46.8 points Overview: How Helicobacter pylori disrupts immunity and promotes gastric cancer
source:Technical divisiondate:2022-05-25views:1456

 Histopathological classification of gastric adenocarcinoma includes intestinal type, diffuse type and mixed type. Helicobacter pylori (Hp) infection, high-salt diet, and high-nitrate diet are the main risk factors;

 Hp virulence factors can activate oncogenic pathways (such as Wnt signaling pathway), and Hp LPS and DNA can also induce inflammatory responses by activating multiple TLRs;

The signaling pathway activated by Hp virulence factors can induce CDX1 and CDX2, and play an important role in the development of chronic gastritis into intestinal metaplasia;

 Hp infection induces dendritic cells, monocytes, myeloid-derived suppressor cells, and neutrophils to enter the stomach, induce neovascularization, and form an immunosuppressive microenvironment.

The immune microenvironment in gastric adenocarcinoma | Nature Reviews Gastroenterology & Hepatology IF: 46.802 


Iron deficiency can increase gastritis and gastric injury caused by Helicobacter pylori (Hp) infection in C57BL/6 and INS-GAS mice;

Iron-deficiency-induced phenotypes were not associated with altered microbiota, but significantly increased levels of cancer-promoting deoxycholic acid (DCA);

DCA exacerbates gastric injury induced by Hp infection. In vitro, DCA promotes the entry of Hp oncoprotein CagA into host cells;

Cholestyramine treatment significantly reduced Hp-induced gastric inflammation and injury in INS-GAS mice under iron deficiency;

In 416,885 subjects, the use of bile acid sequestrants was associated with a dose-dependent reduction in the risk of gastric cancer, and the expression of the bile acid receptor TGR5 was also associated with the severity of human carcinogenic lesions.

JCI - Iron deficiency linked to altered bile acid metabolism promotes Helicobacter pylori–induced inflammation–driven gastric carcinogenesis IF: 14.808


LRPPRC can enhance the resistance of colorectal cancer cell lines to 5FU, and can promote the proliferation, migration and invasion of colorectal cancer in both cell lines and mice;

The prognosis of colorectal cancer patients with P53 mutation and high expression of LRPPRC is poor;

P53 up-regulates the expression of miR-34a to inhibit the expression of LRPPRC, which can bind to the mRNA of MDR1, increase its stability and promote the expression of MDR1 protein;

P53 mutation enhances the resistance of colorectal cancer cells to 5FU by up-regulating LRPPRC expression to increase MDR1 expression;

Gossypol-acetic acid (GAA) can enhance the efficacy of 5FU on colorectal cancer in cell lines and mice by inducing the degradation of LRPPRC.

Targeting the miR-34a/LRPPRC/MDR1 axis collapse the chemoresistance in P53 inactive colorectal cancer | Cell Death & Differentiation (


Loss of APC is associated with increased TDO2 expression in human and mouse normal and malignant intestinal epithelium;

APC deletion activates WNT-β-catenin signaling, which in turn upregulates TCF4-mediated TDO2 gene transcription and expression;

TDO2 activates the Kyn-AhR pathway, increases glycolysis, drives anabolic cancer cell growth, increases CXCL5 secretion, and recruits macrophages to the tumor microenvironment;

TDO2-AhR-CXCL5 promotes tumor growth by recruiting macrophages into the tumor microenvironment of CRC;

APC-depleted CRC models are more sensitive to deletion or pharmacological inhibition of TDO2. Knockout or inhibition of TDO2 damages the proliferation of cancer cells and enhances anti-tumor immunity.

Synthetic Essentiality of Tryptophan 2,3-dioxygenase 2 in APC-Mutated Colorectal Cancer | Cancer Discovery | American Association for Cancer Research ( [IF: 39.397]








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