Radiosensitization of non-small cell lung carcinoma by EGFR inhibition

Molecular targeted cancer therapy is a promising treatment strategy. Considering the central role of the epidermal growth factor receptor in cell proliferation and survival, there are indications that targeted agents like tyrosine kinase inhibitors, i. e., erlotinib, may enhance the antitumor treatment by radiation. The aim of this study is to analyze the inactivation effects of g-rays and to test the radiosensitizing potential of erlotinib on human lung adenocarcinoma cells in vitro. Irradiations were performed with doses ranging from 1 Gy to 8 Gy. In order to increase the radiosensitivity of CRL-5876 lung adenocarcinoma cells, the cells were treated with a clinically relevant concentration of 2 ?M erlotinib. The effects of single and combined treatments were monitored using clonogenic survival, cell viability and proliferation assays at different time points. For the detection and visualization of the phosphorylated histone H2AX (?-H2AX), an important biological marker of DNA double-strand break formation, fluorescence immunocytochemistry, was performed. The response to the treatment was monitored at four time points: 30 min, 2, 6, and 24 h. Irradiations with g-rays resulted in significant cell inactivation regarding all analyzed biological endpoints. Combined treatments revealed consistent cell inactivation. Moreover, compared to g-rays alone, elevated levels of g-H2AX foci were observed after pretreatment with erlotinib, indicating radiosensitization through impaired DNA repair.

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WIP promotes in-vitro invasion ability, anchorage independent growth and EMT progression of A549 lung adenocarcinoma cells by regulating RhoA levels

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2016.12.040 ◽

2017 ◽

Vol 482 (4) ◽

pp. 1353-1359 ◽

Cited By ~ 7

Author(s):

Amrita Salvi ◽

Thirumaran Thanabalu

Keyword(s):

Lung Adenocarcinoma ◽

Anchorage Independent Growth ◽

In Vitro Invasion ◽

Adenocarcinoma Cells ◽

Lung Adenocarcinoma Cells ◽

A549 Lung

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PD-L1 lncRNA splice promotes lung adenocarcinoma progression via enhancing c-Myc activity

10.1101/2020.09.29.282541 ◽

2020 ◽

Author(s):

Shuang Qu ◽

Zichen Jiao ◽

Geng Lu ◽

Bing Yao ◽

Ting Wang ◽

...

Keyword(s):

Lung Adenocarcinoma ◽

Great Promise ◽

Non Coding Rna ◽

Adenocarcinoma Cells ◽

T Cell Immune Responses ◽

Lung Adenocarcinoma Cells ◽

Novel Strategy ◽

L1 Protein

ABSTRACTAlthough blockade of programmed death-ligand 1 (PD-L1) to enhance T cell immune responses shows great promise in tumor immunotherapy, the efficacy of such immune-checkpoint inhibition strategy is limited for patients with solid tumors. The mechanism underlying the limited efficacy of PD-L1 inhibitors remains unclear. Here, we show that human lung adenocarcinoma, regardless of PD-L1 protein positive or negative, all produce a long non-coding RNA isoform of PD-L1 (PD-L1-lnc) via alternative splicing, which promotes lung adenocarcinoma proliferation and metastasis. PD-L1-lnc in various lung adenocarcinoma cells is significantly upregulated by IFNγ in a manner similar to PD-L1 mRNA. Both in vitro and in vivo studies demonstrate that PD-L1-lnc increases proliferation and invasion but decreases apoptosis of lung adenocarcinoma cells. Mechanistically, PD-L1-lnc directly binds to c-Myc and enhances c-Myc transcriptional activity downstream in lung adenocarcinoma cells. Our results provide targeting PD-L1-lnc−c-Myc axis as a novel strategy for lung cancer therapy.

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Kinesin Family Member 18A (KIF18A) Contributes to the Proliferation, Migration, and Invasion of Lung Adenocarcinoma Cells In Vitro and In Vivo

Disease Markers ◽

10.1155/2019/6383685 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9 ◽

Cited By ~ 2

Author(s):

Fu-Tao Chen ◽

Fu-Kuan Zhong

Keyword(s):

Tumor Growth ◽

Lung Adenocarcinoma ◽

Clinical Stage ◽

Migration And Invasion ◽

Expression Levels ◽

Adenocarcinoma Cells ◽

Lung Adenocarcinoma Cells ◽

Tumor Growth And Metastasis

Objective. To determine the expression levels of KIF18A in lung adenocarcinoma and its relationship with the clinicopathologic features of patients undergoing radical colectomy and explore the potential role in the progression of lung adenocarcinoma. Methods. Immunohistochemical assays were performed to explore the expression levels of KIF18A in 82 samples of lung adenocarcinoma and corresponding normal tissues. According to the levels of KIF18A expression in lung adenocarcinoma tissue samples, patients were classified into the KIF18A high expression group and low expression group. Clinical data related to the perioperative clinical features (age, gender, smoking, tumor size, differentiation, clinical stage, and lymph node metastasis), the potential correlation between KIF18A expression levels, and clinical features were analyzed, and the effects of KIF18A on lung adenocarcinoma cell proliferation, migration, and invasion were measured by colony formation assay, MTT assay, wound healing assay, and transwell assays. The possible effects of KIF18A on tumor growth and metastasis were measured in mice through tumor growth and tumor metastasis assays in vivo. Results. KIF18A in lung adenocarcinoma tissues. Further, KIF18A was significantly associated to clinical characteristic features including the tumor size (P=0.033) and clinical stage (P=0.041) of patients with lung adenocarcinoma. Our data also investigated that KIF18A depletion dramatically impairs the proliferation, migration, and invasion capacity of lung adenocarcinoma cells in vitro and inhibits tumor growth and metastasis in mice. Conclusions. Our study reveals the involvement of KIF18A in the progression and metastasis of lung adenocarcinoma and provides a novel therapeutic target for the treatment of lung adenocarcinoma.

