We treated CNE 2 cells

We treated CNE 2 cells Pazopanib price with 5, 10 and 20 M ApoG2 for 24, 48 and 72 h. This treatment resulted in dose and time dependent inhibition of cell proliferation. At 10 and 20 M, ApoG2 inhibited about 60% and 90% of the cell growth, respectively, at 72 h. Moreover, among four NPC cell lines C666 1, CNE 1, CNE 2 and HONE 1, ApoG2 treatment resulted in a tremendous inhibition of cell proliferation in Inhibitors,Modulators,Libraries C666 1, CNE 1 and CNE 2 NPC cell lines. At 10 M, ApoG2 inhibited more than 60% of the cell growth of C666 1, CNE 1 and CNE 2 cells at 72 h. In contrast, only about 30% of HONE 1 cell proliferation was inhibited by 10 M ApoG2 treatment for 72 h. AapoG2 Treatment Induces NPC Cells Arresting in S Phase of Cell Cycle Gossypol reportedly induces cell cycle arrest in prostate cancer cells and colon cancer cells.

To Inhibitors,Modulators,Libraries determine whether ApoG2 could also induce cell cycle arrest in NPC cells, we performed a cell cycle analysis using flow cytom etry. The results showed the same with our previous work that, at 48 h after treatment, ApoG2 did not induce obvious cell apoptosis in NPC cells and little cells were accumulated in sub G1 phase. Instead, ApoG2 induced cell cycle arrest at the DNA synthesis phase in a large percentage of NPC cells at this time. More than 60% of C666 1, CNE 1 and CNE 2 cells were arrested at S phase at 48 h after exposure to 5 and 10 M ApoG2, whereas only 34%, 39% and 35%, respectively, of untreated C666 1, CNE 1 and CNE 2 cells were arrested at S phase.

Because we observed that another NPC cell line, HONE 1, was much less sensitive Inhibitors,Modulators,Libraries to ApoG2 treatment and exhibited a much higher 50% inhibitory concentration value of ApoG2 than C666 1, CNE 1 and CNE 2 cells, we assessed the effect of ApoG2 on the cell cycle in this cell line. Treatment with 10 M ApoG2 induced about 60% HONE 1 cells arresting at S phase, in comparison, only 34% of untreated HONE 1 cells were arrested at S phase of the cell cycle. These data implied Inhibitors,Modulators,Libraries that ApoG2 induced cell cycle arrest is not correlated with the sensitivity of cells to ApoG2, because in both ApoG2 sensitive NPC cells and ApoG2 insensitive HONE 1 cells, ApoG2 treatment could result in significant cell cycle arrest. These data also implied that ApoG2 induced cell cycle arrest was not caused the inhi bition of Bcl 2 proteins Inhibitors,Modulators,Libraries and other molecular mechanisms might be involved in ApoG2 induced cell cycle arrest in NPC cells.

Downregulation of c Myc Expression Leads to Cell Cycle Arrest by ApoG2 in NPC cells Because researchers have reported that cell cycle regulat ing molecules, such as p21, p53, and TGF 1, play roles in gossypol induced cell cycle arrest, we hypothesized that ApoG2 can also modify some cell cycle regulators, resulting in references cell cycle arrest in NPC cells. Consistent with our hypothesis, treatment with 10 M ApoG2 signifi cantly decreased the level of c Myc protein expression at 24 h in CNE 2 cells.

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