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May 29 this year is the 18th "World Gut Health Da.
May 29 this year is the 18th "World Gut Health Da.
One day 40 years ago, a young doctor from Australia picked up a bottle of "drink" and drank it after wo.
In 2005, Marshall, who was over fifty, was awarded the Nobel Prize in Physiology or Medicine for his discovery of Helicobacter pylori, the culprit of gastric ulce.
pylori (Hp) , which has been confirmed to be the initiator of peptic ulcerimportant causative factor for gastric cancer
However, the mechanism by which.
was extracted from bovine tissue in the early stage and was mainly secreted by brain tiss.
FGF was extracted from bovine tissue in the early stage and was mainly secreted by brain tiss.
Clinically, FGF is often used for wound repair after medical cosmetic surgery, and is also widely added to various cosmetic produc.
However, the strong mitogenic ability of FGF also accelerates the carcinogenesis of cel.
doi: 11053.
doi: 11053.
Analysis of public databases showed that high FGFR4 expression in gastric cancer was associated with poor prognosis, specifically, shorter overall survival and disease-free survival in patients with high FGFR4 expressi.
Further mouse experiments confirmed that Hp infection promoted the expression of FGFR4 in gastric cancer cel.
A conjecture came to the researchers' minds: Hp upregulates FGFR4 by activating the STAT3 pathw.
doi: 11053.
doi: 11053.
gast.
202001
As a classic transcription factor, STAT3 often promotes the expression of downstream molecules by binding to the promoter of target gen.
Therefore, the researchers further predicted that the promoter of FGFR4 has the ability to bind STAT3, and verified it using a luciferase reporter ass.
After screening, a total of 6 binding sites entered the candidate li.
Therefore, the researchers further predicted that the promoter of FGFR4 has the ability to bind STAT3, and verified it using a luciferase reporter ass.
After screening, a total of 6 binding sites entered the candidate li.
Binding sites were determined by chromatin co-immunoprecipitation ( ChIP) experimen.
The results showed that 2 of these 6 candidate sites significantly bound STAT After activation of STAT3 with IL-6, the enrichment abundance of these two loci was significantly increased, further demonstrating that Hp induces the activation of STAT3 to upregulate the expression of FGFR
The results showed that 2 of these 6 candidate sites significantly bound STAT After activation of STAT3 with IL-6, the enrichment abundance of these two loci was significantly increased, further demonstrating that Hp induces the activation of STAT3 to upregulate the expression of FGFR
doi: 11053.
gast.
202001
gast.
202001
However, as the receptor of FGF, FGFR4 cannot function alone and requires the participation of FGF to functi.
And FGF has many subtypes, and selecting specific subtype molecules is the focus of follow-up wo.
And FGF has many subtypes, and selecting specific subtype molecules is the focus of follow-up wo.
After experiments and database analysis, the researchers focused on FGF1 The content of FGF19 in gastric cancer was higher than that in normal gastric tissue, and the expression of FGF19 in gastric cancer cells further increased after Hp infecti.
How does FGF19 function? The research team stimulated tumor cells with FGF19, and they found that FGF19 promotes the activation of STAT3 in cells, and this promotion effect is mediated by SRC molecul.
Previous studies have confirmed that STAT3 is activated after.
pylori infection, which in turn upregulates FGFR Up-regulated FGFR4 binds FGF19 and in turn activates STAT3 aga.
Such a positive feedback loop continuously amplifies the biological effects of .
pylori infection, which in turn upregulates FGFR Up-regulated FGFR4 binds FGF19 and in turn activates STAT3 aga.
Such a positive feedback loop continuously amplifies the biological effects of .
doi: 11053.
gast.
202001
gast.
202001
But what role does such a positive feedback loop have on the occurrence and development of gastric cancer? Using cytological experiments, the researchers found that the presence of a positive feedback loop promoted the growth of gastric cancer cel.
Cell cycle and apoptosis are the two research directions most related to cell growth, and the positive feedback loop caused by Hp significantly inhibits the apoptosis of gastric cancer cel.
Inhibition of key molecules of the loop can limit the growth of gastric cancer cells and increase apoptos.
Inhibition of key molecules of the loop can limit the growth of gastric cancer cells and increase apoptos.
So far, the researchers have proposed the key mechanism of.
pylori carcinogenesis: after infection with.
pylori, tumor cells will produce a large amount of FGF19, and the combination with FGFR4 activates the downstream pathway and promotes tumor grow.
At the same time, FGF19 also causes tumor cells to produce more FGFR4, further amplifying the oncogenic effect of FGF1
pylori carcinogenesis: after infection with.
pylori, tumor cells will produce a large amount of FGF19, and the combination with FGFR4 activates the downstream pathway and promotes tumor grow.
At the same time, FGF19 also causes tumor cells to produce more FGFR4, further amplifying the oncogenic effect of FGF1
doi: 11053.
gast.
202001
gast.
202001
How Hp promotes the expression of FGF19 still needs to be further explored, but the discovery of key molecules provides new ideas for the prevention and treatment of gastric canc.
Starting from the cup of "drink" 40 years ago, the true face of Hp is gradually becoming clear in the relay of generations of scientific researche.
Starting from the cup of "drink" 40 years ago, the true face of Hp is gradually becoming clear in the relay of generations of scientific researche.
References:
Chinese Medical Association, et .
Guidelines for primary diagnosis and treatment of Helicobacter pylori infection (201
Chinese Journal of General Practitioners, 2020, 19(5): 397-40 doi: 13760/c.
cn114798-20200223-0015
Guidelines for primary diagnosis and treatment of Helicobacter pylori infection (201
Chinese Journal of General Practitioners, 2020, 19(5): 397-40 doi: 13760/c.
cn114798-20200223-0015
Diagnosis and Treatment Guidelines
Xing Zhang, et .
Induction of FGFR4 by.
pylori via STAT3 with a feedforward activation loop
Induction of FGFR4 by.
pylori via STAT3 with a feedforward activation loop
involving SRC signaling in gastric canc.
Gastroenterolo.
2022; S0016-5085(22)00505- doi: 11053.
gast.
202001
Gastroenterolo.
2022; S0016-5085(22)00505- doi: 11053.
gast.
202001 Leave a comment here
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