scholarly journals Encapsulated miR-200c and Nkx2.1 in a nuclear/mitochondria transcriptional regulatory network of non-metastatic and metastatic lung cancer cells

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Olga D’Almeida ◽  
Omar Mothar ◽  
Esther Apraku Bondzie ◽  
Yolande Lieumo ◽  
Laure Tagne ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Regulatory Network ◽  
Transcriptional Regulatory Network ◽  
Lung Cancer Cells ◽  
Metastatic Lung Cancer ◽  
Transcriptional Regulatory ◽  
Metastatic Lung

scholarly journals In vivoselection for spine-derived highly metastatic lung cancer cells is associated with increased migration, inflammation and decreased adhesion

Oncotarget ◽  
2015 ◽  
Vol 6 (26) ◽  
pp. 22905-22917 ◽  
Author(s):  
Xiaopan Cai ◽  
Jian Luo ◽  
Xinghai Yang ◽  
Huayun Deng ◽  
Jishen Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Metastatic Lung Cancer ◽  
Metastatic Lung

scholarly journals Conditionally reprogrammed cells (CRC) methodology does not allow thein vitroexpansion of patient-derived primary and metastatic lung cancer cells

2018 ◽  
Vol 143 (1) ◽  
pp. 88-99 ◽  
Author(s):  
Giovanni Sette ◽  
Valentina Salvati ◽  
Ilenia Giordani ◽  
Emanuela Pilozzi ◽  
Denise Quacquarini ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Metastatic Lung Cancer ◽  
Metastatic Lung

scholarly journals Nm23-H1 was involved in regulation of KAI1 expression in high-metastatic lung cancer cells L9981

2016 ◽  
Vol 8 (6) ◽  
pp. 1217-1226 ◽  
Author(s):  
Jiacong You ◽  
Rui Chang ◽  
Bin Liu ◽  
Lingling Zu ◽  
Qinghua Zhou
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Metastatic Lung Cancer ◽  
Metastatic Lung

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 ABL allosteric inhibitors synergize with statins to enhance apoptosis of metastatic lung cancer cells

Cell Reports ◽  
2021 ◽  
Vol 37 (4) ◽  
pp. 109880
Author(s):  
Jillian Hattaway Luttman ◽  
Jacob P. Hoj ◽  
Kevin H. Lin ◽  
Jiaxing Lin ◽  
Jing Jin Gu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Metastatic Lung Cancer ◽  
Allosteric Inhibitors ◽  
Metastatic Lung

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 BSCI-05. ABL2-HSF1-E2F signaling axis promotes lung adenocarcinoma brain metastasis

2021 ◽  
Vol 3 (Supplement_3) ◽  
pp. iii2-iii2
Author(s):  
Ann Marie Pendergast ◽  
Jacob Hoj ◽  
Benjamin Mayro
Keyword(s):  
Lung Cancer ◽  
Heat Shock ◽  
Brain Metastasis ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Physical Interaction ◽  
Heat Shock Factor 1 ◽  
Metastatic Lung Cancer ◽  
Allosteric Inhibitors ◽  
Metastatic Lung

Abstract Brain metastases are the most common intracranial tumors in adults and are associated with increased patient morbidity and mortality. Limited therapeutic options are currently available for the treatment of brain metastasis. We have identified an actionable signaling pathway utilized by metastatic tumor cells whereby the transcriptional regulator Heat Shock Factor 1 (HSF1) drives a transcriptional program, divergent from its canonical role as the master regulator of the heat shock response, leading to enhanced expression of a subset of E2F transcription factor family gene targets. We showed that HSF1 is required for survival and outgrowth by metastatic lung cancer cells in the brain parenchyma. Unexpectedly, we identified the ABL2 tyrosine kinase as an upstream regulator of HSF1 protein expression, and showed that the Src-homology 3 (SH3) domain of ABL2 directly interacts with HSF1 protein at a non-canonical, proline-independent SH3 interaction motif. Importantly, knockdown of ABL2 impairs expression of HSF1 protein and HSF1-E2F transcriptional gene targets. Notably, we found that pharmacologic inhibition of the ABL kinases using selective ABL allosteric inhibitors, but not ATP-competitive inhibitors, ablates the physical interaction between ABL2 and HSF1, leading to markedly decreased expression of HSF1, E2F1 and E2F8 proteins in brain-metastatic lung cancer cells, and depletion of HSF1-E2F transcriptional targets. These findings highlight potential differences affecting intra- and inter-molecular protein-protein interactions induced by allosteric versus ATP-competitive kinase inhibitors that have important therapeutic implications. Importantly, the targetable nature of the ABL2-HSF1-E2F signaling network identifies ABL allosteric inhibitors as a potentially effective therapy for the treatment of metastatic lung cancers characterized by high expression of HSF1.

scholarly journals Label-Free Quantitative Proteomics and N-terminal Analysis of Human Metastatic Lung Cancer Cells

2014 ◽  
Vol 37 (6) ◽  
pp. 457-466 ◽  
Author(s):  
Hophil Min ◽  
Dohyun Han ◽  
Yikwon Kim ◽  
Jee Yeon Cho ◽  
Jonghwa Jin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Quantitative Proteomics ◽  
Lung Cancer Cells ◽  
Metastatic Lung Cancer ◽  
Label Free ◽  
Metastatic Lung
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