Elevated THBS2, COL1A2, and SPP1 Expression Levels as Predictors of Gastric Cancer Prognosis

Abstract

Background/Aims:Gastric cancer (GC) is an important health problem. Classification based on molecular subtypes may help to determine the prognosis of patients with GC. Tumor invasion and metastasis are important factors affecting the prognosis of cancer. We aimed to identify genes related to tumor invasion and metastasis, which may serve as indicators of good GC prognosis. Methods:Tumor tissues and adjacent normal tissues were collected from 105 patients with primary GC who were treated by undergoing radical surgery. Samples were used for tissue microarray analysis. Identified genes with altered expression were further analyzed using the Gene Ontology (Go) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. The expression levels of THBS2, COL1A2 and SPP1 were analyzed by RT-PCR, western blot and immunohistochemistry. The overall survival curves of patients with high and low expression of each gene of interest were plotted and compared. Results:Forty-three genes were identified. THBS2, COL1A2 and SPP1 were selected for further analysis. Altered expression levels of THBS2, COL1A2 and SPP1 in tumor tissues were confirmed. Patients with low THBS2 expression had a better prognosis; the expression of COL1A2 and SPP1 might not affect the prognosis of patients with GC. Conclusion:THBS2, but not COL1A2 and SPP1, may serve as an indicator of GC prognosis.

Retracted: Silencing of COL1A2, COL6A3, and THBS2 inhibits gastric cancer cell proliferation, migration, and invasion while promoting apoptosis through the PI3k‐Akt signaling pathway

“…We found that COL1A2, COL6A3, and THBS2 genes were mainly involved in ECM‐receptor interaction and PI3K‐Akt signaling pathway through KEGG pathway‐enrichment analysis. THBS2 was found to express highly in gastric cancer tissues, besides, THBS2, and COL1A2 play a critical role in the ECM‐receptor interaction pathway . It is also reported that focal adhesion pathway (THBS2, PDGFD, MAPK1, COL1A2, and COL6A3), ECM‐receptor interaction pathway (THBS2, COL1A2, COL6A3, and FN1) and TGF‐beta signaling (THBS2, MAPK1, and INHBA) were the key differences in tumor growth and normal expression of gastric cancer at a molecular level .…”

“…THBS2 was found to express highly in gastric cancer tissues, besides, THBS2, and COL1A2 play a critical role in the ECM-receptor interaction pathway. 15 It is also reported that focal adhesion pathway (THBS2, PDGFD, MAPK1, COL1A2, and COL6A3), ECM-receptor interaction after the scratch was drawn (×150); B, BGC-823 cell migration ability in each group. C, SGC-7901 cell migration at the same region 0 h and 24 h after the scratch was drawn (×150); D, SGC-7901 cell migration ability in each group; *, P < 0.05 when compared with the blank group and the NC group; NC, negative control pathway (THBS2, COL1A2, COL6A3, and FN1) and TGFbeta signaling (THBS2, MAPK1, and INHBA) were the key differences in tumor growth and normal expression of gastric cancer at a molecular level.…”

“…26 Additionally, our results also confirmed that COL1A2, COL6A3, and THBS2 are highly expressed in gastric cancer, which was consistent with former studies in which up-regulated COL1A1, COL1A2, and THBS2 contributed to the invasiveness and metastasis in gastric cancer. 15,27,28 Compared with adjacent normal tissues, gastric cancer tissues manifested significantly higher positive expression rates of PI3K, Akt, and p-Akt, with an augmented mRNA expression of COL1A2, COL6A3, and THBS2. However, silencing of COL1A2, COL6A3, or THBS2 could drastically reduce the protein expression of p-Akt, Akt, and PI3K, indicating that PI3K-Akt signaling pathway could be deactivated by the silencing of COL1A2, COL6A3, or THBS2.…”

FGFR2 Promotes Gastric Cancer Progression by Inhibiting the Expression of Thrombospondin4 via PI3K-Akt-Mtor Pathway

“…Expression levels of FGFR2 and TSPs assessed independently have been reported in several studies as prognostic factors for patients with GC [17][18][19][20]. As a follow-on from our previous study, which demonstrated that FGFR2 promotes GC cells invasion and migration by targeting TSPs in vitro [16], we undertook an evaluation of the potential clinical significance and mechanism of the relationship between FGFR2 and TSP4 in GC.…”

Alpha B‐crystallin promotes the invasion and metastasis of gastric cancer via NF‐κB‐induced epithelial‐mesenchymal transition

“…As numerous genetic changes are in relation to cancer cell invasion and metastasis,14, 19, 20, 21, 22 great efforts have been made in the identification of novel key regulators and the potential mechanisms involved in this process over the years. Interestingly, recent studies have revealed that CRYAB is aberrantly overexpressed in various types of cancer, and its expression could promote cell invasion and metastasis 8, 9, 10.…”