Abstract
Gastric intestinal metaplasia (GIM) is a precancerous gastric carcinoma (GC) lesion with pivotal roles in carcinogenesis. CD24, LGR5 and Ki67 are expressed in GIM; we previously demonstrated that aquaporin 3 (AQP3) is expressed in goblet cells and is positively correlated with GIM severity. However, the relationships of AQP3 with GIM classification and with other proteins, and their roles in the transition from GIM to gastric carcinoma (GC) remain unknown. Sixteen patients with intestinal-type GC were enrolled in this study. GIM was determined according to the updated Sydney system; GIM classification was determined via HID-AB staining, and AQP3, CD24, LGR5 and Ki67 expression were determined by immunohistochemistry. Type III GIM was more prevalent around the GC and displayed a positive association with GIM severity. CD24 was found in GIM, but LGR5 and Ki67 were found in tissues regardless of GIM. AQP3 expression showed significant correlation to type III GIM. CD24 expression was correlated with the marked GIM and incomplete GIM, while LGR5 expression decreased with GIM aggravation and did not have relationship with classification of GIM. However, Ki67 presented no association with GIM grade or classification. These observations identify AQP3 and CD24 as biomarkers for carcinogenesis of GIM, and may provide a precise strategy for screening at-risk candidates with GIM.
Highlights
Gastric carcinoma (GC) remains one of the most common malignances and the third leading cause of cancer-related mortality worldwide [1]
CD24, leucinerich-repeat-containing G-protein-coupled receptor 5 (LGR5) and Ki67 are expressed in Gastric intestinal metaplasia (GIM); we previously demonstrated that aquaporin 3 (AQP3) is expressed in goblet cells and is positively correlated with GIM severity
GIM was determined according to the updated Sydney system; GIM classification was determined via High iron diamine-alcian blue (HID-AB) staining, and AQP3, CD24, LGR5 and Ki67 expression were determined by immunohistochemistry
Summary
Gastric carcinoma (GC) remains one of the most common malignances and the third leading cause of cancer-related mortality worldwide [1]. It is well recognized that a multistep process is involved in the progression from normal gastric mucosa to intestinal-type GC, including chronic gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia and invasive carcinoma, which was originally proposed by Correa [2, 3]. During this multistep procession, gastric intestinal metaplasia (GIM) is considered to be a precancerous lesion of GC and to play a pivotal role in GC tumorigenesis [4, 5]. Most studies agree that the incomplete GIM, especially www.impactjournals.com/oncotarget
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
