Selenium-doped hydroxyapatite biopapers with an anti-bone tumor effect by inducing apoptosis
Selenium-doped hydroxyapatite biopapers with an anti-bone tumor effect by inducing apoptosis
复制标题
硒掺杂羟基磷灰石生物纸通过诱导细胞凋亡具有抗骨肿瘤作用
DOI：
10.1039/c9bm00953a
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发表时间：
2019-12-01
影响因子：
6.6
通讯作者：
Chen, Feng
中科院分区：
文献类型：
--
作者：
Zhou, Zi-Fei;Sun, Tuan-Wei;Chen, Feng
一维羟基磷灰石（HA）特别模拟了矿化胶原原纤维的结构，并显示出较高的机械性能，例如韧性。在此，我们报告了由自组装的SE掺杂HA纳米线和壳聚糖建造的Se-Doped Ha/Chitosan（SE-HA/CS）生物体。具有较高柔韧性和可制造性的SE-HA/CS生物体不仅可以通过折叠或使用剪刀进一步加工成任意形状，而且还可以在体外/体内抗骨肿瘤研究中表现出很高的性能。 SE-HA/CS生物具有比正常的人骨髓基质细胞（HBMSC）更倾向于抑制肿瘤细胞（HCS 2/8和SJSA细胞）的生长。研究了这种有意义的抗肿瘤作用的潜在机制，例如活性氧的积累以及凋亡的激活以及所涉及的潜在信号途径（包括caspase家族，BCL-2家族和JNK/STAT3）。结果表明，SE-HA/CS生物具有同步诱导JNK激活和STAT3抑制，并促进这些细胞的凋亡，可以抑制HCS 2/8和SJSA细胞的生长。此外，体内抗肿瘤研究证实，SE-HA/CS生物体显然抑制了患者衍生的异种移植肿瘤模型的生长。
One-dimensional hydroxyapatite (HA) particularly mimics the structure of mineralized collagen fibrils and displays superior mechanical properties such as toughness. Herein, we report Se-doped HA/chitosan (Se-HA/CS) biopapers constructed with self-assembled Se-doped HA nanowires and chitosan. The Se-HA/CS biopapers with high flexibility and manufacturability can not only be further processed into arbitrary shapes by folding or using scissors but also display high performances in in vitro/vivo anti-bone tumor studies. The Se-HA/CS biopapers are more inclined to inhibit the growth of tumor cells (HCS 2/8 and SJSA cells) than that of normal human bone marrow stromal cells (hBMSCs). The potential mechanisms of this meaningful anti-tumor effect were investigated, such as reactive oxygen species accumulation and the activation of apoptosis and the underlying signal pathway involved (including caspase family, Bcl-2 family and JNK/STAT3). The results demonstrate that Se-HA/CS biopapers may inhibit the growth of HCS 2/8 and SJSA cells by synchronously inducing JNK activation and STAT3 inhibition and consequently promote the apoptosis of these cells. Furthermore, the in vivo anti-tumor studies confirm that the Se-HA/CS biopapers obviously suppress the growth of patient-derived xenograft tumor models.