scholarly journals Inhibition of histone deacetylases sensitizes EGF receptor-TK inhibitor-resistant non-small-cell lung cancer cells to erlotinib in vitro and in vivo

2017 ◽  
Vol 174 (20) ◽  
pp. 3608-3622 ◽  
Author(s):  
Weiwei Yu ◽  
Weiqiang Lu ◽  
Guoliang Chen ◽  
Feixiong Cheng ◽  
Hui Su ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Histone Deacetylases ◽  
Egf Receptor ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals The HDAC inhibitor panobinostat (LBH589) inhibits mesothelioma and lung cancer cells in vitro and in vivo with particular efficacy for small cell lung cancer

2009 ◽  
Vol 8 (8) ◽  
pp. 2221-2231 ◽  
Author(s):  
M. Cecilia Crisanti ◽  
Africa F. Wallace ◽  
Veena Kapoor ◽  
Fabian Vandermeers ◽  
Melissa L. Dowling ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Hdac Inhibitor ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung

scholarly journals Irradiation Decreases the Neuroendocrine Biomarker Pro-Opiomelanocortin in Small Cell Lung Cancer Cells In Vitro and In Vivo

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0148404 ◽  
Author(s):  
Suzanne L. Meredith ◽  
Jennifer L. Bryant ◽  
Muhammad Babur ◽  
Philip W. Riddell ◽  
Roya Behrouzi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung

scholarly journals Circ_0003998 Regulates the Progression and Docetaxel Sensitivity of DTX-Resistant Non-Small Cell Lung Cancer Cells by the miR-136-5p/CORO1C Axis

2021 ◽  
Vol 20 ◽  
pp. 153303382199004
Author(s):  
Wei Zhang ◽  
Chao Song ◽  
Xiaona Ren
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Colony Formation ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Colony

Background: Drug resistance in cancer cells is a major challenge for anti-cancer therapy. Circular RNA (circRNA) circ_0003998 has been identified as an important regulator in the chemoresistance development of non-small cell lung cancer (NSCLC). The purpose of this study was to investigate the molecular basis underlying the resistance control of circ_0003998 in NSCLC. Methods: The levels of circ_0003998, miR-136-5p and coronin 1C (CORO1C) were gauged by the quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Cell viability, colony formation and apoptosis were evaluated by the Cell Counting Kit-8 (CCK-8), colony formation and flow cytometry assays, respectively. Targeted relationships among circ_0003998, miR-136-5p and CORO1C were confirmed by the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Animal studies were performed to evaluate the function of circ_0003998 in vivo. Results: Our data indicated that circ_0003998 expression was associated with NSCLC resistance to docetaxel (DTX). The knockdown of circ_0003998 promoted DTX sensitivity, suppressed cell colony formation, and enhanced cell apoptosis of A549/DTX and H1299/DTX cells in vitro. Moreover, circ_0003998 knockdown hampered tumor growth and enhanced DTX sensitivity in vivo. Mechanistically, circ_0003998 directly targeted miR-136-5p, and miR-136-5p was a molecular mediator of circ_0003998 function in vitro. Furthermore, CORO1C was a functionally important target of miR-136-5p in regulating DTX-resistant NSCLC cell colony formation, apoptosis and DTX sensitivity in vitro. Additionally, circ_0003998 modulated CORO1C expression by working as a miR-136-5p sponge. Conclusion: Our present work identified that circ_0003998 regulated DTX-resistant NSCLC cell colony formation, apoptosis and DTX sensitivity at least partially by controlling CORO1C expression by sponging miR-136-5p, illuminating a rationale for developing circ_0003998 as a therapeutic target of chemoresistant NSCLC.

