scholarly journals Unbiased Selection of Peptide–Peptoid Hybrids Specific for Lung Cancer Compared to Normal Lung Epithelial Cells

2015 ◽  
Vol 10 (12) ◽  
pp. 2891-2899 ◽  
Author(s):  
Jaya M. Matharage ◽  
John D. Minna ◽  
Rolf A. Brekken ◽  
D. Gomika Udugamasooriya
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Normal Lung ◽  
Lung Epithelial ◽  
Selection Of

The Downregulation of Long Noncoding RNA Metastasis Associated with Colon Cancer 1 (lncRNA MACC1-AS1) Inhibits the Migration and Invasion of Non-Small Cell Lung Cancer Cells

2021 ◽  
Vol 11 (3) ◽  
pp. 453-457
Author(s):  
Caidi Zhang ◽  
Xinzhong Zou
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Small Cell ◽  
Lung Epithelial Cells ◽  
Normal Lung ◽  
Small Cell Lung ◽  
Lung Epithelial

To explore the effects of lncRNA MACC1-AS1 on the invasion and migration of non-small cell lung cancer (NSCLC), PCR was used to detect and compare lncRNA MACC1-AS1 expression in NSCLC cells to normal lung epithelial cells and assess the knockdown effect of lncRNA MACC1-AS1 in A549 and H1299 cell lines. The Transwell system was employed to compare the invasiveness of the lncRNA MACC1-AS1 knockdown cells to the control cells. The migratory ability of the lncRNA MACC1-AS1 knockdown cells was compared to the control cells via in vitro scratch assay. Western blot was used to detect the E-cadherin/N-cadherin expression. Balb/c mouse model was used to verify the metastasis ability in vivo between the control and lncRNA MACC1-AS1 knockdown groups. The level of lncRNA MACC1-AS1 was markedly higher in lung cancer cells than normal lung epithelial cells. The knockdown of lncRNA MACC1-AS1 reduced the invasiveness and migratory capacity of A549 and H1299 cells. Downregulating lncRNA MACC1-AS1 upregulated E-cadherin but down-regulated N-cadherin in A549 and H1299 cells. Besides, the silencing of lncRNA MACC1-AS1 reduced the A549 cells’ ability to metastasize in vivo. LncRNA MACC1-AS1 can enhance the invasiveness and migratory capability of NSCLC.

scholarly journals Metformin Protects against Radiation-Induced Acute Effects by Limiting Senescence of Bronchial-Epithelial Cells

2021 ◽  
Vol 22 (13) ◽  
pp. 7064
Author(s):  
Christine Hansel ◽  
Samantha Barr ◽  
Alina V. Schemann ◽  
Kirsten Lauber ◽  
Julia Hess ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Tissue ◽  
Cellular Stress ◽  
Lung Epithelial Cells ◽  
Normal Lung Tissue ◽  
Normal Lung ◽  
Metformin Treatment ◽  
Acute Effects ◽  
Lung Epithelial ◽  
Radiation Induced

Radiation-induced damage to normal lung parenchyma remains a dose-limiting factor in thorax-associated radiotherapy (RT). Severe early and late complications with lungs can increase the risk of morbidity in cancer patients after RT. Herein, senescence of lung epithelial cells following RT-induced cellular stress, or more precisely the respective altered secretory profile, the senescence-associated secretory phenotype (SASP), was suggested as a central process for the initiation and progression of pneumonitis and pulmonary fibrosis. We previously reported that abrogation of certain aspects of the secretome of senescent lung cells, in particular, signaling inhibition of the SASP-factor Ccl2/Mcp1 mediated radioprotection especially by limiting endothelial dysfunction. Here, we investigated the therapeutic potential of a combined metformin treatment to protect normal lung tissue from RT-induced senescence and associated lung injury using a preclinical mouse model of radiation-induced pneumopathy. Metformin treatment efficiently limited RT-induced senescence and SASP expression levels, thereby limiting vascular dysfunctions, namely increased vascular permeability associated with increased extravasation of circulating immune and tumor cells early after irradiation (acute effects). Complementary in vitro studies using normal lung epithelial cell lines confirmed the senescence-limiting effect of metformin following RT finally resulting in radioprotection, while fostering RT-induced cellular stress of cultured malignant epithelial cells accounting for radiosensitization. The radioprotective action of metformin for normal lung tissue without simultaneous protection or preferable radiosensitization of tumor tissue might increase tumor control probabilities and survival because higher radiation doses could be used.

