scholarly journals Quantitative Proteomic Analysis of the Metastasis-Inhibitory Mechanism of miR-193a-3p in Non-Small Cell Lung Cancer

2015 ◽  
Vol 35 (5) ◽  
pp. 1677-1688 ◽  
Author(s):  
Wei Deng ◽  
Mingxia Yan ◽  
Tao Yu ◽  
Haiyan Ge ◽  
Hechun Lin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Western Blotting ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Protein Profile ◽  
Differentially Expressed ◽  
Lung Cancer Cells ◽  
Positive Effects ◽  
Regulated Expression

Background: microRNAs can repress the expression of target genes by destabilizing their mRNAs or by inhibiting their translation. Our previous findings suggested that miR-193a-3p inhibited the progression of NSCLC both in vitro and in vivo. However, the biological processes and molecular pathways through which this miRNA exerts its positive effects are unknown. Methods: To explore the molecular mechanisms by which miR-193a-3p inhibited NSCLC metastasis, we investigated the changes in the protein profile of SPC-A-1sci (highly metastatic) cells in response to the up-regulation of miR-193a-3p expression using a proteomics approach (iTRAQ combined with NanoLC-MS/MS). Changes in the profiles of the expressed proteins were verified using western blotting and were analyzed using the DAVID and STRING programs. Results: In the two replicated experiments, 4962/4946 proteins were identified, and the levels of expression of 4923/4902 proteins were quantified. In total, 112 of these proteins were differentially expressed. Among them, the up-regulated levels of expression of two of the 62 proteins with up-regulated expression (PPP2R2A and GSN) and the down-regulated levels of expression four of the 50 proteins with down-regulated expression (LMNB2, UHRF1, G3BP1, and HNRNPU) were verified using western blotting. The bioinformatics analysis revealed the interactions and signaling networks of these differentially expressed proteins. Conclusion: miR-193a-3p inhibited the metastasis of lung cancer cells by deregulating the expression of tumor-related proteins. These findings may improve the understanding of the molecular mechanisms underlying the metastatic-inhibitory effect of miR-193a-3p on lung cancer cells.

scholarly journals circDENND4C Promotes Proliferation and Metastasis of Lung Cancer by Upregulating BRD4 Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Dongjie Ma ◽  
Yingzhi Qin ◽  
Shanqing Li ◽  
Li Li ◽  
Jia He ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Cell Activity ◽  
Lung Cancer Cells ◽  
Biological Behavior ◽  
Invasion And Metastasis ◽  
Proliferation And Metastasis

Objective. To investigate the effects of circDENND4C on the malignant biological behavior of lung cancer and its downstream target genes and molecular mechanisms. Methods. The expression of circDENND4C in lung cancer tissues and cells was detected. After transfection with silenced circDENND4C, the expression levels of circDENND4C, miR-141-3p, and BRD4 in lung cancer cells were detected by qRT-PCR. The targeting relationship between circDENND4C and miR-141-3p as well as miR-141-3p and BRD4 was verified. Cell activity was detected by CCK-8 and EdU assay. Transwell assay was used to detect the invasiveness of A549 and NCI-H1299 in each group. Effects of circDENND4C on proliferation and metastasis of lung cancer in nude mice were studied. Results. In vitro and in vivo results showed that circDENND4C silencing reduced the proliferation, invasion, and metastasis of lung cancer cells. Mechanism studies showed that circDENND4C has a targeting relationship with miR-141-3p. However, miR-141-3p has a targeting relationship with BRD4. circDENND4C indirectly upregulated BRD4 through sponge adsorption of miR-141-3p, thereby promoting metastasis and proliferation of NSCLC. Conclusion. circDENND4C, as an oncogene, promotes the proliferation, invasion, and metastasis of lung cancer cells.

