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 Detailed Characterization of a High-molecular-weight Glycoprotein Secreted by Lung Cancer Cells

1993 ◽  
Vol 84 (9) ◽  
pp. 982-988 ◽  
Author(s):  
Noritaka Nonaka ◽  
Ken-ichi Manaka ◽  
Kunihiko Kobayashi ◽  
Hidematsu Hiraideceased
Keyword(s):  
Lung Cancer ◽  
Molecular Weight ◽  
Cancer Cells ◽  
High Molecular Weight ◽  
Lung Cancer Cells ◽  
Detailed Characterization

Characterization of cultured primary/metastatic lung cancer cells obtained by percutaneous puncture

2017 ◽  
Author(s):  
Adriana Rojas Moreno ◽  
Alejandra Cañas Arboleda ◽  
Angelica Herreño ◽  
Maria Jose Fernandez ◽  
Juan Andres Mejia ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Metastatic Lung Cancer ◽  
Percutaneous Puncture ◽  
Metastatic Lung

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 Structural characterization of centipede oligopeptides and capability detection in human small cell lung carcinoma: inducing apoptosis

RSC Advances ◽  
2019 ◽  
Vol 9 (19) ◽  
pp. 10927-10936
Author(s):  
JingQuan Zhao ◽  
Jianmei Yang ◽  
Zerui Hao ◽  
Yulin An ◽  
Mingqiang Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Carcinoma ◽  
Structural Characterization ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma

SSMO-5 mediated the lung cancer cells apoptosis by activating the caspases and regulating the interaction of p53/MDM2.

scholarly journals Dual-strand tumor suppressor miR-193b-3p and -5p inhibit malignant phenotypes of lung cancer by suppressing their common targets

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Kyung Hee Choi ◽  
Chang Hoon Shin ◽  
Woo Joo Lee ◽  
Haein Ji ◽  
Hyeon Ho Kim
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Heart Development ◽  
Target Genes ◽  
Quantitative Polymerase Chain Reaction ◽  
Metastatic Potential ◽  
Lung Cancer Cells ◽  
Metastatic Lung Cancer ◽  
Metastatic Lung

Abstract Emerging studies suggest that microRNAs (miRNAs) play multiple roles in cancer malignancy, including proliferation and acquisition of metastatic potential. Differentially expressed miRNAs responsible for the malignancy of lung cancer were searched by miRNA microarray using a previously established brain metastatic lung cancer model. Twenty-five miRNAs were down-regulated in brain metastatic lung cancer cells. Among those, miR-193b-3p and -5p were chosen for further studies. Their function in metastatic potential and proliferation was examined using Transwell invasion, wound healing, and colony forming assays. The underlying mechanism of tumor-suppressor miR-193b-3p and -5p was explored using reverse transcriptase quantitative polymerase chain reaction (RT-qPCR), Western blot, Argonaute 2-RNA immunoprecipitation (Ago2-RIP), and reporter assays. Both strands of miR-193b were down-regulated in brain metastatic lung cancer cells and in tissues from lung cancer patients. Overexpression of miR-193b-3p and -5p inhibited invasive and migratory activities and diminished clonogenic ability. Conversely, inhibition of miR-193b-3p or -5p increased the metastatic potential and colony forming ability. Cyclin D1 (CCND1), Ajuba LIM Protein (AJUBA), and heart development protein with EGF like domains 1 (HEG1) were identified as common target genes of miR-193b-3p and -5p. A reporter assay and an Ago2-RIP experiment showed that both miRNAs directly bind to the 3′ untranslated region (3′UTR) of the target mRNA. Knockdown of target gene reduced the proliferative and metastatic potential of primary and metastatic lung cancer cells. Our results demonstrate miR-193b is a dual-strand tumor suppressor and a novel therapeutic target for lung cancer.

scholarly journals An Integrated Expression Profiling Reveals Target Genes of TGF-β and TNF-α Possibly Mediated by MicroRNAs in Lung Cancer Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e56587 ◽  
Author(s):  
Akira Saito ◽  
Hiroshi I. Suzuki ◽  
Masafumi Horie ◽  
Mitsuhiro Ohshima ◽  
Yasuyuki Morishita ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Expression Profiling ◽  
Target Genes ◽  
Lung Cancer Cells ◽  
Tnf Α

scholarly journals P3.02b-122 Characterization of Afatinib Resistant Lung Cancer Cells (PC9/Afa) and Reversal of Resistance by T790M Specific Tyrosine Kinase Inhibitors

2017 ◽  
Vol 12 (1) ◽  
pp. S1267-S1268
Author(s):  
Anya Maan-Yuh Lin ◽  
Ming-Hung Huang ◽  
Hui-Ju Huang ◽  
Bao-Shuo Huang ◽  
Jih-Hsiang Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tyrosine Kinase ◽  
Cancer Cells ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Lung Cancer Cells

Characterization of human lung cancer cells resistant to 4′-O-demethyl-4β-(2′′-nitro-4′′-fluoroanilino)-4-desoxypodophyllotoxin, a unique compound in the epipodophyllotoxin antitumor class

2000 ◽  
Vol 11 (1) ◽  
pp. 19-28 ◽  
Author(s):  
Yoko Tachibana ◽  
Xiao-Kang Zhu ◽  
Preethi Krishnan ◽  
Kuo-Hsiung Lee ◽  
Kenneth F Bastow
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells ◽  
Unique Compound

scholarly journals Characterization of cancer omics and drug perturbations in panels of lung cancer cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Ayako Suzuki ◽  
Keiichi Onodera ◽  
Ken Matsui ◽  
Masahide Seki ◽  
Hiroyasu Esumi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Stress Response ◽  
Cancer Cells ◽  
Chemical Compounds ◽  
Lung Cancer Cells ◽  
New Combinations ◽  
Rna Seq ◽  
Lung Cancers

AbstractTo better understand the disruptions of transcriptional regulations and gene expression in lung cancers, we constructed a multi-omics catalogue of the responses of lung cancer cells to a series of chemical compounds. We generated and analyzed 3,240 RNA-seq and 3,393 ATAC-seq libraries obtained from 23 cell lines treated with 95 well-annotated compounds. To demonstrate the power of the created multi-omics resource, we attempted to identify drugs that could induce the designated changes alone or in combination. The basal multi-omics information was first integrated into co-expression modules. Among these modules, we identified a stress response module that may be a promising drug intervention target, as new combinations of compounds that could be used to regulate this module and the consequent phenotypic appearance of cancer cells have been identified. We believe that the multi-omics profiles generated in this study and the strategy used to stratify them will lead to more rational and efficient development of anticancer drugs.

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