scholarly journals Ex vivo model of non‑small cell lung cancer using mouse lung epithelial cells

2017 ◽  
Author(s):  
Taku Sato ◽  
Mami Morita ◽  
Ryota Tanaka ◽  
Yui Inoue ◽  
Miyuki Nomura ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Small Cell Lung Cancer ◽  
Ex Vivo ◽  
Small Cell ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Small Cell Lung ◽  
Ex Vivo Model ◽  
Lung Epithelial

scholarly journals Down-Regulation of p23 in Normal Lung Epithelial Cells Reduces Toxicities From Exposure to Benzo[a]pyrene and Cigarette Smoke Condensate via an Aryl Hydrocarbon Receptor-Dependent Mechanism

2018 ◽  
Vol 167 (1) ◽  
pp. 239-248 ◽  
Author(s):  
Jinyun Chen ◽  
Poonam Yakkundi ◽  
William K Chan
Keyword(s):  
Epithelial Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Cigarette Smoke ◽  
Lung Epithelial Cells ◽  
Normal Lung ◽  
Cigarette Smoke Condensate ◽  
Down Regulation ◽  
Protein Levels ◽  
Aryl Hydrocarbon ◽  
Lung Epithelial

Abstract The aryl hydrocarbon receptor (AHR) is a ligand-activated signaling molecule which controls tumor growth and metastasis, T cell differentiation, and liver development. Expression levels of this receptor protein is sensitive to the cellular p23 protein levels in immortalized cancer cell lines. As little as 30% reduction of the p23 cellular content can suppress the AHR function. Here we reported that down-regulation of the p23 protein content in normal, untransformed human bronchial/tracheal epithelial cells to 48% of its content also suppresses the AHR protein levels to 54% of its content. This p23-mediated suppression of AHR is responsible for the suppression of (1) the ligand-dependent induction of the cyp1a1 gene transcription; (2) the benzo[a]pyrene- or cigarette smoke condensate-induced CYP1A1 enzyme activity, and (3) the benzo[a]pyrene and cigarette smoke condensate-mediated production of reactive oxygen species. Reduction of the p23 content does not alter expression of oxidative stress genes and production of PGE2. Down regulation of p23 suppresses the AHR protein levels in two other untransformed cell types, namely human breast MCF-10A and mouse immune regulatory Tr1 cells. Collectively, down-regulation of p23 suppresses the AHR protein levels in normal and untransformed cells and can in principle protect our lung epithelial cells from AHR-dependent oxidative damage caused by exposure to agents from environment and cigarette smoking.

scholarly journals Selection of rhinovirus 1A variants adapted for growth in mouse lung epithelial cells

Virology ◽  
2011 ◽  
Vol 420 (2) ◽  
pp. 82-88 ◽  
Author(s):  
Angela L. Rasmussen ◽  
Vincent R. Racaniello
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Lung Epithelial ◽  
Selection Of

Cigarette Smoking Condensate Disrupts Endoplasmic Reticulum–Golgi Network Homeostasis Through GOLPH3 Expression in Normal Lung Epithelial Cells

2016 ◽  
Vol 18 (9) ◽  
pp. 1877-1885 ◽  
Author(s):  
Kyeong-Nam Yu ◽  
Hyeon-Jeong Kim ◽  
Sanghwa Kim ◽  
Orkhouselenge Dawaadamdin ◽  
Ah-Young Lee ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Cigarette Smoking ◽  
Lung Epithelial Cells ◽  
Normal Lung ◽  
Lung Epithelial ◽  
Golgi Network

scholarly journals Induction of cPLA2in Lung Epithelial Cells and Non-small Cell Lung Cancer Is Mediated by Sp1 and c-Jun

2001 ◽  
Vol 276 (46) ◽  
pp. 42737-42743 ◽  
Author(s):  
Stacy A. Blaine ◽  
Marilee Wick ◽  
Christina Dessev ◽  
Raphael A. Nemenoff
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Epithelial Cells ◽  
Small Cell Lung ◽  
Lung Epithelial

scholarly journals Lung Krüppel-like factor (LKLF) is a transcriptional activator of the cytosolic phospholipase A2 α promoter

