Abstract
Investigation of the Cell Stabilization and the Epithelial to Mesenchymal Transition Effect of Flavopiridol in Mouse Lung Squamous Cell Carcinoma
Highlights
Lung malignancy is a leading cause of cancer related morbidity and mortality worldwide
We investigated the effect of flavopiridol on the expression of two putative stem cell markers, plasma membrane-associated glycoproteins CD133 and CD44 in squamous cell lung cancers (SqCLCs) cell line
The percentages of Cd133+/Cd44+ cells in the flavopiridol treated cells when compared with the control untreated cells
Summary
Lung malignancy is a leading cause of cancer related morbidity and mortality worldwide. The three main subtypes of NSCLC are adenocarcinoma, SqCLCs and large-cell carcinoma. More than 55% of lung carcinomas harbor at least one genetic alteration, most of them being histologic subtype specific. This fact suggests that inhibition of cdks involved in the control of cell cycle is not the only mechanism of action. Inhibition of cdk’s with additional functions (i.e. involved in the control of transcription or function of proteins that do not control cell cycle) may contribute to the antitumoral effect. Direct and indirect inhibition of receptor activation (EGFR) and: or a direct inhibition of kinases (pp Src, PKC, Erk-1) involved in the signal transduction pathway could play a role in the antiproliferative activity of flavopiridol [4]. The three main subtypes of Non-small cell lung cancer (NSCLC) are adenocarcinoma, squamous cell lung cancers (SqCLCs) and large-cell carcinoma. The present study focused on the effect of flavopiridol in cell stabilization, cell adhesion, junctional complex and epithelial to mesenchymal transition (EMT) in mouse lung squamous cell carcinoma cell
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