Metaplasia in the Stomach—Precursor of Gastric Cancer?

Yada

et al. 2020

Nature

109

“…10k-n). 46.2% of intestinal metaplasia cases, which is strongly correlated with gastric cancer 23,24 , displayed mild to moderate AQP5 expression (Extended Data Fig. 10o, q).…”

Section: Aqp5 Expression In Human Gastric Cancermentioning

confidence: 96%

AQP5 enriches for stem cells and cancer origins in the distal stomach

Yada

et al. 2020

Nature

109

“…H. pylori is the well-recognized cause of GC and has been classified by World Health Organization as group I carcinogen. H. pylori -infected patients develop GC via multistep processes, including chronic gastritis, atrophic gastritis, intestinal metaplasia (IM), dysplasia, and ultimately GC [ 54 , 55 ]. OPN contributes to immune escape of H. pylori via inhibition of inducible nitric oxide synthase (iNOS) production by macrophage [ 56 ].…”

Section: The Association Of Opn With Apoptosis In Inflammatory Gimentioning

confidence: 99%

Is Osteopontin a Friend or Foe of Cell Apoptosis in Inflammatory Gastrointestinal and Liver Diseases?

Iida

Wagatsuma

Hirayama

et al. 2017

IJMS

Osteopontin (OPN) is involved in a variety of biological processes, including bone remodeling, innate immunity, acute and chronic inflammation, and cancer. The expression of OPN occurs in various tissues and cells, including intestinal epithelial cells and immune cells such as macrophages, dendritic cells, and T lymphocytes. OPN plays an important role in the efficient development of T helper 1 immune responses and cell survival by inhibiting apoptosis. The association of OPN with apoptosis has been investigated. In this review, we described the role of OPN in inflammatory gastrointestinal and liver diseases, focusing on the association of OPN with apoptosis. OPN changes its association with apoptosis depending on the type of disease and the phase of disease activity, acting as a promoter or a suppressor of inflammation and inflammatory carcinogenesis. It is essential that the roles of OPN in those diseases are elucidated, and treatments based on its mechanism are developed.

“…As a common malignant tumor in the world, gastric cancer (GC) ranks the 4th in incidence and the 2nd in mortality. 1,2 The early stage of gastric cancer has no specific manifestations and lacks sensitive serum indicators, and most patients are already in the advanced stage when diagnosed with poor prognosis. 3,4 Gastric cancer is a complex disease caused by many factors such as heredity and environment.…”

Section: Introductionmentioning

confidence: 99%

<p>RPL38 Regulates the Proliferation and Apoptosis of Gastric Cancer via miR-374b-5p/VEGF Signal Pathway</p>

Ji¹,

Zhang²

2020

OTT

Aim: To explore the role of RPL38 on proliferation and apoptosis of gastric cancer cells by regulating miR-374b-5p/VEGF signal pathway. Methods: qRT-PCR was used to measure the expression of RPL38. CCK8 assay, Matrigel invasion assay, and flow cytometry were used to detect the role of RPL38in MKN-45 cells. Western blot was used to measure the protein expression of VEGF, pERK , ERK, p-AKT, AKT in cells. Dual-luciferase assay was performed to verify the relationship between miR-374b-5p and RPL38, miR-374b-5p and VEGF. Results: In our research, we found that RPL38 was upregulation in gastric cancer, loss function of RPL38 could inhibit MKN-45 cell proliferation and invasion, accompany with increasing apoptosis. Then, we verified that RPL38 could interact with miR-374b-5p by performed luciferase assay, there was a negative correlation between RPL38 and miR-374b-5p. Furthermore, we observed that VEGF is a potential target of miR-374b-5p, miR-374b-5p negatively regulated the expression of VEGF, and effected ERK/AKT signal pathways. Next, we found that miR-374b-5p inhibitor or overexpression of VEGF could prevent the antitumor function of si-RPL38. Conclusion: Knockdown of RPL38 inhibits the proliferation and apoptosis of gastric cancer via miR-374b-5p/VEGF signal pathway.