FAM64A aggravates proliferation, invasion, lipid droplet formation, and chemoresistance in gastric cancer: A biomarker for aggressiveness and a gene therapy target.

FAM64A is a mitogen-induced regulator of the metaphase and anaphase transition. Here, we found that FAM64A messenger RNA (mRNA) and protein expression levels were higher in gastric cancer tissue than in normal mucosa (p < .05). FAM64A methylation was negatively correlated with FAM64A mRNA expression (p < .05). The differentially expressed genes of FAM64A were mainly involved in digestion, potassium transporting or exchanging ATPase, contractile fibers, endopeptidase, and pancreatic secretion (p < .05). The FAM64A-related genes were principally categorized into ubiquitin-mediated proteolysis, cell cycle, chromosome segregation and mitosis, microtubule binding and organization, metabolism of amino acids, cytokine receptors, lipid droplet, central nervous system, and collagen trimer (p < .05). FAM64A protein expression was lower in normal gastric mucosa than intestinal metaplasia, adenoma, and primary cancer (p < .05), negatively correlated with older age, T stage, lymphatic and venous invasion, tumor, node, metastasis stage, and dedifferentiation (p < .05), and associated with a favorable overall survival of gastric cancer patients. FAM64A overexpression promoted proliferation, antiapoptosis, migration, invasion, and epithelial-mesenchymal transition via the EGFR/Akt/mTOR/NF-κB, while the opposite effect was observed for FAM64A knockdown. FAM64A also induced chemoresistance directly or indirectly through lipid droplet formation via ING5. These results suggested that upregulation of FAM64A expression might induce aggressive phenotypes, leading to gastric carcinogenesis and its subsequent progression. Thus, FAM64A could be regarded as a prognosis biomarker and a target for gene therapy.

The effects of REG4 expression on chemoresistance of ovarian cancer.

Although ovarian cancer usually responds well to platinum- and taxane-based first-line chemotherapy, most patients develop recurrence and chemoresistance. Regenerating gene 4 (REG4) is a secretory protein involved in cell differentiation and proliferation. We found higher REG4 expression in ovarian cancer than in normal tissues (p < .05). Regenerating gene 4 expression was negatively associated with overall, progression-free or post-progression survival rates of patients with ovarian cancer receiving platinum or paclitaxel treatment (p < .05) according to a Kaplan-Meier plotter. Regenerating gene 4 overexpression resulted in either cisplatin or paclitaxel resistance, and apoptosis resistance in CAOV3 ovarian cancer cells (p < .05). REG4-transfected ovarian cancer cells showed stronger migration and invasion treated with cisplatin or paclitaxel (p < .05). Additionally, cisplatin or paclitaxel exposure led to the overexpression of phosphorylated phosphoinositide 3-kinase (p-PI3K), p-Akt, phosphorylated mammalian target of rapamycin (p-mTOR), glutathione S-transferase-π, survivin, and B-cell lymphoma 2 in REG4 transfectants compared with control cells (p < .05). These findings suggested that REG4 expression was up-regulated in ovarian cancer, and associated with poor survival and chemotherapy resistance. REG4 promoted the occurrence, development, and chemotherapy resistance of ovarian cancer by regulating cell proliferation, apoptosis, migration, and invasion, and PI3K/Akt/m-TOR signalling pathways. IMPACT STATEMENTWhat is already known on this subject? REG4 mRNA expression is up-regulated in many digestive cancers. High REG4 expression was associated with an adverse prognosis, high tumour and nodal stages, poor differentiation, and hepatic and peritoneal metastases of digestive cancers. REG4 expression conferred cancer cells with increased resistance to chemoradiotherapy, especially 5-FU-based treatment, by activating the MAPK/Erk/Bim signalling pathway.What do the results of this study add? REG4 was highly expressed in ovarian cancer. The expression of p-PI3K, p-AKT, p-mTOR, GST-π, survivin, and Bcl-2 was increased in REG4-overexpressing cells. High REG4 expression was significantly associated with inferior OS, PFS, and PPS rates in patients with ovarian cancer receiving platinum chemotherapy. REG4 mediated cisplatin and paclitaxel resistance in CAOV3 ovarian cancer cells. The percentage of apoptotic cells was markedly lower in REG4-transfected compared to mock-transfected cells after cisplatin or paclitaxel treatment.What are the implications of these findings for clinical practice and/or further research? This study aimed to evaluate the prognostic significance of REG4 expression in ovarian cancer treated with platinum and paclitaxel, to explore REG4 chemoresistance mechanisms to platinum and paclitaxel, and to provide a scientific experimental basis for the clinical treatment and outcome evaluation of ovarian cancer. In order to provide comprehensive clinical treatment of ovarian cancer, it is helpful to improve our understanding of multi-drug resistance and identify new cancer diagnostic biomarkers.

