Differential Notch1 and Notch2 expression in non-small cell lung cancer

2019 ◽  
Vol 1 ◽  
pp. 8-12
Author(s):  
J. Pancewicz ◽  
P.L. Bernatowicz
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Nsclc Cell ◽  
Expression Level ◽  
Lung Cancer Cells ◽  
Small Cell Lung

<b>Introduction:</b> NOTCH signaling can be deregulated in non-small cell lung cancer and can have oncogenic or tumor suppressive functions. NOTCH1 is regulated equally with NOTCH2, and the stability of the expression of those Notch receptors could determine the biological functions of lung cancer cells. <br/><b>Purpose:</b> To estimate expression level of NOTCH2 receptor in diverse NSCLC cell lines. Furthermore, we compared the mRNA level of NOTCH2 expression to the level of NOTCH1 expression. <br/><b>Materials and methods:</b> We have evaluated the mRNA manifestation of NOTCH1 and NOTCH2 genes by using quantitative real time method (RT-PCR). Moreover, we associated the results from NSCLC cells with results achieved in non-cancerous human bronchial epithelial cells (HBEpC). <br/><b>Results:</b> The expression level of NOTCH1 and NOTCH2 was downregulated in NSCLC cell lines, when related to HBEpC. Nevertheless, the decrease in NOTCH1 expression was significant, whereas NOTCH2 was not much different from the expression in control cells. <br/><b>Conclusions:</b> We conclude that NOTCH1 and NOTCH2 most likely have different biological function in NSCLC. They are active in NSCLC cell lines; nonetheless both are downregulated in lung cancer cells used in this study. Moreover, NOTCH2 expression is comparatively higher than NOTCH1 expression.

scholarly journals Lnc-GAN1 expression is associated with good survival and suppresses tumor progression by sponging mir-26a-5p to activate PTEN signaling in non-small cell lung cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Rui-Qi Wang ◽  
Xiao-Ran Long ◽  
Ning-Ning Zhou ◽  
Dong-Ni Chen ◽  
Mei-Yin Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Expression Level ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Non Coding Rnas

Abstract Background Long non-coding RNAs (lncRNAs) play vital roles in the development and progression of non-small-cell lung cancer (NSCLC); however, the role of most lncRNAs in NSCLC remains unknown. This study explored the clinical significance, biological function and underlying mechanism of lnc-GAN1 in NSCLC. Methods With a custom lncRNA microarray we found that lnc-GAN1 is markedly downregulated in NSCLC tissues. Then lnc-GAN1 expression level was measured using qRT-PCR in NSCLC tissues and cell lines. Survival was assessed using the Kaplan-Meier method. The biological functions of lnc-GAN1 in lung cancer cells were evaluated in vitro and in vivo. RNA fluorescence in situ hybridization and subcellular localization assays revealed the subcellular distribution of lnc-GAN1 in cells. Bioinformatic analysis was adopted to predict miRNAs and signaling pathways regulated by lnc-GAN1. RNA immunoprecipitation and Dual-luciferase reporter assays were used to assess the interaction between lnc-GAN1 and miR-26a-5p in lung cancer cells. Results lnc-GAN1 is downregulated in HCC tissues and associated with larger tumor size and poor overall survival and disease-free survival; its ectopic expression suppresses cell proliferation, colony formation, and cell cycle progression and induces apoptosis in NSCLC cells; it also inhibits tumor growth in the NSCLC xenograft model. We further proved that lnc-GAN1 is localized in cytoplasm and transcribed independently from its parental gene GAN. Mechanistically, lnc-GAN1 acts as a sponge for miR-26a-5p by two seed sequences, and the two non-coding RNAs have a negative relationship in NSCLC tissues; we further prove that PTEN is a direct target of miR-26a-5p and lnc-GAN1 inhibits cell cycle signaling pathway by activating PTEN, whose expression level correlated negatively with miR-26a-5p level but positively with lnc-GAN1 level in NSCLC samples. Conclusions Lnc-GAN1 is downregulated and associated with poor survival of NSCLC patients, and mechanistically acts as a tumor suppressor via sponging and inhibiting miR-26a-5p to upregulate PTEN. This study provides a potential prognostic biomarker and treatment target for NSCLC.

scholarly journals Antitumor agent yatein from Calocedrus formosana Florin leaf induces apoptosis in non-small-cell lung cancer cells

2019 ◽  
Vol 65 (1) ◽  
Author(s):  
Shang-Tse Ho ◽  
Chi-Chen Lin ◽  
Tung-Lin Wu ◽  
Yu-Tang Tung ◽  
Jyh-Horng Wu
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Hexane Fraction ◽  
Small Cell Lung ◽  
Calocedrus Formosana

Abstract Calocedrus formosana Florin is a softwood tree species with high economic value in Taiwan. Several bioactivities of the extracts of C. formosana have been reported; however, only one study focused on the anti-non-small-cell lung cancer cells’ (anti-NSCLC) effect of C. formosana extract and its active phytocompound. In the present study, the anti-lung cancer effects of C. formosana leaf extract and its active derivative yatein were evaluated. The results revealed that the n-hexane fraction of the crude extract exhibited the highest cytotoxicity potential against two non-small-cell lung cancer (NSCLC) cell lines, namely A549 and CL1-5. Yatein, isolated from the n-hexane fraction, exhibited the highest cytotoxicity in the A549 and CL1-5 cells. In addition, the CL1-5 cells were more sensitive than the A549 cells after yatein treatment. Flow cytometry results revealed that yatein induced apoptosis in the two cell lines. Furthermore, expression of regulatory proteins related to apoptosis, such as caspase 3, caspase 8, caspase 9, and poly (ADP-ribose) polymerase (PARP), increased in the A549 and CL1-5 cells after yatein treatment. These findings provide insight into the in vitro anti-lung tumor efficacy of yatein, thus rendering this phytocompound a potential anticancer lead compound for NSCLC treatment.

