Microenvironment T-Type calcium channels regulate neuronal and glial processes in tumor cells to promote glioblastoma growth
Clicks: 1
ID: 315425
2026
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
0.0
/100
1 views
0 readers
AI Quality Assessment
Not analyzed
Readership in this journal
Ranked #114 of 125 articles by views in journal of neuro-oncology
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 125 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
Abstract Background Glioblastoma (GBM) is the most common primary malignant brain tumor. The aim of this study was to elucidate the role of microenvironment and intrinsic T-type calcium channels (Cav3) in regulating GBM. Methods We grafted syngeneic GBM cells into Cav3.2 knockout mice to assess the role of microenvironment T-Type calcium channels on GBM growth. We grafted syngeneic GBM cells into the hippocampus along Schafer collaterals and performed electrophysiology. We used neurons from WT and Cav3.2 Knockout (KO) mice in co-culture with GBM stem cells (GSC) to assess the effects of Cav3.2 on neuron/GSC synaptic connections and tumor cell growth. We performed single-cell RNA-seq of tumors from WT and Cav3.2 KO mice to elucidate the regulation of tumors by the microenvironment. Results Cav3.2KO in the microenvironment led to significant reduction of GBM growth and prolongation of animal survival. Neuronal Cav3.2 promoted GSC growth in co-culture and neuron/GBM functional synaptic connections in vivo. scRNA-seq showed that microenvironment Cav3.2 regulates neuronal and glial biological processes. Microenvironment Cav3.2 downregulated numerous genes associated with regulating the OPC cell state in GBM tumors. Treatment of GSCs with the Cav3 blocker mibefradil downregulated genes associated with neuronal processes. The Cav3 blocker drug mibefradil synergized with temozolomide (TMZ) and radiation to reduce in vivo tumor growth and prolong animal survival. Conclusions The data reveal a role for microenvironment Cav3 in promoting GBM progression through regulating neuronal and glial processes. Targeting both intrinsic and microenvironment Cav3 with the inhibitor mibefradil significantly enhanced the anti-GBM effects of TMZ and radiation.
| Reference Key |
openalex_W7162942084
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | Collin Dube, Y Zhang, Shekhar Saha, Tyler C J Deutsch, Matthew Yorek, Michelle Lai, Myron Gibert, Miguel Escalante, Kadie Hudson, Doris Wong, Paweł Marcinkiewicz, Ulaş Yener, Yunan Sun, Esther Xu, Aditya Sorot, Elizabeth Mulcahy, Benjamin Kefas, Farina Hanif, Fadilla Guessous, Ashley Vernon, David Schiff, Hui Zong, Benjamin Purow, Eric Holland, Swapnil Sonkusare, Harald Sontheimer, Manoj K. Patel, Roger Abounader |
| Journal | journal of neuro-oncology |
| Year | 2026 |
| DOI |
10.1093/neuonc/noag131
|
| URL | |
| Keywords | Keywords not found |
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.