Association of single nucleotide polymorphisms in the MVP gene with platinum resistance and survival in patients with epithelial ovarian cancer.

The human major vault protein (MVP) has been linked to the development of multidrug resistance in cancer cells, and overexpression of MVP has been observed in ovarian cancer tissues. The aim of the present study was to investigate the association between single nucleotide polymorphisms (SNPs) in the MVP gene and the tumor response to platinum-based chemotherapy and survival of patients affected by epithelial ovarian cancer (EOC), in addition to confirm whether tetra-primer amplification-refractory mutation system (ARMS)-polymerase chain reaction (PCR) is an accurate genotyping method. For this purpose, two polymorphisms in the MVP gene, namely reference SNP (rs)1057451 and rs4788186, were selected from the data obtained by the International haplotype map (HapMap) Project regarding Chinese Han population, and were evaluated by tetra-primer ARMS-PCR. Upon validation by DNA sequencing, the association of these polymorphisms with platinum resistance, progression-free survival (PFS) and overall survival (OS) in patients with EOC was assessed. The results of tetra-primer ARMS-PCR were in agreement with those derived from DNA sequencing. No significant differences were observed between platinum-sensitive and platinum-resistant cohorts in terms of allele and genotype distribution of these two polymorphisms in the MVP gene, which were not associated with PFS or OS. However, a trend toward prolonged PFS was observed in patients carrying the heterozygous AG allele at the rs4788186 locus. These results suggest that rs1057451 and rs4788186 variants in the MVP gene are not associated with favorable therapeutic response to platinum or longer survival in Chinese Han patients affected by EOC. In addition, the data of the present study confirm that tetra-primer ARMS-PCR is a trustworthy and economical genotyping method.

Association between polymorphisms of BAG-1 and XPD and chemotherapy sensitivity in advanced non-small-cell lung cancer patients treated with vinorelbine combined cisplatin regimen.

BCL-2 Associated athanogene 1 (BAG-1) and Xeroderma pigmentosum group D (XPD) are involved in the nucleotide excision repair pathway and DNA repair. We aimed to investigate whether polymorphisms in BAG-1 and XPD have effects on chemotherapy sensitivity and survival in patients with advanced non-small-cell lung cancer (NSCLC) treated with vinorelbine combined cisplatin (NP) regimen. A total of 142 patients with diagnosed advanced NSCLC were recruited in the current study. NP regimen was applied for all eligible patients. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used for BAG-1 (codon 324) and XPD (codons 312 and 751) genotyping. The treatment response was evaluated according to the RECIST guidelines. Progression-free survival (PFS) and overall survival (OS) were record as median and end point, respectively. As for BAG-1 codon 324, the chemotherapy sensitivity in NSCLC patients with CT genotype was 0.383 times of those with CC genotype (P < 0.05). With respect to XPD codon 751, the chemotherapy sensitivity in NSCLC patients with Lys/Gln genotype was 0.400 times of those with Lys/Lys genotype (P < 0.05). In addition, NSCLC patients carrying combined C/C genotype at codon 324 in BAG-1, Asp/Asp of XPD codon 312, and Lys/Lys of XPD codon 751 produced a higher efficacy of NP chemotherapy compared to those carrying mutation genotypes (all P < 0.05). Further, there were significant differences in PFS between patients with combined C/C genotype of BAG-1 codon 324, Lys/Lys genotype of XPD codon 751, and Asp/Asp genotype of XPD codon 312 and patients carrying BAG-1 codon 324 C/T genotype, XPD codon751 Lys/Gln genotype, and XPD codon312 Asp/Asn genotype (P < 0.05). Multivariate Cox regression analysis indicated that the combined wild-type of codon 324 XPD, codon 751 XPD, and codon 312 BAG-1 is the protective factor for OS and PFS, and clinical stages is the risk factor for OS and PFS. In conclusion, our research demonstrated the combined effects of BAG-1 and XPD polymorphisms on chemotherapy sensitivity and survival in patients with advanced NSCLC, which might be the important predictive markers for platinum-based chemotherapy efficacy.