2005 ◽  
Vol 387 (1) ◽  
pp. 239-246 ◽  
Author(s):  
Marilee J. WICK ◽  
Stacy BLAINE ◽  
Vicki VAN PUTTEN ◽  
Milene SAAVEDRA ◽  
Raphael A. NEMENOFF
Keyword(s):  
Epithelial Cells ◽  
Phospholipase A2 ◽  
Promoter Activity ◽  
Cytosolic Phospholipase A2 ◽  
Dominant Negative ◽  
Lung Epithelial Cells ◽  
Mitogen Activated Protein Kinase ◽  
Normal Lung ◽  
Cytosolic Phospholipase ◽  
Lung Epithelial

Increased expression of cPLA2 (cytosolic phospholipase A2) has been shown to be the cause of tumorigenesis of NSCLC (non-small-cell lung cancer). Our laboratory has previously demonstrated that oncogenic forms of Ras increase transcription of cPLA2 in normal lung epithelial cells and NSCLC lines through activation of the ERK (extracellular-signal-regulated kinase) and JNK (c-Jun N-terminal kinase) MAPK (mitogen-activated protein kinase) family. We have also defined a minimal region of the cPLA2 promoter that is critical for this induction. To identify potential transcription factors that bind to this region and regulate expression, a yeast one-hybrid screen was performed with a rat lung cDNA library. Multiple members of the Krüppel family were identified, with LKLF (lung Krüppel-like factor) being isolated a number of times. Overexpression of LKLF in lung epithelial cells or Drosophila SL-2 cells increased cPLA2 promoter activity. Conversely, expression of a dominant negative form of LKLF inhibited induction of cPLA2 promoter activity by oncogenic Ras in normal lung epithelial cells and NSCLC. By electrophoretic mobility-shift assay analysis, it was found that LKLF bound to a GC-rich region of the cPLA2 promoter located between −37 and −30 upstream from the transcription start site. Expression of siRNA (small interfering RNA) directed against LKLF inhibited basal expression of cPLA2 in lung epithelial cells and blocked induction by H-Ras. In NSCLC, siRNA against LKLF co-operated with siRNA against Sp1 (stimulatory protein 1) to inhibit cPLA2 promoter activity. Finally, recombinant LKLF was a substrate for ERKs. These results indicate that LKLF is an important regulator of cPLA2 expression and participates in the induction of this protein, which is critical for increased eicosanoid production associated with lung tumorigenesis.

scholarly journals CHUK/IKK-α loss in lung epithelial cells enhances NSCLC growth associated with HIF up-regulation

2019 ◽  
Vol 2 (6) ◽  
pp. e201900460
Author(s):  
Evangelia Chavdoula ◽  
David M Habiel ◽  
Eugenia Roupakia ◽  
Georgios S Markopoulos ◽  
Eleni Vasilaki ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Epithelial Cells ◽  
Transcriptome Profiling ◽  
Lung Epithelial Cells ◽  
Tumor Promoter ◽  
Alveolar Type ◽  
Hypoxic Conditions ◽  
Lung Epithelial

Through the progressive accumulation of genetic and epigenetic alterations in cellular physiology, non–small-cell lung cancer (NSCLC) evolves in distinct steps involving mutually exclusive oncogenic mutations in K-Ras or EGFR along with inactivating mutations in the p53 tumor suppressor. Herein, we show two independent in vivo lung cancer models in which CHUK/IKK-α acts as a major NSCLC tumor suppressor. In a novel transgenic mouse strain, wherein IKKα ablation is induced by tamoxifen (Tmx) solely in alveolar type II (AT-II) lung epithelial cells, IKKα loss increases the number and size of lung adenomas in response to the chemical carcinogen urethane, whereas IKK-β instead acts as a tumor promoter in this same context. IKKα knockdown in three independent human NSCLC lines (independent of K-Ras or p53 status) enhances their growth as tumor xenografts in immune-compromised mice. Bioinformatics analysis of whole transcriptome profiling followed by quantitative protein and targeted gene expression validation experiments reveals that IKKα loss can result in the up-regulation of activated HIF-1-α protein to enhance NSCLC tumor growth under hypoxic conditions in vivo.

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