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Apoptotic cell death is a highly regulated process, which plays a crucial role in many biological events. Etoposide is an antineoplastic drug, which targets the DNA unwinding enzyme, topoisomerase II. The aim of the present research approach to investigate the expression of the apoptosis-related genes BCL2 (Bcl-2), FAS, Caspase-3, BAX and the new member BCL2L12, cloned by our group, along with treatment of HL-60 leukemia cells with etoposide. The kinetics of apoptosis induction and cell toxicity was evaluated by DNA laddering and MTT method, respectively. The mRNA expression levels of the genes were analyzed by RT-PCR using gene-specific primers. Beta-actin was used as a control gene. An important downregulation of BCL2L12 was observed at 4 h of drug treatment, whereas BAX was upregulated at the same time point. No alteration in the expression pattern of the other apoptosis-related genes was detected. Since, the main anticarcinogenic effect of etoposide is due to the induction of apoptosis, these changes observed in the mRNA expression levels of the genes may be an underlying mechanism.

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This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 2.0 France Licence.

This work is the first to shed light on the potential clinical usefulness of DDC, as an efficient tumor biomarker in gastric cancer. The provided evidence underlines the propitious predictive value of DDC expression in the survival of stomach adenocarcinoma patients.

Embryonic Stem (ES) or induced Pluripotent Stem (iPS) cells are important sources for cardiomyocyte generation, targeted for regenerative therapies. Several in vitro protocols are currently utilized for their differentiation, but the value of cell-based approaches remains unclear. Here, we characterized a cardiovascular progenitor population derived during ES differentiation, after selection based on VE-cadherin promoter (Pvec) activity. ESCs were genetically modified with an episomal vector, allowing the expression of puromycin resistance gene, under Pvec activity. Puromycin-surviving cells displayed cardiac and endothelial progenitor cells characteristics. Expansion and self-renewal of this cardiac and endothelial dual-progenitor population (CEDP) were achieved by Wnt/β-catenin pathway activation. CEDPs express early cardiac developmental stage-specific markers but not markers of differentiated cardiomyocytes. Similarly, CEDPs express endothelial markers. However, CEDPs can undergo differentiation predominantly to cTnT+ (~47%) and VE-cadherin+ (~28%) cells. Transplantation of CEDPs in the left heart ventricle of adult rats showed that CEDPs-derived cells survive and differentiate in vivo for at least 14 days after transplantation. A novel, dual-progenitor population was isolated during ESCs differentiation, based on Pvec activity. This lineage can self-renew, permitting its maintenance as a source of cardiovascular progenitor cells and constitutes a useful source for regenerative approaches.

Gastric cancer constitutes one of the most common neoplasms globally. Kallikrein-related peptidases have attracted interest as potential tumor markers and future targets for novel cancer therapeutics. We have recently reported KLK13 clinical importance as a favorable prognostic biomarker for gastric cancer patients' survival. By aiming to explore how the molecular profile of KLK13 is modified in stomach cancer cells treated with antineoplastic drugs, we examined, for the first time, the mRNA alterations of this gene following gastric cancer cells' exposure to the prominent chemotherapeutic substances epirubicin, oxaliplatin, or methotrexate. The antiproliferative effects of these agents, on AGS cells' growth, were determined by the 3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide and trypan blue assays. Total RNA, isolated from the harvested cells, was reverse-transcribed to cDNA. KLK13 levels were quantified via real-time PCR using the SYBR Green chemistry. The relative changes of KLK13 expression were calculated with the comparative C (t) (2(-ddCt)) method. Distinct KLK13 profiles resulted from AGS cells' incubation with epirubicin or methotrexate for 24, 36, and 48 h. KLK13 expression increased in a time-dependent manner up to 5.70 times (for epirubicin) or 5.76 times (for methotrexate) at 48 h compared with the corresponding untreated cells. According to our results, KLK13 expression is implicated in the molecular pathways that are triggered after administration of anticancer agents on gastric cancer cells. Moreover, our data support the possibility that KLK13 may be exploited as a future molecular predictor of gastric cancer cells' response to chemotherapy.