Triosephosphate isomerase (TPI) is highly expressed in many types of human tumors and is involved in migration and invasion of cancer cells. However, TPI clinicopathological significance and malignant function in gastric cancer (GC) have not been well defined. The present study aimed to examine TPI expression in GC tissue and its biological functions. Furthermore, we investigated its downstream genes by gene chip technology. Our results showed that TPI expression was higher in gastric cancer tissues than adjacent tissues, although no statistical differences were found between TPI expression and clinicopathological factors. TPI overexpression in human gastric carcinoma cell line BGC-823 enhanced cell proliferation, invasion and migration, but did not change cell cycle distribution, while TPI knockdown suppressed proliferation, invasion and migration, induced apoptosis and increased G2/M arrest of human gastric carcinoma cell line MGC-803. Since the cell division cycle associated 5 (CDCA5) was identified as the one with the most decreased expression after TPI knockdown, we investigated its role in MGC-803 cells. The results showed that CDCA5 knockdown also inhibited proliferation, migration, induced apoptosis and increased G2/M arrest similarly to TPI knockdown. CDCA5 overexpression promoted MGC-803 cell proliferation, clone formation and migration abilities. These results indicated that TPI expression level might affect GC cell behavior, suggesting that both TPI and CDCA5 might be considered as potential tumor markers related with GC development and might be potential new targets in GC treatment.

Triosephosphate isomerase (TPI) is highly expressed in many human cancers and is involved in migration and invasion of cancer cells. However, TPI clinicopathological significance and prognostic value in gastric cancer (GC) are not yet well defined. The aim of the present work was to evaluate TPI expression in GC tissue and its prognostic value in GC patients.TPI expression was analyzed in 92 primary GC tissues and 80 adjacent normal mucosa tissues from GC patients undergoing gastrectomy by immunohistochemical analysis of tissue microarrays (TMAs). Univariate and multivariate analyses were performed to investigate TPI prognostic significance in GC patients.Immunohistochemical staining score showed that TPI expression in cancer tissues was significantly higher than in adjacent normal mucosa (P < .001). Univariate analysis revealed that TPI expression, depth of invasion, lympho node metastasis, tumor node metastasis (TNM) stage, and tumor diameter were associated with negative prognostic predictors for overall survival in GC patients (P < .05). High TPI expression represented a significant predictor of shorter survival in GC patients with positive lymphatic metastasis (P = .022) and tumor diameter >5 cm (P = .018). Cox multivariate analysis identified TPI expression, TNM stage, and tumor diameter as independent prognostic factors in GC patients.TPI expression might be considered as a novel prognostic factor to evaluate GC patients’ survival.

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Two unsymmetrical oxovanadium complexes incorporating salicylaldehyde derivate and phenanthroline [VO(DESAA)(phen)] (1), (DESAA = 4-(diethylamino)salicylaldehyde anthranilic acid, phen = phenanthroline) and [VO(CLSAA)(phen)] (2), (CLSAA = 5-chlorosalicylaldehyde anthranilic acid)] have been synthesized and characterized. The interactions of the complexes with CT-DNA were studied using different techniques. Complexes 1 and 2 interact with CT-DNA by intercalative modes and can efficiently cleave pBR322 DNA after light irradiation. The two complexes showed high cytotoxic activities against myeloma cell (Ag8.653) and gliomas cell (U251) lines. Interestingly, complex 1 exhibited greater antitumor efficiency, larger binding affinity with CT-DNA, and better cleaving ability than those of complex 2. In addition, their antitumor mechanism has been analyzed by using cell cycle analysis, apoptosis, and Annexin V-FITC/PI assay. The results showed that complex 1 can cause G2/M-phase arrest of the cell cycle, exhibit a significantly induced apoptosis in Ag8.653 cells, and display typical morphological apoptotic characteristics. These complexes induced proliferative suppression of Ag8.653 cells via the induction of apoptosis.

Gastric cancer (GC) is the third leading cause of cancer-associated mortality. In a previous study, we identified that α-enolase (ENO1) promoted cell migration in GC, but the underlying molecular mechanisms remain to be fully elucidated. In the present study, small interfering RNAs were identified to interfere with ENO1 expression. The cDNA expression profiling was performed using an Affymetrix mRNA array platform to identify genes that may be associated with ENO1 in human GC cell line MGC-803. The differentially expressed genes (DEGs) were identified using the reverse transcription-quantitative polymerase chain reaction, followed by a series of bioinformatic analyses. As a result, there were 448 DEGs, among which 183 (40.85%) were downregulated. The most significant functional terms for the DEGs were the nuclear lumen for cell components (P=2.83×10−4), transcription for biological processes (P=3.7×10−7) and transcription factor activity for molecular functions (P=1.16×104). In total, six significant pathways were enriched, including the most common cancer-associated forkhead box O signaling pathway (P=0.0077), microRNAs in cancer (P=0.0183) and the cAMP signaling pathway (P=0.0415). Furthermore, a network analysis identified three hub genes (HUWE1, PPP1CB and HSPA4), which were all involved in tumor metastasis. Taken together, the DEGs, significant pathways and hub genes identified in the present study shed some light on the molecular mechanisms of ENO1 involved in the pathogenesis of GC.