Effect of the -2081G/A polymorphism of the TLR4 gene and its interaction with Helicobacter pylori infection on the risk of gastric cancer in Chinese individuals.

AIMS: Toll-like receptor 4 (TLR4) plays an important role in gastric carcinoma. Using a case-control study, we analyzed the genotypic distribution of TLR4 rs10983755 (-2081G/A) and rs11536878 in a Chinese population and investigated the effect of their interactions with Helicobacter pylori infection on susceptibility to gastric cancer (GC) and atrophic gastritis (AG). METHODS: In this study, 409 and 581 cases of GC and AG, respectively, were selected for analyses along with an equal number of matched controls. The TLR4 polymorphisms were genotyped using Sequenom MassARRAY. Serum levels of anti-H. pylori IgG were determined by enzyme-linked immunosorbent assay. RESULTS: The TLR4-2081G/A polymorphism was negatively associated with GC (AG+AA vs. GG: odds ratio [OR]=0.70, 95% confidence interval [CI]=0.53-0.93, p=0.012). A decreased risk of GC was observed in H. pylori negative and TLR4-2081(AG+AA) genotype subjects [H. pylori(-)/AG+AA vs. H. pylori(+)/GG: OR=0.16, 95% CI=0.09-0.27, p<0.001]. The rs11536878 polymorphism was not associated with GC or AG. CONCLUSIONS: The TLR4-2081G/A polymorphism seems to affect the risk of gastric carcinogenesis and may to some degree play a protective role against H. pylori infection.

Effects of MTHFR genetic polymorphisms on toxicity and clinical response of irinotecan-based chemotherapy in patients with colorectal cancer.

AIMS: This meta-analysis aims to evaluate the effects of common polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene on the toxicity and clinical responses of irinotecan-based chemotherapy in patients with colorectal cancer (CRC). METHODS: The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched from their inception through November 1st, 2013 without language restrictions. Meta-analysis was conducted with the use of the STATA 12.0 software. Crude odds ratios (ORs) and their 95% confidence intervals (95% CIs) were calculated. Seven clinical cohort studies with a total of 815 CRC patients met the inclusion criteria. Two common polymorphisms (677 C>T and 1298 A>C) in the MTHFR gene were assessed. RESULTS: The results from our meta-analysis suggested that MTHFR genetic polymorphisms might significantly decrease the rate of grade 3/4 toxicity of irinotecan-based chemotherapy in CRC patients (OR=0.53, 95% CI: 0.32-0.89, p=0.015). Furthermore, we also demonstrated that MTHFR genetic polymorphisms strongly correlated with good clinical responses (complete response+partial response) to irinotecan-based chemotherapy in CRC patients (OR=1.47, 95% CI: 1.05-2.04, p=0.024). CONCLUSIONS: Our findings provide empirical evidence that MTHFR genetic polymorphisms may decrease the toxicity of irinotecan-based chemotherapy and increase the clinical benefits for CRC patients. Thus, MTHFR genetic polymorphisms may be screened to predict the clinical responses to irinotecan-based chemotherapy in CRC patients.

Role of MDM2 T309G polymorphism in susceptibility and prognosis of nonsmall cell lung cancer: a meta-analysis.