Knockdown CYP2S1 inhibits lung cancer cells proliferation and migration

2021 ◽  
pp. 1-9
Author(s):  
Huan Guo ◽  
Baozhen Zeng ◽  
Liqiong Wang ◽  
Chunlei Ge ◽  
Xianglin Zuo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Lung Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

BACKGROUND: The incidence of lung cancer in Yunnan area ranks firstly in the world and underlying molecular mechanisms of lung cancer in Yunnan region are still unclear. We screened a novel potential oncogene CYP2S1 used mRNA microassay and bioinformation database. The function of CYP2S1 in lung cancer has not been reported. OBJECTIVE: To investigate the functions of CYP2S1 in lung cancer. METHODS: Immunohistochemistry and Real-time PCR were used to verify the expression of CYP2S1. Colony formation and Transwell assays were used to determine cell proliferation, invasion and migration. Xenograft assays were used to detected cell growth in vivo. RESULTS: CYP2S1 is significantly up-regulated in lung cancer tissues and cells. Knockdown CYP2S1 in lung cancer cells resulted in decrease cell proliferation, invasion and migration in vitro. Animal experiments showed downregulation of CYP2S1 inhibited lung cancer cell growth in vivo. GSEA analysis suggested that CYP2S1 played functions by regulating E2F targets and G2M checkpoint pathway which involved in cell cycle. Kaplan-Meier analysis indicated that patients with high CYP2S1 had markedly shorter event overall survival (OS) time. CONCLUSIONS: Our data demonstrate that CYP2S1 exerts tumor suppressor function in lung cancer. The high expression of CYP2S1 is an unfavorable prognostic marker for patient survival.

scholarly journals PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer

2021 ◽  
Vol 30 ◽  
pp. 096368972110017
Author(s):  
Jianhao Huang ◽  
Yonghua Zheng ◽  
Xiao Zheng ◽  
Bao Qian ◽  
Qi Yin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Human Lung ◽  
Akt Signaling ◽  
Lung Cancer Cells ◽  
Signaling Cascades ◽  
Human Lung Cancer ◽  
Mesenchymal Transition ◽  
Human Lung Cancer Cells

The type II protein arginine methyltransferase 5 (PRMT5) has been engaged in various human cancer development and progression types. Nevertheless, few studies uncover the biological functions of PRMT5 in the epithelial-mesenchymal transition (EMT) of human lung cancer cells, and the associated molecular mechanisms and signaling cascades are entirely unknown. Here, we show that PRMT5 is the ectopic expression in human lung cancer tissues and cell lines. Further study reveals that silencing PRMT5 by lentivirus-mediated shRNA or blocking of PRMT5 by specific inhibitor GSK591 attenuates the expression levels of EMT-related markers in vivo, using the xenograft mouse model. Moreover, our results show that down-regulation of PRMT5 impairs EGFR/Akt signaling cascades in human lung cancer cells, whereas re-expression of PRMT5 recovers those changes, suggesting that PRMT5 regulates EMT probably through EGFR/Akt signaling axis. Altogether, our results demonstrate that PRMT5 serves as a critical oncogenic regulator and promotes EMT in human lung cancer cells. More importantly, our findings also suggest that PRMT5 may be a potential therapeutic candidate for the treatment of human lung cancer.

scholarly journals Microarray analysis of differentially expressed long non‑coding RNAs in daidzein‑treated lung cancer cells

2021 ◽  
Vol 22 (5) ◽  
Author(s):  
Laifang Li ◽  
Jun Liu ◽  
Xiaobo Wang ◽  
Xiaowei Xiong ◽  
Shaoxin Huang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Microarray Analysis ◽  
Differentially Expressed ◽  
Lung Cancer Cells ◽  
Non Coding Rnas

scholarly journals Identification and characterization of RASSF1C piRNA target genes in lung cancer cells

Oncotarget ◽  
2017 ◽  
Vol 8 (21) ◽  
pp. 34268-34282 ◽  
Author(s):  
Mark E Reeves ◽  
Mathew Firek ◽  
Abdullaati Jliedi ◽  
Yousef G Amaar
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Target Genes ◽  
Lung Cancer Cells ◽  
Identification And Characterization

scholarly journals LncRNA XIST acts as a microRNA-520 sponge to regulate the cisplatin resistance in NSCLC cells by mediating BAX through ceRNA network