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The effects of the electro-photodynamic in vitro treatment on human lung adenocarcinoma cells

Bioelectrochemistry ◽

10.1016/j.bioelechem.2009.12.006 ◽

2010 ◽

Vol 79 (1) ◽

pp. 90-94 ◽

Cited By ~ 15

Author(s):

Jolanta Saczko ◽

Mariola Nowak ◽

Nina Skolucka ◽

Julita Kulbacka ◽

Malgorzata Kotulska

Keyword(s):

Lung Adenocarcinoma ◽

Human Lung ◽

Human Lung Adenocarcinoma ◽

Adenocarcinoma Cells ◽

Human Lung Adenocarcinoma Cells ◽

Lung Adenocarcinoma Cells ◽

In Vitro Treatment

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Inhibition of SIRT1 Signaling Sensitizes the Antitumor Activity of Silybin against Human Lung Adenocarcinoma Cells In Vitro and In Vivo

Molecular Cancer Therapeutics ◽

10.1158/1535-7163.mct-13-0942 ◽

2014 ◽

Vol 13 (7) ◽

pp. 1860-1872 ◽

Cited By ~ 20

Author(s):

Zhenxing Liang ◽

Yang Yang ◽

Haibin Wang ◽

Wei Yi ◽

Xiaolong Yan ◽

...

Keyword(s):

Antitumor Activity ◽

Lung Adenocarcinoma ◽

Human Lung ◽

Human Lung Adenocarcinoma ◽

Adenocarcinoma Cells ◽

Human Lung Adenocarcinoma Cells ◽

Lung Adenocarcinoma Cells

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The in vitro photodynamic effect of laser activated gallium, indium and iron phthalocyanine chlorides on human lung adenocarcinoma cells

Journal of Photochemistry and Photobiology B Biology ◽

10.1016/j.jphotobiol.2013.08.003 ◽

2013 ◽

Vol 128 ◽

pp. 58-63 ◽

Cited By ~ 23

Author(s):

K. Maduray ◽

B. Odhav

Keyword(s):

Lung Adenocarcinoma ◽

Human Lung ◽

Iron Phthalocyanine ◽

Photodynamic Effect ◽

Human Lung Adenocarcinoma ◽

Adenocarcinoma Cells ◽

Human Lung Adenocarcinoma Cells ◽

Lung Adenocarcinoma Cells

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C/EBPα Suppresses Lung Adenocarcinoma Cell Invasion and Migration by Inhibiting β-Catenin

Cellular Physiology and Biochemistry ◽

10.1159/000479457 ◽

2017 ◽

Vol 42 (5) ◽

pp. 1779-1788 ◽

Cited By ~ 6

Author(s):

Jinchang Lu ◽

Chunling Du ◽

Junxia Yao ◽

Bo Wu ◽

Yanhong Duan ◽

...

Keyword(s):

Transcription Factor ◽

Lung Adenocarcinoma ◽

Cell Invasion ◽

Migration And Invasion ◽

Adenocarcinoma Cell ◽

Invasion And Migration ◽

Adenocarcinoma Cells ◽

Lung Adenocarcinoma Cells ◽

And Migration

Background/Aims: The transcription factor CCAAT/enhancer-binding protein α (C/EBPα) is a basic leucine zipper transcription factor that plays essential roles in tumor progression. Although decreased or absent C/EBPα expression in many cancers suggests a possible role for C/EBPα as a tumor suppressor, the functions of C/EBPα in lung adenocarcinoma remain unclear. Methods: Here, C/EBPα expression levels in 26 lung adenocarcinoma and para-carcinoma tissue samples were detected by qRT-PCR and immunohistochemistry. Cell transwell assays, wound healing assay and three-dimensional spheroid invasion assay were performed to assess the effects of C/EBPα on migration and invasion in lung adenocarcinoma cells in vitro. Western blotting was applied to analyze the potential mechanisms. Results: C/EBPα was found to be decreased in lung adenocarcinoma tissues compared to para-carcinoma tissues. Overexpression of C/EBPα significantly inhibited the migration and invasion of lung adenocarcinoma cells. In addition, C/EBPα overexpression suppressed the epithelial–mesenchymal transition (EMT) that was characterized by a gain of epithelial and loss of mesenchymal markers. Further study showed that C/EBPα suppressed the transcription of β-catenin and downregulated the levels of its downstream targets. Conclusion: Our data suggest that C/EBPα inhibits lung adenocarcinoma cell invasion and migration by suppressing β-catenin-mediated EMT in vitro. Thus, C/EBPα may be helpful as a potential target for treatment of lung adenocarcinoma.

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