AIMS: This meta-analysis was performed to evaluate the relationships of a common polymorphism (T309G, rs2279744 T>G) in the murine double minute 2 (MDM2) gene with susceptibility and prognosis of nonsmall cell lung cancer (NSCLC). METHODS: The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched for relevant articles published before November 1st, 2013 without any language restrictions. Meta-analysis was conducted using the STATA 12.0 software. Crude odds ratios (ORs) or hazard risk (HR) with their 95% confidence intervals (95% CI) were calculated. Seven clinical studies with a total 3732 NSCLC patients and 1472 healthy controls met the inclusion criteria. RESULTS: The results of our meta-analysis suggested that MDM2 T309G polymorphism might be strongly correlated with an increased risk of NSCLC (G allele vs. T allele: OR=1.63, 95% CI: 1.42-1.89, p<0.001; TG+GG vs. TT: OR=1.54, 95% CI: 1.31-1.80, p<0.001; respectively). Furthermore, we observed significant associations of MDM2 T309G polymorphism with poor overall survival (TT vs. GT: HR=1.22, 95% CI: 101-1.43, p<0.001; TT vs. GG: HR=1.31, 95% CI: 1.04-1.59, p<0.001; TT vs. GT+GG: HR=1.44, 95% CI: 1.13-1.76, p<0.001; respectively) and progression-free survival (TT vs. GT+GG: HR=1.26, 95% CI: 0.82-1.69, p<0.001) of NSCLC patients. CONCLUSIONS: Our findings provide convincing evidence that the MDM2 T309G polymorphism may contribute to individual differences in NSCLC susceptibility and prognosis. Thus, the MDM2 T309G polymorphism may be a promising potential biomarker for NSCLC diagnosis and prognosis.

The role of expression and polymorphism of the BAG-1 gene in response to platinum-based chemotherapeutics in NSCLC.

We investigated the correlation between BAG-1 expression and sensitivity to platinum-based chemotherapeutics in patients with non-small cell lung cancer (NSCLC). mRNA and protein expression of BAG-1 in lung tissue of NSCLC postoperative patients (I-IIIA stage) or healthy subjects were detected using reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry, respectively. Cox regression analysis was used to quantify the association of prognostic factors with survival in NSCLC patients. Venous blood samples from patients newly diagnosed with advanced NSCLC (IIIB-IV stage) were collected before chemotherapy to analyze allelic frequency and gene polymorphisms. Compared to healthy controls (11.67%, 14 cases), levels of mRNA and protein of BAG-1 in lung tissues was significantly higher in NSCLC patients (61.67%, 74 cases) (χ²=5.601, P<0.05). Moreover, BAG-1 expression was identified as an independent prognostic factor for survival in NSCLC patients. As time to progression and survival rate was dramatically increased, patients with a positive expression of BAG-1 exhibited a prolonged survival period (TTP, 49.3 months; 5-year survival rat, 16.21%) compared with those without BAG-1 expression (χ²=7.243, P<0.05). Two BAG-1 digestion patterns (CC and CT) were identified and confirmed. patients (77.46%) had a C/C genotype at BAG-1 codon 324, while 22.54% had the C/T genotype. The T/T genotype was not present in these patients. The progression risk of patients carrying the C/C genotype at Bag-1 codon 324 was 1.87 times higher than that of patients carrying the C/T genotype (P<0.001). Follow-up examination showed that the chemotherapeutic sensitivity of patients carrying the C/C genotype was 2.852 times higher than that of patients carrying the C/T genotype (95% CI, 1.133-7.182; P=0.026). Significant differences were found in the median progression-free survival (PFS) and overall survival (OS) of these two cohorts of patients. Compared to patients carrying the C/T genotype of BAG-1, patients carrying the C/C genotype at Bag-1 codon 324 exhibited better responses to platinum-based chemotherapy. Hence, the expression of BAG-1 was closely associated with the sensitivity to platinum-based chemotherapeutics in NSCLC patients.

[The effect of thalidomide in preventing delayed nausea and vomiting induced by GP regimen of chemotherapy for non-small cell lung cancer].

