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Gastric cancer (GC) is one of the most common cancers in the world. The cathepsin F (CTSF) gene has recently been found to participate in the progression of several types of cancer. However, the clinical characteristics and function of CTSF in GC as well as its molecular mechanisms are not clear. Six GC cell lines and 44 paired adjacent noncancerous and GC tissue samples were used to assess CTSF expression by quantitative polymerase chain reaction (qPCR). We used lentivirus-mediated small hairpin RNA (Lenti-shRNA) against CTSF to knock down the expression of CTSF in GC cells. Western blot and qPCR were used to analyze the mRNA and related protein expression. The biological phenotypes of gastric cells were examined by cell proliferation and apoptosis assays. Microarray-based mRNA expression profile screening was also performed to evaluate the potential molecular pathways in which CTSF may be involved. The CTSF mRNA level was associated with tumor differentiation, depth of tumor invasion, and lymph node metastasis. Downregulation of CTSF expression efficiently inhibited apoptosis and promoted the proliferation of GC cells. Moreover, a total of 1,117 upregulated mRNAs and 1,143 downregulated mRNAs were identified as differentially expressed genes (DEGs). Further analysis identified the involvement of these mRNAs in cancer-related pathways and various other biological processes. Nine DEGs in cancer-related pathways and three downstream genes in the apoptosis pathway were validated by Western blot, which was mainly in agreement with the microarray data. To our knowledge, this is the first report investigating the effect of CTSF on the growth and apoptosis in GC cells and its clinical significance. The CTSF gene may function as a tumor suppressor in GC and may be a potential therapeutic target in the treatment of GC.

Purpose Dysregulation of miR‐148a‐3p in gastric cancer was reported. However, the diagnostic potential and biological function of miR‐148a‐3p in gastric cancer progression is not fully studied. Methods Bioinformatics analysis and RT‐qPCR assay were performed to analyze the expression of miR‐148a‐3p in gastric cancer tissues and plasma of gastric cancer patients. Receiver operating characteristic curve analysis was performed to analyze the diagnostic value of miR‐148a‐3p. In vitro proliferation, apoptosis, migration, invasion, sphere formation assay and Western blotting assay were performed to evaluate the biological function of miR‐148a‐3p in gastric cancer progression. Results miR‐148a‐3p was significantly down‐regulated in both gastric cancer patients' tissue and plasma samples. Plasma miR‐148a‐3p showed promising efficacy for gastric cancer diagnosis. Overexpression of miR‐148a‐3p could inhibit the proliferative phenotype, metastatic phenotype, and cancer stem‐like properties of gastric cancer cells. Conclusions miR‐148a‐3p inhibits cancer progression and is a novel diagnostic biomarker for gastric cancer.

E-Cadherin (CDH1) plays a key role in cell adhesion, which is vital to the normal development and maintenance of cells. Down regulation of CDH1, may lead to dysfunction of the cell-cell adhesion system, resulting in increased susceptibility to tumor development and subsequent tumor cell invasion and metastasis. The CDH1 C-160A polymorphism could decrease its transcription efficiency and may increase susceptibility to cancer development, but its relevance to gastric cancer is generally disputed. Consequently, we performed a meta-analysis of published case-control studies, including 4218 gastric cancer cases and 5461 controls. Overall, no significant association was observed between the CDH1 C-160A polymorphism and risk of gastric cancer in all genetic models. In the stratified analysis by total sample size, a significant association was observed in the small sample size subgroup (total sample size < 300), but the results should be interpreted with caution. In conclusion, this meta-analysis failed to confirm the association between the CDH1 C-160A polymorphism and risk of gastric cancer. Large-scale and well-designed studies are needed to confirm our findings.

