Department of Oral Pathology, School of Dentistry, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea.
Cell Biochem Funct. 2014 Apr;32(3):229-35. doi: 10.1002/cbf.2996. Epub 2013 Sep 13.
In the present study, we examined the effects of methanol extracts of Picrasma quassioides (MEPQ) on apoptosis in human cervical cancer cells. The results showed that MEPQ decreased the viability and induced caspase-dependent apoptosis in HEp-2 cells. MEPQ decreased specificity protein 1 (Sp1) in HEp-2 cells, whereas Sp1 mRNA was not changed. We found that MEPQ reduced Sp1 protein through proteasome-dependent protein degradation, but not the inhibition of protein synthesis. Also, MEPQ increased the expressions of Bad and truncated Bid (t-Bid) but did not alter other Bcl-2 family members. The knock-down of Sp1 by both Sp1 interfering RNA and Mithramycin A, Sp1 specific inhibitor clearly increased Bad and t-Bid expression to decrease cell viability and induce apoptosis. In addition, MEPQ inhibited cell viability and induced apoptotic cell death through the modulation of Sp1 in KB cells. These results suggest that MEPQ may be a potential anticancer agent for human cervical cancer.
在本研究中,我们考察了密蒙花甲醇提取物(MEPQ)对人宫颈癌细胞凋亡的影响。结果表明,MEPQ 降低了 HEp-2 细胞的活力并诱导了 caspase 依赖性细胞凋亡。MEPQ 降低了 HEp-2 细胞中的特异性蛋白 1(Sp1),而 Sp1mRNA 没有改变。我们发现 MEPQ 通过蛋白酶体依赖性蛋白降解减少 Sp1 蛋白,但不抑制蛋白质合成。此外,MEPQ 增加了 Bad 和截断 Bid(t-Bid)的表达,但不改变其他 Bcl-2 家族成员。Sp1 干扰 RNA 和 Mithramycin A(Sp1 特异性抑制剂)均降低了 Sp1 的表达,明显增加了 Bad 和 t-Bid 的表达,从而降低了细胞活力并诱导了细胞凋亡。此外,MEPQ 通过调节 KB 细胞中的 Sp1 抑制了细胞活力并诱导了凋亡性细胞死亡。这些结果表明,MEPQ 可能是一种用于治疗人类宫颈癌的潜在抗癌剂。