2020 ◽  
Author(s):  
Ting-Ting Liu ◽  
Rui Li ◽  
Xiao Liu ◽  
Xi-Jia Zhou ◽  
Chen Huo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Functional Enrichment ◽  
Differentially Expressed ◽  
Lung Cancer Cells ◽  
Venn Diagram ◽  
Cerna Network ◽  
Kaplan Meier ◽  
Lncrna Xist

Abstract Background: In recent years, LncRNA acts as a member of competing endogenous RNA (ceRNA), playing an important role in drug resistance of lung cancer. The aim of this study was to identify potential biomarkers about cisplatin resistant lung cancer cells using a comprehensive ceRNA network.Methods: GSE6410 (GPL-201) analyzed gene expression changes about cispaltin resistance in A549 NSCLC cells. GSE43249 (GPL-14613) included noncoding RNA expression profiling derived from the cisplatin resistant A549 lung cells. GEO2R, an online analysis tool, analyzed the differentially expressed mRNAs and miRNAs (DEmRNAs and DEmiRNAs). To explore the functional enrichment implication of differentially expressed mRNAs, we used the GO and KEGG pathway analysis. Through miRDB、Targetscan、Starbase、miRWalk, we found targeted miRNAs. The Kaplan-Meier curve method was used to show clinical survival analysis of targeted RNAs (P<0.05). The Starbase database predicted potential lncRNAs mediated targeted miRNAs. Eventually, the novel ceRNA network of lncRNAs, miRNAs, mRNA was constructed by cytoscape3.7.2.Results:118 differentially expressed mRNAs were the basis of the mediated ceRNA network. DAVID and Kaplan-Meier picked out BAX, an apoptosis regulator. Venn Diagram demonstrated 8 miRNAs commomly regulating Bax. Starbase predicted lncRNA XIST mediated miRNAs. Finally, lncRNA XIST maybe a useful biomarker regulating cisplatin resistance in lung cancer cells.Conclusions: LncRNA XIST competitively bound to miRNA 520 in the regulation of cisplatin resistance by BAX , participating apoptosis in the p53 signaling pathway.

scholarly journals LncRNA XIST acts as a microRNA-520 sponge to regulate the cisplatin resistance in NSCLC cells by mediating BAX through ceRNA network

2020 ◽  
Author(s):  
Ting-Ting Liu ◽  
Rui Li ◽  
Xiao Liu ◽  
Xi-Jia Zhou ◽  
Chen Huo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Functional Enrichment ◽  
Differentially Expressed ◽  
Lung Cancer Cells ◽  
Venn Diagram ◽  
Cerna Network ◽  
Kaplan Meier ◽  
Lncrna Xist

Abstract Background In recent years, LncRNA acts as a member of competing endogenous RNA (ceRNA), playing an important role in drug resistance of lung cancer. The aim of this study was to identify potential biomarkers about cisplatin resistant lung cancer cells using a comprehensive ceRNA network. Methods GSE6410 (GPL-201) analyzed gene expression changes about cispaltin resistance in A549 NSCLC cells. GSE43249 (GPL-14613) included noncoding RNA expression profiling derived from the cisplatin resistant A549 lung cells. GEO2R, an online analysis tool, analyzed the differentially expressed mRNAs and miRNAs (DEmRNAs and DEmiRNAs). To explore the functional enrichment implication of differentially expressed mRNAs, we used the GO and KEGG pathway analysis. Through miRDB、Targetscan、Starbase、miRWalk, we found targeted miRNAs. The Kaplan-Meier curve method was used to show clinical survival analysis of targeted RNAs (P < 0.05). The Starbase database predicted potential lncRNAs mediated targeted miRNAs. Eventually, the novel ceRNA network of lncRNAs, miRNAs, mRNA was constructed by cytoscape3.7.2. Results 118 differentially expressed mRNAs were the basis of the mediated ceRNA network. DAVID and Kaplan-Meier picked out BAX, an apoptosis regulator. Venn Diagram demonstrated 8 miRNAs commomly regulating Bax. Starbase predicted lncRNA XIST mediated miRNAs. Finally, lncRNA XIST maybe a useful biomarker regulating cisplatin resistance in lung cancer cells. Conclusions LncRNA XIST competitively bound to miRNA 520 in the regulation of cisplatin resistance by BAX, participating apoptosis in the p53 signaling pathway.

