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We found that the overexpression of FMR4 in both cell lines resulted in an increase in cell proliferation compared to the control vector treated cells (P<0.0001) (Figure 6C D).
However, the addition of EGF to TGF-β treatment in both cell lines resulted in indications of the acquisition of mesenchymal characteristics on both the protein and mRNA levels.
Subsequent miR-9-3p transfected lysates from both cell lines resulted in evidence of a significant reduction in markers of autophagic flux (TT: Figure 2A and B and MZ-CRC-1: C and D).
Downregulation of PDGFRα in both cell lines resulted in a statistically significant decrease in invasion of approximately 70%, while PDGFRβ knockdown inhibited invasion by approximately 40% (not determined to be statistically significant).
Mohapatra and colleagues [ 27] reported that XIAP depletion did not result in increased apoptosis in p53 wild type LNCaP or p53 deficient PC-3 prostate cancer cells although over-expression of p53 in both cell lines resulted in apoptosis following XIAP depletion.
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Although both cell lines result from HPV-mediated transformation, the two lines respond quite differently to treatments with chemotherapeutic drugs.
The rationale for developing this dual EGFR/HER2 TKI was to sustain synergistic inhibition of cancer cells by simultaneously targeting receptors in both cell lines, resulting in more potent inhibition in cell growth than could be achieved by targeting either EGFR or HER2 alone [ 56].
However, cortisol treatments did not exert any significant changes in the gene expression of mTOR, rictor or raptor in both cell lines (results not shown).
In both cell lines, results indicated an enrichment of genes associated with biosynthetic processes, cell cycle and growth, signaling, protein synthesis, stress response, biological regulation and metabolism (Table 1).
To test this possibility we assessed the status of p53 activation after the expression of HDAC7 in both SD-1 and Namalwa cells and found that the presence of HDAC7 in both the cell lines resulted in the phosphorylation and acetylation of p53 at serine 392 and lysine 382, respectively, two post-translational modifications indicative of p53 activation.
Silencing of LDHA gene in both prostate cancer cell lines resulted in significant radiosensitisation.
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