OBJECTIVE: To observe the effect of thalidomide in preventing nausea and vomiting induced by emetogenic cisplatin (CDDP) chemotherapy in patients with advanced non-small cell lung cancer. METHODS: This study was carried out as a prospective, randomized control clinical trial. 61 patients with advanced non-small cell lung cancer were scheduled to receive chemotherapy (gemcitabin 1000 mg/m(2) i.v. gtt d1, 8 and CDDP 75 mg/m(2) i.v. gtt d1, GP regimen). The patients were randomly divided into a treatment and control groups. All patients in both groups received ramosetron 0.3 mg intravenously (i.v.) and metoclopramide 20 mg intramuscularly (i.m.) 30 min prior to chemotherapy to prevent nausea and emesis on day 1. In the treatment group, addition of thalidomide (50 mg p.o. bid) were administered on days 1 to 5 after the start of chemotherapy. RESULTS: Acute nausea was effectively controlled in 74.2% of the patients in the control group and in 90.0% of treatment group. Acute vomiting was effectively controlled in 90.3% of the patients in the control group and in 93.3% of treatment group. No statistically significant differences showed in effective control of acute nausea and vomiting between the 2 groups (P = 0.108; P = 1.000). Delayed nausea was effectively controlled in 19.4% of the patients in control group and in 56.7% in the treatment group. Delayed vomiting was effectively controlled in 48.4% of the patients in control group and 76.7% in treatment group. Statistically there was a significant differences in effective control of delayed nausea and vomiting between the 2 groups (P = 0.003, P = 0.023). Both antiemetic regimens were well tolerated, and no significant difference was observed in adverse events between the 2 groups (P > 0.05). CONCLUSION: Our results demonstrate that thalidomide is highly effective in controlling delayed nausea and vomiting episodes in patients induced by moderately emetogenic chemotherapy. Moreover, no serious toxic effects are induced by this treatment.

Effects of allitridi on cell cycle arrest of human gastric cancer cells.

AIM: To determine the effect of allitridi on cell cycle of human gastric cancer (HGC) cell lines MGC803 and SGC7901 and its possible mechanism. METHODS: Trypan blue dye exclusion was used to evaluate the proliferation, inhibition of cells and damages of these cells were detected with electron microscope. Flow cytometry and cell mitotic index were used to analyze the change of cell cycle, immunohistochemistry, and RT-PCR was used to examine expression of the p21(WAF1) gene. RESULTS: MGC803 cell growth was inhibited by allitridi with 24 h IC50 being 6.4 microg/mL. SGC7901 cell growth was also inhibited by allitridi with 24 h IC50 being 7.3 microg/mL. After being treated with allitridi at the concentration of 12 microg/mL for 24 h, cells were found to have direct cytotoxic effects, including broken cellular membrane, swollen and vesiculated mitochondria and rough endoplasmic reticula, and mass lipid droplet. When cells were treated with allitridi at the concentration of 3, 6, and 9 microg/mL for 24 h, the percentage of G0/G1 phase cells was decreased and that of G2/M phase cells was significantly increased (P = 0.002) compared with those in the group. When cells were treated with allitridi at the concentration of 6 microg/mL, cell mitotic index was much higher (P = 0.003) than that of control group, indicating that allitridi could cause gastric cancer cell arrest in M phase. Besides, the expression levels of p21(WAF1) gene of MGC803 cells and p21(WAF1) gene of SGC7901 cells were remarkably upregulated after treatment. CONCLUSION: Allitridi can cause gastric cancer cell arrest in M phase, and this may be one of the mechanisms for inhibiting cell proliferation. Effect of allitridi on cells in M phase may be associated with the upregulation of p21(WAF1) genes. This study provides experimental data for clinical use of allitridi in the treatment of gastric carcinoma.

Effect of staurosporine on cycle of human gastric cancer cells.

AIM: To study the effect of staurosporine (ST) on the cell cycle of human gastric cancer cell lines MGC803 and SGC7901. METHODS: Cell proliferation was evaluated by trypan blue dye exclusion method. Apoptotic morphology was observed under a transmission electron microscope. Changes of cell cycle and apoptotic peaks of cells were determined by flow cytometry. Expression of p21WAF1 gene was examined using immunohistochemistry and RT-PCR. RESULTS: The growth of MGC803 and SGC7901 cells was inhibited by ST. The inhibitory concentrations against 50% cells (IC50) at 24 h and 48 h were 54 ng/ml and 23 ng/ml for MGC803, and 61 ng/ml and 37 ng/ml for SGC7901. Typical apoptotic bodies and apoptotic peaks were observed 24 h after cells were treated with ST at a concentration of 200 ng/ml. The percentage of cells at G0/G1 phase was decreased and that of cells at G2/M was increased significantly in the group treated with ST at the concentrations of 40 ng/ml, 60 ng/ml, 100 ng/ml for 24 h, compared with the control group (P<0.01). The expression levels of p21WAF1 gene in both MGC803 and SGC7901 cells were markedly up-regulated after treatment with ST. CONCLUSION: ST can cause arrest of gastric cancer cells at G2/M phase, which may be one of the mechanisms that inhibit cell proliferation and cause apoptosis in these cells. Effect of ST on cells at G2/M phase may be attributed to the up-regulation of p21WAF1 gene.

