Ophiopogonin B
Ophiopogonin B is often used in Chinese traditional medicine to treat pulmonary disease, it is a prospective inhibitor of PI3K/Akt and may be used as an alternative compound to treat NSCLC. It may be considered a potential inhibitor of gastric cancer progression, and may be used as an alternative compound for its treatment. Ophiopogonin B induces apoptosis, mitotic catastrophe and autophagy , has inhibitory effect on adhesion, invasion and migration of A549 cells in vitro.
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Oncol Rep. 2013 Feb;29(2):430-6.
Ophiopogonin B-induced autophagy in non-small cell lung cancer cells via inhibition of the PI3K/Akt signaling pathway.[Pubmed:
23151908]
Ophiopogonin B (OP-B) is a bioactive component of Radix Ophiopogon Japonicus, which is often used in Chinese traditional medicine to treat pulmonary disease. However, whether or not Ophiopogonin B has any potential antitumor activity has not been reported.
METHODS AND RESULTS:
Here, we show that the non-small cell lung cancer (NSCLC) cell lines NCI-H157 and NCI-H460 treated with Ophiopogonin B grow more slowly and accumulate vacuoles in their cytoplasm compared to untreated control cells. Flow cytometric analysis showed that the cells were arrested in G0/G1 phase. Nuclear morphology, Annexin-V/PI staining, and expression of cleaved caspase-3 all confirm that Ophiopogonin B does not induce apoptosis. Instead, based on results from both transmission electron microscopy (TEM) and the expression of microtubule-associated protein 1 light chain 3-II (LC3-II), we determined that Ophiopogonin B treatment induced autophagy in both cell lines. Next, we examined the PI3K/Akt/mTOR signaling pathway and found that Ophiopogonin B inhibited phosphorylation of Akt (Ser473, Thr308) in NCI-H157 cells and also inhibited several key components of the pathway in NCI-H460 cells, such as p-Akt(Ser473, Thr308), p-p70S6K (Thr389). Additionally, insulin-mediated activation of the PI3K/Akt/mTOR pathway provides evidence that activation of this pathway may correlate with induction of autophagy in H460 cells.
CONCLUSIONS:
Therefore, Ophiopogonin B is a prospective inhibitor of PI3K/Akt and may be used as an alternative compound to treat NSCLC.
Mol Med Rep. 2016 Jun;13(6):4981-6.
Effects of ophiopogonin B on the proliferation and apoptosis of SGC‑7901 human gastric cancer cells.[Pubmed:
27121658 ]
Ophiopogonin B (OP‑B) is a bioactive component of Radix Ophiopogon japonicus, which is often used in traditional Chinese medicine to treat cancer.
METHODS AND RESULTS:
The present study aimed to investigate the antitumor activity of OP‑B in gastric cancer. Cell Counting kit‑8, flow cytometry with Annexin V‑fluorescein isothiocyanate, Hoechst staining, mitochondrial membrane potential (MMP) detection, and reactive oxygen species (ROS) assay were used to detect the biological function of SGC‑7901 gastric cancer cells. The results demonstrated that high concentrations of OP‑B (5, 10 and 20 μmol/l) exerted potent antiproliferative effects on SGC‑7901 cells in a dose‑dependent manner. Furthermore, apoptotic rates were increased and cell morphology was altered following treatment with OP‑B. In addition, OP‑B‑induced apoptosis of SGC‑7901 cells was associated with loss of MMP and increased ROS generation. Western blotting indicated that treatment with OP‑B increased the protein expression levels of caspase‑3 and B‑cell lymphoma 2 (Bcl‑2)‑associated X protein, whereas the expression levels of Bcl‑2 and the phosphorylation levels of extracellular signal‑regulated kinases 1/2 and c‑Jun N‑terminal kinases 1/2 were decreased.
CONCLUSIONS:
These results suggest that OP‑B may be considered a potential inhibitor of gastric cancer progression, and may be used as an alternative compound for its treatment.
