Effect of intraoperative blood salvage on erythrocyte morphosis observed under atomic force microscope

AIM: To investigate the effect of intraoperative blood salvage (IOBS) on the morphosis of erythrocytes with atomic force microscopic (AFM) observation. METHODS: Blood samples from the patients with spinal operation were collected before operation (T1) and 1 h after IOBS (T4). Unprocessed blood (T2) and processed blood (T3) in the cell saver were also measured. An AFM with nanometer resolution was used to examine the ultrastructure of membrane surface of the erythrocytes in the samples. RESULTS: The percentage of heteromorphous erythrocytes in T1 samples was the lowest. There were significant differences in AFM images and height profile of a single erythrocyte between salvaged blood and venous blood. AFM images at 1 μm range showed that the distribution of the particles on the erythrocyte membrane surface in unprocessed blood in cell saver was significantly different from the other blood samples. CONCLUSION: There are significant changes in the AFM images of erythrocytes and the ultrastructure of the membrane surface in salvaged blood.     

Effects of propofol on invasion and migration of human gastric cancer SGC-7901 cells

AIM: To investigate the effects of propofol on invasion and migration of gastric cancer cell line SGC-7901. METHODS: Cultured gastric cancer cell line SGC-7901 was randomly divided into 4 groups, and then diffe-rent concentrations (1, 3, 5 and 7 mg/L) of propofol were added and incubated for 24 h. The cell viability was measured by MTT assay. The invasion and migration abilities of the SGC-7901 cells were detected by Transwell assay and wound-healing assay. The expression of cysteine-rich angiogenic inducer 61 (CYR61), CD44v6 and matrix metalloproteinase-7 (MMP-7) in the SGC-7901 cells were examined by immunocytochemistry and Western blot.RESULTS: Propofol at 5 mg/L does not affect the viability of SGC-7901 cells, whereas significantly suppresses the invasion and migration abilities, and down-regulates the expression of CD44v6 and MMP-7 (P<0.05). CONCLUSION: The decreased invasion and migration abilities of SGC-7901 cells were partly due to the inhibition of CD44v6 and MMP-7 expression.     

Observation of molecular interaction between gold nanoparticle and VEGF165 with atomic force microscope

AIM: To investigate the molecular interaction between gold nanoparticles (GNP) and vascular endothelial growth factor 165(VEGF₁₆₅) under atomic force microscope (AFM). METHODS: Before and after incubation with VEGF₁₆₅, GNP were screened by integrated tools including AFM, ultraviolet-visible absorption spectroscopy and particle size analysis under near-physiological condition. In addition, GNP at different concentrations were incubated with VEGF₁₆₅, then added to starved human umbilical vein endothelial cells(HUVECs). The ultrastructural changes of HUVECs surface were examined by AFM. The effects of GNP on the growth of HUVECs were assessed by MTT assay. RESULTS: After treated with VEGF₁₆₅, the GNP absorption peak revealed a slight red shift, and the size distribution of GNP was increased from 20 nm to 30 nm. By AFM imaging, the diameter of GNP was (22.05±1.52) nm in average while the average diameter of GNP-VEGF₁₆₅ was (33.91±2.61) nm. Binding of GNP and VEGF₁₆₅, and the formation of GNP-VEGF₁₆₅ core-shell complex were indicated by the AFM imaging. AFM screening showed the changes of ultrastructure on HUVECs surface. The group of VEGF₁₆₅ displayed the signs of cell proliferation. Granulation of cell surface, increase in cell-to-cell contact, formation of pseudopodia and appearance of membranes pores were all observed. The proliferation of HUVECs was inhibited by GNP with MTT assay. CONCLUSION: GNP bind to VEGF₁₆₅ through chemical bonds to block or inactivate the receptor binding sites of VEGF₁₆₅. Therefore, GNP inhibit VEGF₁₆₅-induced proliferation of HUVECs.     

