scholarly journals Transcriptome profiling reveals Silibinin dose-dependent response network in non-small lung cancer cells

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10373
Author(s):  
Jagan Mohan Kaipa ◽  
Vytaute Starkuviene ◽  
Holger Erfle ◽  
Roland Eils ◽  
Evgeny Gladilin
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Transcriptome Profiling ◽  
Small Cell Lung ◽  
Silybum Marianum ◽  
Systematic Analysis ◽  
Response Network ◽  
Dose Dependent

Silibinin (SIL), a natural flavonolignan from the milk thistle (Silybum marianum), is known to exhibit remarkable hepatoprotective, antineoplastic and EMT inhibiting effects in different cancer cells by targeting multiple molecular targets and pathways. However, the predominant majority of previous studies investigated effects of this phytocompound in a one particular cell line. Here, we carry out a systematic analysis of dose-dependent viability response to SIL in five non-small cell lung cancer (NSCLC) lines that gradually differ with respect to their intrinsic EMT stage. By correlating gene expression profiles of NSCLC cell lines with the pattern of their SIL IC50 response, a group of cell cycle, survival and stress responsive genes, including some prominent targets of STAT3 (BIRC5, FOXM1, BRCA1), was identified. The relevancy of these computationally selected genes to SIL viability response of NSCLC cells was confirmed by the transient knockdown test. In contrast to other EMT-inhibiting compounds, no correlation between the SIL IC50 and the intrinsic EMT stage of NSCLC cells was observed. Our experimental results show that SIL viability response of differently constituted NSCLC cells is linked to a subnetwork of tightly interconnected genes whose transcriptomic pattern can be used as a benchmark for assessment of individual SIL sensitivity instead of the conventional EMT signature. Insights gained in this study pave the way for optimization of customized adjuvant therapy of malignancies using Silibinin.

Corrigendum to “Phenotypic mismatch repair hMSH2 and hMLH1 gene expression profiles in primary non-small cell lung carcinomas” [Lung Cancer 64 (2009) 282–288]

Lung Cancer ◽  
2010 ◽  
Vol 67 (1) ◽  
pp. 126
Author(s):  
Dimitra Vageli ◽  
Zoe Daniil ◽  
Jubrail Dahabreh ◽  
Eleni Karagianni ◽  
Dimitra N. Vamvakopoulou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Mismatch Repair ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Small Cell ◽  
Small Cell Lung ◽  
Lung Carcinomas ◽  
Hmlh1 Gene

scholarly journals Saikosaponin D inhibits proliferation and induces apoptosis of non-small cell lung cancer cells by inhibiting the STAT3 pathway

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052093716
Author(s):  
Shibo Wu ◽  
Weizhuang Chen ◽  
Kaitai Liu ◽  
Feng Ren ◽  
Dawei Zheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Small Cell ◽  
Small Cell Lung ◽  
Dapi Staining ◽  
Proliferation And Apoptosis ◽  
Dose Dependent

Objective To study the effects of saikosaponin D (SSD) on proliferation and apoptosis in human non-small cell lung cancer cell lines, and to explore underlying mechanisms. Methods Following treatment with saikosaponin D, A549 and H1299 cells were assessed for anti-proliferation effects using cell cycle kit-8 assays, changes in nuclear morphology using 4′,6-diamidino-2-phenylindole (DAPI) staining, and cell apoptosis using annexin V/propidium iodide double staining. Proliferation- and apoptosis-related proteins were detected by immunoblotting. Results Saikosaponin D had dose-dependent inhibitory effects on A549 cells (IC50, 3.57 µM) and H1299 cells (IC50, 8.46 µM). DAPI staining revealed decreased cell numbers, and most H1299 cells became round after treatment with 20 µM saikosaponin D. As saikosaponin D concentration increased, the proportions of cells in G0/G1 phase, and cells undergoing apoptosis, increased. Levels of phosphorylated p44/42 and signal transducer and activator of transcription (STAT)3 were significantly downregulated in both cell lines, while total STAT3 levels were not significantly affected. The cleaved form of caspase 3 was significantly upregulated. Conclusions Saikosaponin D inhibits proliferation, inducing cell cycle arrest and apoptosis, in lung cancer cells in a dose-dependent manner, possibly through inhibition of STAT3 phosphorylation and activation of caspase 3.

scholarly journals Gene Expression Profiles of Non-Small Cell Lung Cancer: Survival Prediction and New Biomarkers

Oncology ◽  
2010 ◽  
Vol 79 (3-4) ◽  
pp. 283-292 ◽  
Author(s):  
Kristjan Välk ◽  
Tõnu Vooder ◽  
Raivo Kolde ◽  
Mari-Ann Reintam ◽  
Cathleen Petzold ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cancer Survival ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Small Cell ◽  
Survival Prediction ◽  
Small Cell Lung ◽  
New Biomarkers ◽  
Lung Cancer Survival
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