Key result
Nitidine chloride increases ovarian cancer cell apoptosis ~10-fold and inhibits proliferation via Akt signaling.
Why the study?
There was no previous evidence of nitidine chloride involvement in the apoptosis or proliferation of ovarian cancer cells and the underlying molecular mechanisms.
Does nitidine chloride inhibit proliferation and induce apoptosis in ovarian cancer cells?
Does nitidine chloride inhibit proliferation and induce apoptosis in ovarian cancer cells?
Absolute Event Rate: 22% vs 2.3%
p-value: p=0.0010
Nitidine chloride demonstrates anti-tumor properties in ovarian cancer cells by inhibiting proliferation and inducing apoptosis via the Akt pathway, with synergistic effects when combined with doxorubicin.
NC effects in ovarian cancer cell lines may inform Akt-targeted strategies; leaves open clinical translation pending in vivo and human studies.
Nitidine chloride (NC) exhibits anti-tumor properties in various types of tumor. However, to the best of our knowledge there is no previous evidence of NC involvement in the apoptosis or proliferation of ovarian cancer cells and the underlying molecular mechanisms. The present study aimed to investigate the influence of NC on the viability and apoptosis of ovarian cancer cells and the synergistic effect NC and doxorubicin (DOX) may have on ovarian cancer cells. The viability and proliferation of ovarian cancer cells were examined using a methyl thiazolyl tetrazolium assay and 3H-thymidine incorporation assay. The apoptotic rate of ovarian cancer cells was detected by flow cytometry. The expression of apoptosis‑associated proteins and Akt serine/threonine kinase 1 (Akt) were determined by western blot analysis following NC treatment. The inhibitory effect of NC on the proliferation of ovarian cancer cells was demonstrated in a time and dose‑dependent manner. The pro-apoptotic effect of NC on ovarian cancer cells was also observed. It was determined that NC significantly downregulated the protein expression levels of B‑cell CLL/lymphoma 2 (Bcl-2) and upregulated the expression of Bcl‑2‑associated X protein, p53, caspase‑3 and ‑9. NC suppressed Akt phosphorylation. Additionally, the present study demonstrated that the effect of NC on the proliferation and apoptosis of ovarian cancer cells was Akt‑dependent by using the phosphatidylinositol-4,5-bisphosphate 3-kinase/Akt signaling pathway inhibitor, LY294002. NC exhibited a synergistic inhibitory effect on the viability of ovarian cancer cells when combined with DOX. The current study demonstrated that NC inhibited the proliferation and induced the apoptosis of ovarian cancer cells via the Akt signaling pathway and highlighted its potential clinical application for the treatment of ovarian cancer.
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Ding et al. (2016) studied Ovarian cancer. Nitidine chloride vs. Control (0 µM) was evaluated on Apoptotic rate (p=0.0010). Nitidine chloride significantly increased the apoptotic rate of A2780 ovarian cancer cells from 2.3% to 22.0% at 20 µM and inhibited proliferation via the Akt signaling pathway.
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