Effect of ruthenium-polypyridine complex on apoptosis of gastric cancer SGC-7901 cells

AIM:To study the effect of ruthenium-pyridine complex Ru1 on apoptosis of gastric cancer SGC-7901 cells. METHODS:MTT assay and crystal violet staining method were used to detect the viability and cell number of SGC-7901 cells treatment with Ru1. Annexin V-FITC and PI staining was performed to test the apoptosis rate of SGC-7901 cells. The protein expression of Bax and Bcl-2 was detected by Western blot. RESULTS:The results of MTT assay and crystal violet staining showed that the ruthenium-pyridine complexes significantly reduced the viability and cell number of SGC-7901 cells. Treatment with Ru1 for 24 h significantly increased the apoptotic rate of SGC-7901 cells (P<0.05). Ru1 up-regulated the expression of Bax protein and down-regulated the expression of Bcl-2 protein in the SGC-7901 cells (P<0.05). CONCLUSION:Ru1 induces apoptosis of SGC-7901 cells by affecting the expression of Bax and Bcl-2 proteins.     

Double TdR blocking induces synchronization of cell cycle in human gastric cancer SGC-7901 cells

AIM: To investigate the effects of double thymidine deoxyribonucleoside (TdR) blocking on the cell cycle of human gastric cancer SGC-7901 cells.METHODS: SGC-7901 cells in the logarithm period were selected in the study and treated with TdR at concentration of 2 mmol/L, 4 mmol/L or 8 mmol/L for 15 h as the first blocking. After incubation in TdR-free medium for 10 h, the cells were treated with TdR at same concentrations again for another 15 h as the second blocking. The blocked cells were released by washing in fresh medium twice and incubation in TdR-free medium containing 10% fetal bovine serum for 12 h. The cells were collected and the cell cycle was detected by flow cytometry.RESULTS: By double TdR (2 mmol/L, 4 mmol/L and 8 mmol/L) blocking to synchronize the cell cycle, the cells in G₀/G₁ phase accounted for 77.3%, 77.5% and 77.0%, respectively. After further incubation for 12 h in TdR-free medium, the proportion of the cells in each phase of the cell cycles returned to normal range. CONCLUSION: The method of double TdR blocking is an ideal access in short term to acquire a large number of cells in G₀/G₁ phase.     

Effect of beclin-1 gene silencing on TuAKe-injured gastric cancer SGC-7901 cells

AIM: To observe the effect of beclin-1 silencing by the technique of RNA interference on the injury of human gastric cancer SGC-7901 cell by Sheliugu extract (the extract from tuber of Amorphophallus konjac, TuAKe). METHODS: To knock down the expression of beclin-1 gene, SGC-7901 cells were transfected with lentiviral vector carrying beclin-1-shRNA. The beclin-1 gene knock-down and non-knock-down SGC-7901 cells were treated with TuAKe. The cell viability was analyzed by CKK-8 assay. The percentages of apoptotic cells were detected by flow cytometry. The expression of beclin-1 and LC3 was detected by Western blot. RESULTS: The beclin-1 gene silencing decreased the protein expression of beclin-1 and increased the protein expression of LC3 in the SGC-7901 cells, leading to the decrease in cell viability and the increase in apoptotic rate (P<0.05). TuAKe increased the protein expression of beclin-1 and LC3 in the SGC-7901 cells, and decreased the protein expression of LC3 in the SGC-7901 cells with beclin-1 gene silencing, thus inhibiting the cell viability and increasing the apoptotic rate (P<0.05). CONCLUSION: Beclin-1 gene silencing inhibits the activation of beclin-1-related signaling pathway in gastric cancer SGC-7901 cells, and aggravates the injury of cell viability induced by TuAKe.     

