting ABCA1 in Lung Adenocarcinoma

2019 ◽  
Vol 18 ◽  
pp. 153303381989259 ◽  
Author(s):  
Keqiang Liu ◽  
Weiqiang Zhang ◽  
Jian Tan ◽  
Jingbo Ma ◽  
Jing Zhao
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Adenosine Triphosphate ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Adenocarcinoma Cell ◽  
Matrigel Invasion ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

Objective: The aim of this study was to investigate the microRNA-200b-3p expression in lung adenocarcinoma and the possible functional associations of microRNA-200b-3p with cell proliferation, migration, and invasion. Methods: Quantitative real-time polymerase chain reaction was used to detect the expression of microRNA-200b-3p in lung adenocarcinoma samples and in the human lung adenocarcinoma cell lines A549 and H1299. A549 and H1299 cells were transfected with either a microRNA-200b-3p mimic or a negative control microRNA or either an empty vector or an adenosine triphosphate-binding cassette transporter A-1 overexpression vector. A Cell Counting Kit-8 assay was employed to assess the ability of cell proliferation. Transwell assays and transwell-Matrigel invasion assay were, respectively, utilized to assess the capacity of migration and invasion in A549 and H1299 cells. Results: The results showed that microRNA-200b-3p expression was significantly upregulated in tumor tissues compared with that in adjacent normal tissues. Overexpression of microRNA-200b-3p promoted lung adenocarcinoma cell proliferation and metastasis. Furthermore, adenosine triphosphate-binding cassette transporter A-1 was a direct target of microRNA-200b-3p, and this binding was verified by luciferase reporter analysis. Overexpression of adenosine triphosphate-binding cassette transporter A-1 obviously suppressed lung adenocarcinoma cell proliferation, migration, and invasion. Lung adenocarcinoma cell phenotypes induced by microRNA-200b-3p overexpression could be partially remitted by the co-overexpression of microRNA-200b-3p and adenosine triphosphate-binding cassette transporter A-1. Conclusion: This study first identified that microRNA-200b-3p is upregulated in lung adenocarcinoma cells and associated with cell proliferation and metastasis. MicroRNA-200b-3p promoted lung adenocarcinoma cell proliferation and metastasis by suppressing adenosine triphosphate-binding cassette transporter A-1. MicroRNA-200b-3p may function as a novel molecular marker and therapeutic target for lung adenocarcinoma treatment.

scholarly journals ACOT11 promotes cell proliferation, migration and invasion in lung adenocarcinoma

2020 ◽  
Vol 9 (5) ◽  
pp. 1885-1903
Author(s):  
Chaoyang Liang ◽  
Xiaowei Wang ◽  
Zhenrong Zhang ◽  
Fei Xiao ◽  
Hongxiang Feng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Migration And Invasion

scholarly journals Evaluation of the Oncogene Function of GOLPH3 and Correlated Regulatory Network in Lung Adenocarcinoma

2021 ◽  
Vol 11 ◽  
Author(s):  
Tong Zhang ◽  
Yue Wang ◽  
Yangyang Chen ◽  
Shuo Jin ◽  
Ying Gao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Survival Analysis ◽  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Interaction Network ◽  
Cell Receptor ◽  
Migration And Invasion ◽  
Biological Regulation ◽  
Protein Protein Interaction ◽  
Human Protein Atlas

