Ad.mda-7 inhibited growth and decreased survival in a broad array of human
tumor cells, without eliciting detrimental effects in normal cells. This study demonstrates that Ad.mda-7 can effectively impede the proliferation and induce apoptosis of human cervical
carcinoma cells, but the underlying mechanisms inducing cell death at
protein level are unknown. Using
proteome analysis, an investigation aimed at a better understanding of the antiproliferative mechanisms by Ad.mda-7 was carried out in CaSki
cervical cancer cells. A total of 43 differentially expressed
proteins were visualized by 2-DE and
silver stain., 29
proteins of which were identified via matrix-assisted
laser desorption/ionization-time of flight mass spectrometry(MALDI-TOF-MS) analysis, 15 were upregulated (eg.,
Tumor suppressor p53, Apoptosis regulator BAX,
Adenylate kinase isoenzyme 1(AK1), Growth arrest and DNA-damage-inducible
protein GADD45 gamma (GADD45gamma)) and 14 were downregulated (e.g.,
Eukaryotic translation initiation factor 5A(eIF-5A),
Protein DJ-1,
Annexin V, Transcription
elongation factor B
polypeptide 2 (TCEB2), TRAF family member-associated NFkappaB activator (
TRAF2),c-Myc-responsive
protein Rcl (RCL)). Among the identified
proteins, the
protein and
mRNA alterations of six
proteins were further confirmed by Western blot and semi-quantitative RT-PCR. Together, at both the
mRNA and
protein levels, p53, BAX, AK1, GADD45gamma and BCCIP were upregulated, while
eIF-5A was downregulated following Ad.mda-7 treatment. Our findings may offer new insights into the antiproliferative mechanisms by Ad.mda-7 and its mode of action in cervical
carcinoma cells.