[Allicin induced cell cycle arrest in human gastric cancer cell lines].

OBJECTIVE: To study the effect of allicin on cell cycle of human gastric cancer cell lines, MGC-803 and SGC-7901, and its possible mechanisms. METHODS: The gastric cancer cell lines MGC-803 and SGC-7901 were treated with allicin. Proliferation inhibitory rate was detected by trypan-blue exclusion. Morphologic changes were observed by electron microscopy. The cell cycle was examined by flow cytometry and Giemsa staining. Expression of p21WAF1, p16INK4 protein and mRNA was detected by immunohistochemistry and RT-PCR. RESULTS: The gastric cancer cells were inhibited after exposure to allicin for 24 hr, The IC50 was 6.4 microg/ml in MGC-803 cells and 7.3 microg/ml in SGC-7901cells. After exposure to allicin of 12 microg/ml for 24 hr, it caused the cytotoxic effect on the cells, including cellular membrane breakagy. After exposure to allicin of 3 microg/ml, 6 microg/ml and 9 microg/ml for 24 hr, compared with the control group, the proportion of cells in the G0/G1 phase was decreased and that in the G2/M phase was increased significantly (P < 0.01). After exposure to allicin of 6 microg/ml for 24 hr, compared with the control group, cell division index was much higher, suggesting that allicin could induce cell arrest in M phase. The expression levels of p21WAF1 and p16INK4 protein and mRNA in MGC-803 cells and p21WAF1 protein and mRNA in SGC-7901 cells were markedly up-regulated. CONCLUSION: Allicin induce cell arrest of gastric cancer in M phase, which may be related to the up-regulated expression of p21WAF1 and p16INK4 genes.

[Effect of staurosporine on cell cycle of human gastric cancer cells].

BACKGROUND & OBJECTIVE: Protein kinase C (PKC) has been considered to be a potentially suitable target for anticancer therapy. This study was designed to investigate the effect of PKC inhibitor staurosporine (ST) on the inhibition of proliferation, the induction of apoptosis, and the change of cell cycle in human gastric cancer cell lines MGC-803 and SGC-7901. METHODS: The inhibition rates of cell proliferation were evaluated by trypan blue exclusion. The apoptotic bodies were observed under light microscope and electron microscope. The apoptotic peaks of the cells and the changes of cell cycle were analyzed using flow cytometry. RESULTS: ST inhibited cell growth of MGC-803, IC(50) of 24 hours was 54 ng/ml and IC(50) of 48 hours was 23 ng/ml. ST inhibited cell growth of SGC-7901, IC(50) of 24 hours was 61 ng/ml and IC(50) of 48 hours was 37 ng/ml. MGC-803 cells were treated by ST at the concentrations of 40, 60, and 100 ng/ml for 24 hours, the percentages of G(0)/G(1) phage were 23.6+/-1.8%, 11.6+/-0.7%, and 3.3+/-0.2%, respectively (54.3+/-3.1% in control group); the percentages of G(2)/M phage were 22.6+/-4.0%, 35.5+/-0.4%, and 36.8+/-5.5%, respectively (13.5+/-0.2 in control group). SGC-7901 cells were treated by ST at the concentrations of 40, 60, and 100 ng/ml for 24 hours, the percentages of G(0)/G(1) phage were 27.1+/-1.4%, 17.0+/-3.4%, 13.7+/-0.7%, respectively (52.5+/-4.4% in control group); the percentages of G(2)/M were 21.9+/-2.6%, 39.5+/-4.9%, and 38.4+/-3.1%, respectively (13.5+/-2.2% in control roup). Compared with the control group, the percentages of G(0)/G(1) phage of two cell lines decreased and that of G(2)/M cells increased significantly in the ST treated group(P< 0.01). Treated by ST at the concentration of 200 ng/ml, the apoptotic peaks and typical apoptotic bodies were observed. CONCLUSION: ST significantly inhibits the proliferation and induces apoptosis of MGC-803 cells and SGC-7901 cells; ST induces G(2)/M phase arrest.