scholarly journals Polyisoprenylated Cysteinyl Amide Inhibitors Deplete K-Ras and Induce Caspase-dependent Apoptosis in Lung Cancer Cells

2019 ◽  
Vol 19 (10) ◽  
pp. 838-851 ◽  
Author(s):  
Augustine T. Nkembo ◽  
Felix Amissah ◽  
Elizabeth Ntantie ◽  
Rosemary A. Poku ◽  
Olufisayo O. Salako ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Fold Increase ◽  
Lung Cancer Cells ◽  
Ras Signaling ◽  
Extrinsic Pathway ◽  
Lung Cancers ◽  
Protein Levels

Background: Non-small cell lung cancers (NSCLC) harboring mutation-induced dysregulation of Ras signaling present some of the most difficult-to-manage cases, since directly targeting the constitutively active mutant Ras proteins has not resulted in clinically useful drugs. Therefore, modulating Ras activity for targeted treatment of cancer remains an urgent healthcare need. Objective: In the current study, we investigated a novel class of compounds, the polyisoprenylated cysteinyl amide inhibitors (PCAIs), for their anticancer molecular mechanisms using the NSCLC cell panel with K-Ras and/or other mutant genes. Methods: The effect of the PCAIs on intracellular K-Ras levels, cell viability, apoptosis, spheroid and colony formation were determined. Results: Treatment of the lung cancer cells with the PCAIs, NSL-RD-035, NSL-BA-036, NSL-BA- 040 and NSL-BA-055 resulted in concentration-dependent cell death in both K-Ras mutant (A549, NCI-H460, and NCI-H1573), N-Ras mutant (NCI-H1299) and other (NCI-H661, NCI-H1975, NCIH1563) NSCLC cells. The PCAIs at 1.0 -10 μM induced the degeneration of 3D spheroid cultures, inhibited clonogenic cell growth and induced marked apoptosis via the extrinsic pathway. The most potent of the PCAIs, NSL-BA-055, at 5 μM induced a seven-fold increase in the activity of caspase- 3/7 and a 75% selective depletion of K-Ras protein levels relative to GAPDH in A549 cells that correlated with PCAIs-induced apoptosis. NSL-BA-040 and NSL-BA-055 also induced the phosphorylation of MAP kinase (ERK 1/2). Conclusion: Taken together, PCAIs may be potentially useful as targeted therapies that suppress NSCLC progression through disruption of Ras-mediated growth signaling.

scholarly journals Investigating the intracellular effects of hyperbranched polycation–DNA complexes on lung cancer cells using LC-MS-based metabolite profiling

2019 ◽  
Vol 15 (1) ◽  
pp. 77-87 ◽  
Author(s):  
Ali Alazzo ◽  
Mohammad Ahmad Al-Natour ◽  
Keith Spriggs ◽  
Snjezana Stolnik ◽  
Amir Ghaemmaghami ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Gene Delivery ◽  
Cancer Cells ◽  
Metabolite Profiling ◽  
Molecular Mechanisms ◽  
Lung Cancer Cells ◽  
Dna Complexes ◽  
Gene Delivery Vectors

A metabolomics approach is used to assess the molecular mechanisms underlying the effects of polycation gene delivery vectors on lung cancer cells.

Sign in / Sign up

Export Citation Format

Share Document