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Cytotoxicity was assessed, for both cell lines, by the AlamarBlue® assay (Invitrogen, Eugene, OR) according to the manufacturer instructions.
Both BBS mutations impaired leptin-mediated pSTAT3 activation in both cell lines by affecting either the trafficking or the quantities of leptin receptor in these cells.
The rescue effect was induced in both cell lines by the CM, which was abrogated if BAY-11-7082 waddedded to the CM.
Transport inhibition studies showed dose dependent inhibition of fructose transport in both cell lines by the newly synthesized 6-deoxy-6-fluoro-d-fructose (6FDF).
The presence of Mycoplasma contamination was tested in both cell lines by PCR using the primers 5′-ACTCCTACGGGAGGCAGCAGT-3′ and 5′-TGCACCATCTGTCACTCTGTTAACCTC-3′, which amplifies the spacer regions between the 16S and 23S ribosomal RNA genes.
CTCFL/BORIS was one methylated CTA that became significantly upregulated in both cell lines by both drugs.
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However, the mRNA content of FasL was strongly upregulated in both cells lines by oxaliplatin treatment, being these effects more pronounced in the resistant cell line (20-fold) than in the normal one (4-fold) (Figure 6B).
The majority of cells from both cell lines died by apoptosis induced by treatment with the derivatives.
Growth stimulation by AA in both cell lines, and by LA in MAC13, was effectively inhibited by both the cyclo-oxygenase and lipoxygenase inhibitor indomethacin, and the lipoxygenase inhibitor BWA4C in a dose-dependent manner.
Intracellular ROS generation in both cell lines increased by hyperthermia treatment and decreased by N-acetyl-L-cysteine (NAC) treatment.
Efatutazone suppressed increased TGF-β2 secretion from both cell lines (shown by ELISA) and downregulation of TGF-β2 transcription (observed by quantitative RT-PCR).
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Justyna Jupowicz-Kozak
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