Targeting pyruvate kinase M2 contributes to radiosensitivity of non-small cell lung cancer cells in vitro and in vivo

2015 ◽  
Vol 356 (2) ◽  
pp. 985-993 ◽  
Author(s):  
Mao-Bin Meng ◽  
Huan-Huan Wang ◽  
Wen-Hao Guo ◽  
Zhi-Qiang Wu ◽  
Xian-Liang Zeng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Pyruvate Kinase ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Pyruvate Kinase M2

scholarly journals miR-144-5p Enhances the Radiosensitivity of Non-Small-Cell Lung Cancer Cells via Targeting ATF2

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Lei Song ◽  
Liping Peng ◽  
Shucheng Hua ◽  
Xiaoping Li ◽  
Lianjun Ma ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Stem Cell Differentiation ◽  
Small Cell ◽  
Nsclc Cell ◽  
Small Cell Lung

MicroRNAs (miRNAs or miRs) regulate gene expression at the posttranscriptional level and are involved in many biological processes such as cell proliferation and migration, stem cell differentiation, inflammation, and apoptosis. In particular, miR-144-3p is downregulated in various cancers, and its overexpression inhibits the proliferation and metastasis of cancer cells. However, the role of miR-144-5p in non-small-cell lung cancer (NSCLC), especially radiosensitivity, is unknown. In this study, we found that miR-144-5p was downregulated in NSCLC clinical specimens as well as NSCLC cell lines exposed to radiation. Enhanced expression of miR-144-5p promoted the radiosensitivity of NSCLC cells in vitro and A549 cell mouse xenografts in vivo. Furthermore, we identified activating transcription factor 2 (ATF2) as the direct and functional target of miR-144-5p using integrated bioinformatics analysis and a luciferase reporter assay. In addition, restoration of ATF2 expression inhibited miR-144-5p-induced NSCLC cell sensitivity to radiation in vitro and in vivo. Our findings suggest that deregulation of the miR-144-5p/ATF2 axis plays an important role in NSCLC cell radiosensitivity, thus representing a new potential therapeutic target for NSCLC.

A pilot study on the anticancer effects of novel candidate agent COH-SR4 in lung cancer.

2012 ◽  
Vol 30 (30_suppl) ◽  
pp. 28-28
Author(s):  
David Berz
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Anticancer Effects ◽  
Resected Tumor

28 Background: Non-small cell lung cancer is the leading cause of cancer deaths in the US. The success of current treatment strategies is limited by frequent aberrations in multiple signaling pathways. This includes loss-of-function mutations in the tumor suppressor p53 and activating mutations in multiple growth factor receptors, which converge to activate PI3K/Akt pathway. This calls for the development of novel, more active treatments. We investigated the anti-cancer effects of a novel compound called 1, 3 bis (3, 5-dichlorophenyl) urea (COH-SR4) in lung cancer. Methods: The anticancer effects of COH-SR4 were tested in p53-null H358 lung cancer cells. The antiproliferative effects were investigated in vitro by MTT assay. The bio-availability and antitumor effects were determined in vivo following the administration of 4 mg/kg of COH-SR4 to mice and H358-nu/nu nude mice xenografts. Results: The treatment with COH-SR4 resulted in effective inhibition of the proliferative potential of H358 lung cancer cells [IC50: 23+2 µM], effectively inducing apoptosis. The 4 mg/kg COH-SR4 administration resulted in a free serum concentration of 1+ 0.3 µM. Regression of established H358-xenografts was achieved without any overt toxicity. The histopathology of resected tumor sections revealed an increase in pAMPK (T172) and a decrease in the nuclear proliferative marker Ki 67 and angiogenesis marker CD31. Western blot analyses of resected tumor lysates revealed a decrease in pAkt (S473) and anti-apoptotic protein Bcl2 along with an increase in pAMPK (T172), pro-apoptotic Bax and cleaved PARP levels. In addition, COH-SR4 lead to a decrease in the levels of the cell cycle regulators CDK4 and cyclin B1 as well as the mesenchymal marker vimentin, whilst increasing the epithelial marker E-cadherin. Conclusions: COH-SR4 represents a novel agent for the treatment of non small cell lung cancer. We demonstrated pronounced anti-proliferative and pro-apoptotic activity in vitro and in vivo as well as the capability to promote physiologic, epithelial differentiation. This implies not only therapeutic, but also preventive potential. Further studies are needed to establish the best possible clinical applications of COH-SR4 in lung cancer.

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