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Neurofibromatosis type 1 (NF1) is a genetic disease that can cause brown spots on the skin and abnormal growth of nerves.
It is caused by mutations in the same name gene NF1.
The incidence of neurofibromatosis type 1 is about one in four thousand to one in three thousand.
Image source: https:// annual drama: spy drama-synapses lurking beside the tumor? About 15% of patients with neurofibromatosis 1 (NF1) develop poorly differentiated optic neuromas (called optic gliomas (OPG)) in early childhood.
Recent studies have shown that neurons are essential cellular components of the tumor microenvironment.
And its activity can increase tumor growth.
On May 26, 2021, Michelle Monje, Department of Neurology and Neuroscience, Stanford University, and David H.
Gutmann, Department of Neurology, Washington University School of Medicine, jointly published an article in the journal Nature revealing nerve fibers Oncological type 1 gene mutations promote the growth of nerve activity-dependent optic neuroma.
In order to study the effect of neuronal activity on the growth of low-grade glioma and the formation of glioma, they used a type of optic neuroma called poorly differentiated, which has Nf1-OPG transgenic mice with high tumor incidence.
The tumor cells in this model mouse grow near retinal ganglion cells (RGC).
The formation of mouse Nf1 optic glioma requires two conditions to be met at the same time: neural progenitor cells The somatic cell Nf1 in Nf1 has a loss of function; heterozygous Nf1 mutations also exist in non-neoplastic (stromal) cells, similar to patients with NF1 cancer susceptibility syndrome.
Light-activated RGC promotes tumor growth.
They injected optogenetic virus into RGC of Nf1-OPG transgenic mice, and evaluated the tumor growth rate at 12 weeks after activating RGC at 6 weeks of age.
The results showed that the volume of the optic nerve became larger after light-activated RGC, and the proliferation of glioma cells increased significantly, which indicated that the nerve activity of RGC promoted the growth of optic neuroma.
Dark environment inhibits tumor growth.
More interestingly, sunlight affects tumor growth in Nf1-OPG transgenic mice: tumors grow faster under full light (24 hours of light), but tumors grow in complete darkness (24 mouse dark environment) It becomes slower and the proliferation of tumor cells decreases.
Could it be said that wearing sunglasses to avoid light can inhibit tumor growth? Previous studies have found that cortical neuronal activity drives the growth of well-differentiated tumors through paracrine BDNF and synaptoadhesin NLGN3.
NLGN3 is a cell adhesion protein on the postsynaptic membrane, which can mediate the formation and maintenance of synapses between neurons.
Researchers found that light-activated RGC can indeed cause the levels of BDNF and NLGN3 to increase, and incubating NLGN3 in vitro can also promote the growth of poorly differentiated optic neuroma.
In addition, the expression of NLGN3 was up-regulated in patients with Nf1 optic neuroma.
Knockout of NLGN3 inhibits tumor growth After knocking out NLGN3, the tumor growth of Nf1-OPG transgenic mice seems to have been pressed the pause button: the volume of the optic nerve is no different from normal, and the proliferation of tumor cells is significantly reduced.
This indicates that NLGN3 is involved in the tumor development process of poorly differentiated optic neuroma.
After the researchers injected tetrodotoxin into the vitreous body to inhibit neuronal activity, the expression of NLGN3 secreted by the optic nerve was significantly reduced.
Optogenetics technology did not affect the secretion of NLGN3 after activating the optic nerve of normal mice, but NLGN3 expression was up-regulated in NF1 mutant mice.
Completely in the dark environment does not affect the secretion of NLGN3 in normal mice.
NLGN3 expression is up-regulated in NF1 mutant mice. These results indicate that Nf1 mutation abnormally increases the up-regulation of NLGN3, which is regulated by neuronal activity in the optic nerve.
Disintegrin and metalloprotease 10 (ADAM10) is a "sheddase" that can hydrolyze more than 30 transmembrane proteins.
NLGN3 is shed from the neurons by ADAM10.
After treatment with GI254023X (ADAM10 inhibitor), it can prevent the growth of tumors in Nf1-OPG transgenic mice and inhibit the proliferation of tumor cells.
Expert comment: German Cancer Research Center, Department of Neurology, Heidelberg University Hospital, Germany: Varun Venkataramani and Frank Winkler (extracted part) This is an exciting study.
This article uses a tumor gene model mouse to reveal the discovery that light-induced neuronal activity not only promotes tumor growth, but is also responsible for the tumor initiation process.
Gene knocking out NLGN3 or inhibiting NLGN3 can slow the growth of tumors.
What's more interesting is that tumor growth slows down in the dark.
So, what is the clinical significance of this research? Should NF1 patients be told that they need to wear sunglasses or cover their eyes? Should somehow reduce the overall neuronal activity of cancer patients? [References] 1.
https://doi.
org/10.
1038/d41586-021-01353-92.
https://doi.
org/10.
1038/s41586-021-03580-6, the pictures in the text are all from the reference Baidu Netdisk link: https://pan.
baidu.
com/s/1ADBwF5om6VXov1yy0caIHQ extraction code: 6b2r
Neurofibromatosis type 1 (NF1) is a genetic disease that can cause brown spots on the skin and abnormal growth of nerves.