Perifosine inhibits cell proliferation and triggers apoptosis in human gastric cancer cell line SGC-7901 cells

AIM: To investigate the effect of perifosine, a novel inhibitor of Akt, on the cell proliferation and apoptosis in human gastric cancer cell line SGC-7901.METHODS: Cell growth inhibition was detected by MTT assay. Cell cycle was analyzed by flow cytometry. Annexin V-FITC apoptosis detection kit was used to determine apoptosis in the cells. Protein expression was examined by Western blotting.RESULTS: Akt phosphorylation was dose-dependently inhibited by perifosine in SGC-7901 cells. The results of MTT and cell cycle analysis indicated that perifosine inhibited the growth of human gastric cancer cells in a dose-dependent manner. Perifosine arrested the cell cycle progression at G₂ phase. Apoptosis induction became more effective with increasing the concentration of perifosine. The caspase cascade and its downstream effector poly(ADP-ribose) polymerase (PARP) were also activated upon perifosine treatment, and the level of Bcl-2 was down-regulated, whereas the protein level of Bax was up-regulated.CONCLUSION: The small molecule Akt inhibitor perifosine shows substantial anti-tumor activity in human gastric cancer cell line SGC-7901. Perifosine induces caspase-dependent apoptosis, and the key regulators include caspase-3, caspase-9 and Bcl-2.     

Effect of integrin β1 on multidrug resistance in gastric cancer SGC-7901 cells

AIM: To study the effect of integrin β1 on multidrug resistance in gastric cancer and its possible mechanisms. METHODS: The expression of integrin β1 at mRNA and protein levels in the SGC-7901 cells and SGC-7901/DDP cells was determined by qPCR and Western blot. The expression of integrin β1 in the SGC-7901/DDP cells was silenced by antisense oligodeoxynucleotide. The cell viability was detected by the CCK-8 assay, the cell apoptosis were analyzed by flow cytometry, and the protein levels of integrin β1, Bcl-2/Bax, cleaved caspase-3/caspase-3, cytochrome C (Cyt-C) and p-AKT/AKT were determined by Western blot.RESULTS: The expression of integrin β1 at both mRNA and protein levels was significantly upregulated in SGC-7901/DDP cells. The expression of integrin β1 was increased in SGC-7901 cells treated with chemotherapeutic agents such as cisplatin, paclitaxel and 5-fluorouracil. Knockdown of integrin β1 induced apoptosis of SGC-7901/DDP cells with an increased sensitivity to the chemotherapeutic agents. Meanwhile, knockdown of integrin β1 downregulated the protein levels of Bcl-2/Bax, p-AKT^Ser473 and p-AKT^Thr308, while promoted the release of Cyt-C and upregulated the protein level of cleaved caspase-3. CONCLUSION: Knockdown of integrin β1 increases the sensitivity of SGC-7901/DDP cells to the chemotherapeutic agents, and promotes the cell apoptosis via mitochondrial apoptosis pathway. The mechanism may be related to the attenuation of AKT pathway by inhibiting phosphorylations of AKT at Ser473 and Thr308.     

Effects of DSF/Cu on surface ultrastructures and mechanical properties of human breast cancer and normal breast epithelial cells

AIM: To study the effects of disulfiram/copper complex (DSF/Cu) on ultrastructures and mechanical properties of human breast cancer and normal breast epithelial cells by atomic force microscopy (AFM) based on the nanoscale resolution and piconewton force measurement level. METHODS: The change of cell cycle and apoptotic rate of MCF-7 cells and MCF-10A cells induced by DSF/Cu were compared by flow cytometry. The cell surface morphology, ultrastructure, height, width and roughness were detected by AFM. The effects of DSF/Cu on the hardness (Young's modulus) of the 2 kinds of cells were determined by AFM with indentation technique. RESULTS: DSF/Cu significantly induced apoptosis of the MCF-7 cells in a dose-dependent manner, whereas had little effect on the MCF-10A cells. The cell cycle analysis showed that DSF/Cu induced G₂/M arrest in the MCF-7 cells, but led to G₀/G₁ arrest in the MCF-10A cells. The AFM images showed that the MCF-7 cells shrank and showed smaller and smoother morphology, and the filopodia were retracted obviously, even some became into lamellipodia, or disappeared completely after treated with DSF/Cu at concentrations of 400 and 800 nmol/L. The quantitative analysis indicated that the MCF-7 cells showed smaller width and larger height, and the root mean square roughness and average roughness were decreased significantly in a dose-dependent manner after treated with DSF/Cu at concentrations of 400 and 800 nmol/L. However, little effect in the MCF-10A cells was observed. The biomechanics test at a single cell level demonstrated that the Young's modulus of the MCF-7 cells and MCF-10A cells were both increased, yet the proportion increased in the MCF-7 cells was much higher than that in the MCF-10A cells after treated with DSF/Cu at concentrations of 400 and 800 nmol/L. CONCLUSION: DSF/Cu has strong antitumor effect on breast cancer with high efficiency and low toxicity by changing the properties of the biomechanics specifically.     

