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*For medical professionals only to read and reference
, and the knowledge is rising!
).
Study screenshots
of all brain tumors.
The most aggressive type of glioma is called GBM, and it affects the brain and is almost incurable
.
The epidermal growth factor receptor (EGFR) signaling pathway has previously been shown to be highly active
in most GBMs.
The signaling pathway is like a cellular chain of command through which a string of proteins is triggered in sequences to stimulate specific cellular functions
.
Irregular activation of certain pathways often leads to the development of diseases, including cancer
.
Previous studies have shown that the EGFR pathway hinders the natural process by which cells stop dividing, called aging, a mechanism that is essential
for hindering the growth and spread of cancer cells.
Blocking the function of the EGFR pathway promotes aging and helps inhibit tumor growth
.
Study author Suyun Huang (MD, Paul M.
Corman, Ph.
D.
, Chair of Cancer Research and member of the Massey Cancer Biology Research Program) said
from 23 tumor-free samples and 157 glioma samples of different grades from epilepsy patients.
Compared to tumor-free samples, 40 differentially expressed lncRNAs
were identified in different grades of glioma.
The study also analyzed lncRNA profiles in glioma cases in normal brain tissue from the Cancer Genome Atlas Database (TCGA) and the Genotype Tissue Expression Project (GTEx
) database.
The study found:
This study shows that lncEPAT acts as a genetic regulator, allowing EGFR to evade the anti-tumor effects of USP16 and accelerate cancer progression, and targeting lncEPAT may be an effective anti-aging therapeutic target for GBM
.
In preclinical models, Huang also found that lncEPAT consumption increased USP16 activity and inhibited the growth
of GBM cells.
, and the knowledge is rising!
Executive Summary
).
Study screenshots
status quo
of all brain tumors.
The most aggressive type of glioma is called GBM, and it affects the brain and is almost incurable
.
The epidermal growth factor receptor (EGFR) signaling pathway has previously been shown to be highly active
in most GBMs.
The signaling pathway is like a cellular chain of command through which a string of proteins is triggered in sequences to stimulate specific cellular functions
.
Irregular activation of certain pathways often leads to the development of diseases, including cancer
.
Previous studies have shown that the EGFR pathway hinders the natural process by which cells stop dividing, called aging, a mechanism that is essential
for hindering the growth and spread of cancer cells.
Blocking the function of the EGFR pathway promotes aging and helps inhibit tumor growth
.
Study author Suyun Huang (MD, Paul M.
Corman, Ph.
D.
, Chair of Cancer Research and member of the Massey Cancer Biology Research Program) said
- EGFR signaling dysregulation is associated with poorer outcomes and increased resistance to conventional therapies in patients with GBM; Therefore, targeted EGFR is considered a promising therapeutic strategy;
- However, the underlying cellular processes by which EGFR promotes tumor growth are largely unknown
.
conclusion
from 23 tumor-free samples and 157 glioma samples of different grades from epilepsy patients.
Compared to tumor-free samples, 40 differentially expressed lncRNAs
were identified in different grades of glioma.
The study also analyzed lncRNA profiles in glioma cases in normal brain tissue from the Cancer Genome Atlas Database (TCGA) and the Genotype Tissue Expression Project (GTEx
) database.
The study found:
- A specific protein called ubiquitin-specific protease 16 (USP16) regulates aging and attenuates the growth of glioma cells;
- A separate strip of long noncoding RNA—a molecule that controls gene activity—called lncEPAT, was also identified, activated by EGFR and highly functional
in GBM. - lncEPAT interacts with USP16 protein and is regulated by USP16-mediated H2A deubiquitination, which provides new ideas
for EGFR activation to regulate H2A ubiquitination and gene transcription. - lncEPAT attenuates USP16-induced cellular senescence, thereby promoting GBM cell growth and tumorigenesis
.
This study shows that lncEPAT acts as a genetic regulator, allowing EGFR to evade the anti-tumor effects of USP16 and accelerate cancer progression, and targeting lncEPAT may be an effective anti-aging therapeutic target for GBM
.
In preclinical models, Huang also found that lncEPAT consumption increased USP16 activity and inhibited the growth
of GBM cells.
prospect
- We have convincing evidence that the cancer-driving function of lncEPAT in GBM depends on the inactivation of the USP16 protein;
- EGFR-induced, overexpressed lncEPAT provides a promising new target for the pro-aging treatment of GBM
.
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