It is caused by mutations in the same name gene NF1.
The incidence of neurofibromatosis type 1 is about one in four thousand to one in three thousand.
Image source: https:// annual drama: spy drama-synapses lurking beside the tumor? About 15% of patients with neurofibromatosis 1 (NF1) develop poorly differentiated optic neuromas (called optic gliomas (OPG)) in early childhood.
Recent studies have shown that neurons are essential cellular components of the tumor microenvironment.
And its activity can increase tumor growth.
On May 26, 2021, Michelle Monje, Department of Neurology and Neuroscience, Stanford University, and David H.
Gutmann, Department of Neurology, Washington University School of Medicine, jointly published an article in the journal Nature revealing nerve fibers Oncological type 1 gene mutations promote the growth of nerve activity-dependent optic neuroma.
In order to study the effect of neuronal activity on the growth of low-grade glioma and the formation of glioma, they used a type of optic neuroma called poorly differentiated, which has Nf1-OPG transgenic mice with high tumor incidence.
The tumor cells in this model mouse grow near retinal ganglion cells (RGC).
The formation of mouse Nf1 optic glioma requires two conditions to be met at the same time: neural progenitor cells The somatic cell Nf1 in Nf1 has a loss of function; heterozygous Nf1 mutations also exist in non-neoplastic (stromal) cells, similar to patients with NF1 cancer susceptibility syndrome.
Light-activated RGC promotes tumor growth.
They injected optogenetic virus into RGC of Nf1-OPG transgenic mice, and evaluated the tumor growth rate at 12 weeks after activating RGC at 6 weeks of age.
The results showed that the volume of the optic nerve became larger after light-activated RGC, and the proliferation of glioma cells increased significantly, which indicated that the nerve activity of RGC promoted the growth of optic neuroma.
Dark environment inhibits tumor growth.
More interestingly, sunlight affects tumor growth in Nf1-OPG transgenic mice: tumors grow faster under full light (24 hours of light), but tumors grow in complete darkness (24 mouse dark environment) It becomes slower and the proliferation of tumor cells decreases.
Could it be said that wearing sunglasses to avoid light can inhibit tumor growth? Previous studies have found that cortical neuronal activity drives the growth of well-differentiated tumors through paracrine BDNF and synaptoadhesin NLGN3.
NLGN3 is a cell adhesion protein on the postsynaptic membrane, which can mediate the formation and maintenance of synapses between neurons.
Researchers found that light-activated RGC can indeed cause the levels of BDNF and NLGN3 to increase, and incubating NLGN3 in vitro can also promote the growth of poorly differentiated optic neuroma.
In addition, the expression of NLGN3 was up-regulated in patients with Nf1 optic neuroma.
Knockout of NLGN3 inhibits tumor growth After knocking out NLGN3, the tumor growth of Nf1-OPG transgenic mice seems to have been pressed the pause button: the volume of the optic nerve is no different from normal, and the proliferation of tumor cells is significantly reduced.
This indicates that NLGN3 is involved in the tumor development process of poorly differentiated optic neuroma.
After the researchers injected tetrodotoxin into the vitreous body to inhibit neuronal activity, the expression of NLGN3 secreted by the optic nerve was significantly reduced.
Optogenetics technology did not affect the secretion of NLGN3 after activating the optic nerve of normal mice, but NLGN3 expression was up-regulated in NF1 mutant mice.
Completely in the dark environment does not affect the secretion of NLGN3 in normal mice.
NLGN3 expression is up-regulated in NF1 mutant mice. These results indicate that Nf1 mutation abnormally increases the up-regulation of NLGN3, which is regulated by neuronal activity in the optic nerve.
Disintegrin and metalloprotease 10 (ADAM10) is a "sheddase" that can hydrolyze more than 30 transmembrane proteins.
NLGN3 is shed from the neurons by ADAM10.
After treatment with GI254023X (ADAM10 inhibitor), it can prevent the growth of tumors in Nf1-OPG transgenic mice and inhibit the proliferation of tumor cells.
Expert comment: German Cancer Research Center, Department of Neurology, Heidelberg University Hospital, Germany: Varun Venkataramani and Frank Winkler (extracted part) This is an exciting study.
This article uses a tumor gene model mouse to reveal the discovery that light-induced neuronal activity not only promotes tumor growth, but is also responsible for the tumor initiation process.
Gene knocking out NLGN3 or inhibiting NLGN3 can slow the growth of tumors.
What's more interesting is that tumor growth slows down in the dark.
So, what is the clinical significance of this research? Should NF1 patients be told that they need to wear sunglasses or cover their eyes? Should somehow reduce the overall neuronal activity of cancer patients? [References] 1.
https://doi.
org/10.
1038/d41586-021-01353-92.
https://doi.
org/10.
1038/s41586-021-03580-6, the pictures in the text are all from the reference Baidu Netdisk link: https://pan.
baidu.
com/s/1ADBwF5om6VXov1yy0caIHQ extraction code: 6b2r
