Gold quantum dots impair the tumorigenic potential of glioma stem-like cells via β-catenin downregulation in vitro

金量子点体外通过下调 β-catenin 抑制胶质瘤干细胞样细胞的致瘤潜能

阅读:4
作者:Rizwan Wahab, Neha Kaushik, Farheen Khan, Nagendra Kumar Kaushik, Su-Jae Lee, Eun Ha Choi, Abdulaziz A Al-Khedhairy

Background

Over the past several decades, the incidence of solid cancers has rapidly increased worldwide. Successful removal of tumor-initiating cells within tumors is essential in the field of cancer therapeutics to improve patient disease-free survival rates. The biocompatible multivarient-sized gold nanoparticles (MVS-GNPs) from quantum dots (QDs, <10 nm) to nanosized (up to 50 nm) particles have vast applications in various biomedical areas including cancer treatment. The role of MVS-GNPs for inhibition of tumorigenic potential and stemness of glioma was investigated in this study.

Conclusion

In summary, G-QDs may exhibit possible contribution on suppressing the growth of tumor-initiating cells. These data reveal a unique therapeutic approach for the elimination of residual resistant stem-like cells during cancer treatment.

Methods

Herein, MVS-GNPs synthesized and characterized by means of X-ray diffraction pattern (XRD) and transmission electron microscopy (TEM) techniques. Afterwards, interaction of these GNPs with glioma stem-cell like cells along with cancer cells were evaluated by MTT, cell motility, self-renewal assays and biostatistics was also applied.

Results

Among these GNPs, G-QDs contributed to reduce metastatic events and spheroid cell growth, potentially blocking the self-renewal ability of these cells. This study also uncovers the previously unknown role of the inhibition of CTNNB1 signaling as a novel candidate to decrease the tumorigenesis of glioma spheroids and subsequent spheroid growth. The accurate and precise biostatistics results were obtained at quantify level.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。