Cervical cancer ranks seventh overall among all types of cancer in women. Although several treatments, including radiation, surgery and chemotherapy, are available to eradicate or reduce the size of cancer, many cancers eventually relapse. Thus, it is essential to identify possible alternative therapeutic approaches for cancer. We sought to identify alternative and effective therapeutic approaches, by first synthesizing palladium nanoparticles (PdNPs), using a novel biomolecule called saponin. The synthesized PdNPs were characterized by several analytical techniques. They were significantly spherical in shape, with an average size of 5 nm. Recently, PdNPs gained much interest in various therapies of cancer cells. Similarly, histone deacetylase inhibitors are known to play a vital role in anti-proliferative activity, gene expression, cell cycle arrest, differentiation and apoptosis in various cancer cells. Therefore, we selected trichostatin A (TSA) and PdNPs and studied their combined effect on apoptosis in cervical cancer cells. Cells treated with either TSA or PdNPs showed a dose-dependent effect on cell viability. The combinatorial effect, tested with 50 nM TSA and 50 nMPdNPs, had a more dramatic inhibitory effect on cell viability, than either TSA or PdNPs alone. The combination of TSA and PdNPs had a more pronounced effect on cytotoxicity, oxidative stress, mitochondrial membrane potential (MMP), caspase-3/9 activity and expression of pro- and anti-apoptotic genes. Our data show a strong synergistic interaction between TSA and PdNPs in cervical cancer cells. The combinatorial treatment increased the therapeutic potential and demonstrated relevant targeted therapy for cervical cancer. Furthermore, we provide the first evidence for the combinatory effect and cytotoxicity mechanism of TSA and PdNPs in cervical cancer cells.
Angiogenin was isolated as a tumor angiogenic factor solely on the basis of its angiogenic activity. Its expression is essential for melanoma progression and metastasis. Many studies have mainly focused on how it induces angiogenesis, which allows further melanoma growth and metastasis. Here, we investigated the effects of angiogenin on melanoma cell growth and studied its influence on the expression and function of the basic fibroblast growth factor. We transfected the angiogenin gene in the sense and antisense orientation into A375 cells, and obtained stable angiogenin under-expressing and over-expressing transfectants. We found that in the angiogenin antisense transfectants, the cell proliferation was decreased and the basic fibroblast growth factor-induced cell proliferation was inhibited, but the expression of basic fibroblast growth factor was increased. In contrast, in the angiogenin sense transfectants, the cell proliferation was increased, and the basic fibroblast growth factor-induced cell proliferation was also increased. The expression of basic fibroblast growth factor, however, was decreased. In conclusion, we demonstrated that, besides its angiogenic activity, angiogenin also directly contributes to A375 cell proliferation and is required for the basic fibroblast growth factor to induce cell proliferation. We also demonstrated that the endogenous angiogenin expression levels affect the expression of basic fibroblast growth factor in A375 cells. By targeting angiogenin, therefore, one may find a potential therapeutic approach to human malignant melanoma.
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