hsp90 inhibitor nms-e973 exerts the anticancer effect against glioblastoma via induction of puma-mediated apoptosis
Clicks: 268
ID: 254486
2018
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Emerging Content
30.0
/100
268 views
44 readers
AI Quality Assessment
Not analyzed
Readership in this journal
EmergingRanked #55 of 171 articles by views in jurnal tam
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 171 in total.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
Libo Sun,1 Shoujun Yang,2 Guonan Chi,1 Xingyi Jin1 1First Department of Neurosurgery, China-Japan Union Hospital of Jilin University, Changhun, Jilin, People’s Republic of China; 2Department of Rehabilitation, China-Japan Union Hospital of Jilin University, Changhun, Jilin, People’s Republic of China Background: Glioblastoma is one of the most aggressive and common malignancies of the central nervous system in humans. Owing to the correlation of high Hsp90 expression with prognosis and clinical pathology features of diverse types of cancer, targeting Hsp90 with small-molecule inhibitors has become a promising anticancer strategy.Purpose: In this study, we aimed to explore the possibility of anticancer effect of NMS-E973 in giloblastoma and elucidate the mechanism.Methods: Cell based MTT assay and colony formation assay were used to detect cell viability. Apoptosis was analyzed by nuclear staining with Hoechst 33258 and Annexin V/propidium iodide staining followed by flow cytometry. Western-blot and RT-PCR were used to detect gene expression. Xenograft assay was used to explore the anticancer effect of NMS-E973 in vivo.Results: We found that NMS-E973 induces apoptosis and inhibits cell growth in glioblastoma cells in cell culture and xenograft models. As a proapoptotic Bcl-2 member, PUMA was induced by NMS-E973 in a p53-dependent manner in glioblastoma in cell culture, thereby inducing apoptosis in glioblastoma cells. Furthermore, PUMA was induced by NMS-E973 treatment in xenograft tumors, and deficiency in PUMA significantly suppressed the antitumor effects of NMS-E973.Conclusion: Our study suggests that PUMA-mediated apoptosis is important for the therapeutic responses of NMS-E973. Induction of PUMA might be a potential biomarker for predicting NMS-E973 responses. Keywords: NMS-E973, PUMA, glioblastoma, apoptosis
| Reference Key |
l2018oncotargetshsp90
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | ;Sun L;Yang S;Chi G;Jin X |
| Journal | jurnal tam |
| Year | 2018 |
| DOI |
DOI not found
|
| URL | |
| Keywords |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.