Int J Oncol. 2016 Jul;49(1):316-24.
Ophiopogonin B induces apoptosis, mitotic catastrophe and autophagy in A549 cells.[Pubmed:
27175570 ]
Ophiopogonin B (OP-B), a saponin compound isolated from Radix Ophiopogon japonicus, was verified to inhibit cell proliferation in numerous non-small cell lung cancer (NSCLC) cells in our previous study. However, the precise mechanisms of action have remained unclear.
METHODS AND RESULTS:
In the present study, we mainly investigated the effects of OP-B on adenocarcinoma A549 cells to further elaborate the underlying mechanisms of OP-B in different NSCLC cell lines. Detection by high content screening (HCS) and TUNEL assay verified that OP-B induced apoptosis in this cell line, while detection of Caspase-3, Bcl-2 and Bax showed that OP-B induced cell death was caspase and mitochondrial independent. Further experiments showed that OP-B induced cell cycle arrest in the S and G2/M phases by inhibiting the expression of Myt1 and phosphorylation of Histone H3 (Ser10), which resulted in mitotic catastrophe in the cells. Transmission electron microscopy (TEM) observation of cell micro-morphology combined with detection of Atgs by western blot analysis showed that OP-B induced autophagy in this cell line. Autophagy inhibition by the lysosome inhibitor CQ or Beclin1-siRNA knockdown both attenuated cell viability, demonstrated that autophagy also being the vital reason resulted in cell death. More importantly, the xenograft model using A549 cells provided further evidence of the inhibition of OP-B on tumor proliferation. Immunohistochemistry detection of LC3 and Tunel assay both verified that high dose of OP-B (75 mg/kg) induced autophagy and apoptosis in vivo, and western blot detection of p-Histone H3 (Ser10), Survivin and XIAP further indicated the molecular mechanism of OP-B in vivo.
CONCLUSIONS:
As our findings revealed, multiple types of cell death overlapped in OP-B treated A549 cells, it displayed multitarget characteristics of the compounds extracted from the Chinese herbal, which may be used as candidate anticancer medicine in clinic.
Yao Xue Xue Bao. 2013 Jun;48(6):855-9.
Molecular mechanism of ophiopogonin B induced cellular autophagy of human cervical cancer HeLa cells.[Pubmed:
23984518 ]
METHODS AND RESULTS:
This study is to investigate the antitumor activity of Ophiopogonin B (OP-B). MTT assay, flow cytometric analysis, acridine orange staining, Lyso-Tracker Red staining and HeLa-GFP-LC3 transfect cells assay were used to detect the proliferation activity, apoptosis and autophagy of HeLa cells. The results showed that Ophiopogonin B exerted potent antiproliferative activity on HeLa cells, the cell growth inhibition effect of Ophiopogonin B was not due to apoptosis and OP-B could induce autophagy of HeLa cells. Ophiopogonin B also induced the protein expression up-regulation of Beclin-1 and promoted LC3 I transformation LC3 II, which were representative proteins of autophagy. Furthermore, 3-MA, an inhibitor of autophagy, not only inhibited Ophiopogonin B-mediated autophagy but also almost completely reversed the antiproliferative effect of Ophiopogonin B, suggesting that the growth inhibition effect of Ophiopogonin B was autophagy dependent. Western blotting demonstrated that Ophiopogonin B inhibited the phosphorylation of Akt and its' downstream vital protein, such as mTOR and p70S6K. In addition, Ophiopogonin B also induced the protein expression up-regulation of PTEN, which is a negative regulation protein for Akt/mTOR signaling pathway. However, Ophiopogonin B did not affect the protein expression of total Akt. Collectively, the antitumor effects of Ophiopogonin B were autophagy-dependent via repression Akt/mTOR signaling pathway.
CONCLUSIONS:
Therefore, Ophiopogonin B is a prospective inhibitor of Akt/mTOR and may be used as an alternative compound to treat cervical carcinoma.