The Key microRNAs Regulated the Development of Non-small Cell Lung Cancer by Targeting TGF-β-induced epithelial–mesenchymal Transition

2019 ◽  
Vol 22 (4) ◽  
pp. 238-244 ◽  
Author(s):  
Gang Chen ◽  
Bo Ye
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Nsclc Cell ◽  
Normal Lung ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Mesenchymal Transition

Purpose: Epithelial-to-Mesenchymal Transition (EMT) was reported to play a key role in the development of Non-Small Cell Lung Cancer (NSCLC). The process of EMT is regulated by the changes of miRNAs expression. However, it is still unknown which miRNA changed the most in the process of canceration and whether these changes played a role in tumor development. Methods: A total of 36 SCLC patients treated in our hospital between 11th, 2015 and 10th, 2017 were enrolled. The samples of cancer tissues and paracancer tissues of patients were collected and analyzed. Then, the miRNAs in normal lung cells and NSCLC cells were also analyzed. In the presence of TGF-β, we transfected the miRNA mimics or inhibitor into NSCLC cells to investigate the role of the significantly altered miRNAs in cell migration and invasion and in the process of EMT. Results: MiR-330-3p was significantly up-regulated in NSCLC cell lines and tissues and miRNA- 205 was significantly down-regulated in NSCLC cell lines and NSCLC tissues. Transfected miRNA-205 mimics or miRMA-330-3p inhibitor inhibited the migration and invasion of NCIH1975 cell and restrained TGF-β-induced EMT in NSCLC cells. Conclusion: miRNA-330-3p and miRNA-205 changed the most in the process of canceration in NSCLC. Furthermore, miR-330-3p promoted cell invasion and metastasis in NSCLC probably by promoting EMT and miR-205 could restrain NSCLC likely by suppressing EMT.

Paeonol Inhibits Migration, Invasion and Bone Adhesion of Small Cell Lung Cancer Cells

2015 ◽  
Vol 10 (2) ◽  
pp. 126-130
Author(s):  
Yong Tian ◽  
Cong Chen ◽  
Yu Zhang ◽  
Zhen Zhang ◽  
Haiyan Xie
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung

scholarly journals Melatonin Downregulates PD-L1 Expression and Modulates Tumor Immunity in KRAS-Mutant Non-Small Cell Lung Cancer

2021 ◽  
Vol 22 (11) ◽  
pp. 5649
Author(s):  
Yi-Chun Chao ◽  
Kang-Yun Lee ◽  
Sheng-Ming Wu ◽  
Deng-Yu Kuo ◽  
Pei-Wei Shueng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Tumor Immunity ◽  
Cell Lung Cancer ◽  
Kras Mutation ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Syngeneic Mouse Model

Non-small cell lung cancer (NSCLC) patients harboring a KRAS mutation have unfavorable therapeutic outcomes with chemotherapies, and the mutation also renders tolerance to immunotherapies. There is an unmet need for a new strategy for overcoming immunosuppression in KRAS-mutant NSCLC. The recently discovered role of melatonin demonstrates a wide spectrum of anticancer impacts; however, the effect of melatonin on modulating tumor immunity is largely unknown. In the present study, melatonin treatment significantly reduced cell viability accompanied by inducing cell apoptosis in KRAS-mutant NSCLC cell lines including A549, H460, and LLC1 cells. Mechanistically, we found that lung cancer cells harboring the KRAS mutation exhibited a higher level of programmed death ligand 1 (PD-L1). However, treatment with melatonin substantially downregulated PD-L1 expressions in both the presence and absence of interferon (IFN)-γ stimulation. Moreover, KRAS-mutant lung cancer cells exhibited higher Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) levels, and PD-L1 expression was positively correlated with YAP and TAZ in lung cancer cells. Treatment with melatonin effectively suppressed YAP and TAZ, which was accompanied by downregulation of YAP/TAZ downstream gene expressions. The combination of melatonin and an inhibitor of YAP/TAZ robustly decreased YAP and PD-L1 expressions. Clinical analysis using public databases revealed that PD-L1 expression was positively correlated with YAP and TAZ in patients with lung cancer, and PD-L1 overexpression suggested poor survival probability. An animal study further revealed that administration of melatonin significantly inhibited tumor growth and modulated tumor immunity in a syngeneic mouse model. Together, our data revealed a novel antitumor mechanism of melatonin in modulating the immunosuppressive tumor microenvironment by suppressing the YAP/PD-L1 axis and suggest the therapeutic potential of melatonin for treating NSCLC.

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