Background: Gastric cancer (GC) accounts for high mortality, which seriously threatens people’s health. This study set out to probe into the effect and mechanism of miR-27b-3p on invasion and migration of GC. Methods: The miRNA sequence data of GC was acquired from The Cancer Genome Atlas (TCGA) database. The differential expression of miRNAs (DEMis) was acquired through R packages “edgeR” and “limma.” TargetScan, picTar, RNA22, PITA, and miRanda were performed to predict the target gene of miR-27b-3p. Western-blot and RT-PCR were applied to detect the expression level of the selected candidate. Transwell assays evaluated the effect of miR-27b-3p and runt-related transcription factor 1 (RUNX1) on cell migration and invasion. The rescue assay was achieved by co-culture with mimics of miR-27b-3p and vector of RUNX1. The psiCHECK2 vector was used in the luciferase report assay. Results: We found miR-27b-3p was down-regulated in GC and associated with GC patients' poor survival based on the TCGA data and bioinformatics analysis. Furthermore, RUNX1 was the target gene of miR-27b-3p, which was proved by the luciferase report assay. miR-27b-3p and RUNX1 jointly participate in the regulation of the Hippo pathway. The up-regulated miR-27b-3p could inhibit epithelial–mesenchymal transition (EMT) as well as invasion and migration. However, an overexpressed RUNX1 could weaken this phenomenon. Conclusion: miR-27b-3p was down-regulated in GC, and it could regulate the Hippo pathway and affect EMT by inhibiting RUNX1 expression.

ABSTRACT. This study was designed to detect the stiffness of single living gastrointestinal stromal tumor (GIST) cells in vitro using an atomic force microscope as a probe tool. We determined that the stiffness of living GIST cells was 3913 Pa, the stiffness of the membrane was 642 Pa, and the stiffness of the cytoplasm was 17,550 Pa. For comparison, we also determined the stiffness of a normal stomach cell, which was 7374 Pa, and that of in vitro GIST cells after 2 h of exposure, which was 10,680 Pa. Measuring the mechanical properties of individual GIST cells might provide more complementary information for the diagnosis and treatment of GISTs from the perspective of physical characteristics.

Gastrointestinal stromal tumors (GISTs) are defined as spindle cell and/or epithelioid tumors originated from interstitial Cajal cells or precursors in the digestive tract. This study was conducted to identify genes differing in expression between the gastric tumors and the adjacent non-cancerous mucosas in patients with primary gastric GIST. The gene expression profile was determined by using oligonucleotide-based DNA microarrays and further validated by quantitative real-time PCR. The Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis was performed to predict signaling pathways involved in gastric GIST. Our data showed that the expression levels of 957 genes (RAB39B, member RAS oncogene family; VCAN, versican; etc.) were higher and that of 526 genes (CXCL14, chemokine C-X-C motif ligand 14; MTUS1, microtubule-associated tumor suppressor 1; etc.) were lower in the gastric tumor tissues as compared with normal gastric tissues. Results from KEGG pathway analysis revealed that the differentially expressed genes were enriched into 16 signaling transduction pathways, including Hedeghog and Wnt signaling pathways. Our study may provide basis for identification of novel biomarkers associated with primary gastric GIST pathogenesis and for exploration of underlying mechanisms involved in this gastric sarcoma.

Background: Gastric cancer (GC) is a common gastrointestinal malignancy. Evidence suggests that long non-coding RNAs (lncRNAs) influence mRNA expression to induce GC progression. We aim to investigate the function and regulatory mechanism of TP73-AS1 in GC. Materials and methods:We detected TP73-AS1, miR-27b-3p, and TMED5 (Transmembrane P24 Trafficking Protein 5) by real-time polymerase chain reaction (RT-PCR). Similarly, the protein levels of CRIM1 and wnt/β-catenin were detected by western-blot. The colony formation and Cell-Counting Kit-8 (CCK-8) assay detected cell proliferation. Transwell and scrape assay tested cell migration and invasion. Dual-luciferase reporter assays confirmed directed binding targets. Tumor xenograft in nude mice checked the result in vivo. Results: TP73-AS1 over-expressed in GC. Suppressed TP73-AS1 inhibited cell proliferation, migration, and invasion. However, down-regulated miR-424 could reverse the effects of weakenTP73-AS1 on the progression of GC. Moreover, TMED5 was also up-regulated in GC. Both TP73-AS1 and TMED5 were the direct target of miR-27b-3p. Meanwhile, miR-27b-3p was a negative correlation with TP73-AS1 and TMED5. The TP73-AS1/miR-27b-3p/TMED5 axis regulate wnt/β-catenin pathway. Conclusion: TP73-AS1 promoted GC proliferation, migration, and invasion by sponging miR-27b-3p to regulate TMED5. TP73-AS1 was a potential onco-lncRNA in GC.