BackgroundGolgi phosphoprotein 3 (GOLPH3) is an oncoprotein localized in the Golgi apparatus. Abnormal GOLPH3 expression is potentially related to carcinogenesis. However, the potential biological regulation network of GOLPH3 in lung adenocarcinoma (LUAD) remains to be determined.MethodsExpression of GOLPH3 was identified in LUAD via TIMER, Oncomine, Lung Cancer Explorer (LCE), Human Protein Atlas (HPA), and UALCAN database. Survival analysis was performed using the Kaplan–Meier plotter. GOLPH3 alterations were analyzed through cBioPortal. LinkedOmics was used to perform functional analysis and predict interacted targets. The protein–protein interaction network was constructed by GeneMANIA. In addition, candidate miRNAs and lncRNAs targeting GOLPH3 were generated to construct competing endogenous RNA (ceRNA) network, and survival analysis of ceRNA was performed using LnCeVar. The mRNA or protein expression of TUG1, miR-142-5p, and GOLPH3 in Beas-2B and LUAD cells was verified using qPCR or Western blotting. CCK-8 assay, wound healing assay, and transwell assay were used to detect the ability of cell proliferation, migration, and invasion.ResultsOverexpression of GOLPH3 was identified in LUAD. UALCAN analysis showed that upregulated GOLPH3 was linked to different pathological features of LUAD patients. Importantly, high GOLPH3 expression indicated a negative correlation with the first progression (FP) in LUAD patients. GOLPH3 alterations were also found. Moreover, co-expressed genes with GOLPH3 were analyzed; and they were involved in ribosome and oxidative phosphorylation pathways. Functional network analysis indicated GOLPH3 regulated T-cell receptor signaling pathway and interferon signaling pathway with kinase and transcription factor targets. Notably, TUG1/miR-142-5p/GOLPH3 affected overall survival of LUAD patients. GOLPH3 expression was decreased in the cells with overexpression of miR-142-5p and TUG1 knockdown. GOLPH3 reduction inhibited cell proliferation, migration, and invasion.ConclusionsUpregulation of GOLPH3 has a positive correlation with clinicopathological subtypes and poor FP in LUAD. GOLPH3 promoted LUAD progression. Moreover, TUG1 may act as ceRNA to regulate GOLPH3 expression by competitive binding miR-142-5p.

Long noncoding RNA LINC00968 inhibits proliferation, migration and invasion of lung adenocarcinoma through  targeting  miR-22-5p / CDC14A  axis

2020 ◽  
Author(s):  
Chao Wu ◽  
Xuzhao Bian ◽  
Liyuan Zhang ◽  
Yang Wu ◽  
Tianli Pei ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Division ◽  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Cell Division Cycle ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Over Expression ◽  
Node Metastasis

Abstract Background Lung adenocarcinoma (LUAD) is a high aggressive human cancer which usually diagnosed at advanced stages. Accumulating evidences indicate that long noncoding RNAs (lncRNAs) are crucial participants in LUAD progression. Methods The mRNA levels of LINC00968, miR-22-5p and cell division cycle 14A (CDC14A) were measured using quantitative real-time PCR. Cell proliferation was evaluated using cell counting kit-8 and flow cytometry. Cell migration and cell invasion were assessed by wound healing and transwell assay, respectively. The interactions between LINC00968 and miR-22-5p were validated by RNA immunoprecipitation, RNA pull down and luciferase reporter assay. Results We found that lncRNA LINC00968 was significantly down-regulated in LUAD tissues and cell lines. LINC00968 level was positively correlated to survival rate, and negatively correlated to tumor node metastasis stage, tumor size and lymph node metastasis of LUAD patients. LINC00968 over-expression in LUAD cells inhibited cell proliferation and induced cell cycle arrest at G1 phase. LINC00968 over-expression also suppressed migration, invasion and epithelial mesenchymal transition (EMT) as evidenced by elevated E-cadherin, decreased N-cadherin, TWIST and SNAIL levels. We further validated that LINC00968 localized in cytoplasma and acted as an upstream of microRNA miR-22-5p, which was up-regulated in LUAD tissues and cell lines. Besides, elevated miR-22-5p expression abolished the effect of LINC00968 over-expression on LUAD progression including in vivo tumor growth. In addition, we first validated that cell division cycle 14A (CDC14A), which was down-regulated in LUAD tissues, was a downstream target of miR-22-5p. We over-expressed CDC14A in LUAD cells and miR-22-5p induced LUAD progression was partially reversed. Conclusion our study demonstrated that LINC00968 inhibited proliferation, migration and invasion of LUAD by sponging miR-22-5p and further restoring CDC14A. This novel regulatory network might provide us with promising diagnostic and therapeutic target in LUAD treatment.

scholarly journals Long Noncoding RNA RGMB-AS1 Indicates a Poor Prognosis and Modulates Cell Proliferation, Migration and Invasion in Lung Adenocarcinoma

PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0150790 ◽  
Author(s):  
Ping Li ◽  
Guojun Zhang ◽  
Juan Li ◽  
Rui Yang ◽  
Shanshan Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Poor Prognosis ◽  
Migration And Invasion
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