PI3K/mTOR dual inhibitor PF-04691502 induces apoptosis of human gastric cancer SGC-7901 cells

AIM:To determine the antitumor effect of PF-04691502, a dual inhibitor of phosphatidylinositol 3-kinase (PI3K)/Akt and mammalian target of rapamycin (mTOR), on the viability and apoptosis of human gastric cancer cell line SGC-7901.METHODS:Cell viability was analyzed by MTT assay. Cell cycle was detected by flow cytometry, and Annexin V-FITC/PI dual staining was used to detect cell apoptosis. Protein expression of p21, cyclin D1, caspase-3, caspase-8, caspase-9 and poly(ADP-ribose) polymerase (PARP) was determined by Western blotting. RESULTS:MTT assay and cell cycle analysis results indicated that PF-04691502 inhibited the viability of SGC-7901 cells in a dose-dependent manner, and arrested the cells in G1 phase. PF-04691502 down-regulated the expression of cyclin D1 and up-regulated the expression of p21. In addition, SGC-7901 cells treated with PF-04691502 showed typical characteristics of apoptosis, accompanied by activation of caspases and cleavage of PARP. CONCLUSION: The PI3K/mTOR dual inhibitor PF-04691502 induces the apoptosis and inhibited the growth of SGC-7901 cells, implicating its potential therapeutic value for the treatment of cancer.     

Effects of artesunate on proliferation,apoptosis and chemotherapeutic drug sensitivity of human hepatocellular carcinoma HepG2 cells

AIM: To investigate the effects of artesunate on proliferation and apoptosis in human hepatocelluar carcinoma cell line HepG2 and to study the sensitizing effect of artesunate on HepG2 cells to chemotherapeutic drugs. METHODS: The proliferation of HepG2 cells was determined by the assay of cell counting kit-8 (CCK-8) and the colony formation test. The morphology of HepG2 cells with Hoechst 33258 staining was observed under fluorescent microscope. Annexin V/propidium iodide (PI) was used to analyze the apoptosis and the cell cycle. The sensitizing effects of artesunate on HepG2 cells to chemotherapeutic drugs were determined by CCK-8 assay. RESULTS: When treated with artesunate for 48 h, the proliferation of HepG2 cells was significantly inhibited in a dose-dependent manner. The IC₅₀ was 19.2 μmol/L. Compared with the control cells, the colony formation of HepG2 cells treated with artesunate for 7 days was significantly inhibited. The nuclear fragmentation, karyopyknosis, chromosomal condensation, cell shrinkage, and attachment loss in HepG2 cells treated with artesunate were observed. The cells in G₂ phase increased obviously, and the percentages of hypodiploid cells and early apoptotic rates were significantly higher in artesunate treatment groups than those in control group. The IC₅₀ of 5-FU, carboplatin and epirubicin combined with artesunate was 3.33, 2.02 and 1.71 times sensitized as compared with control group, respectively. CONCLUSION: Artesunate effectively inhibits proliferation and induces apoptosis of HepG2 cells. Aresunate also sensitizes HepG2 cells to chemotherapeutic drugs.     

MicroRNA-146a promotes apoptosis of gastric cancer SGC-7901 cells by targeting TAK1

AIM: To explore the effect of microRNA-146a (miR-146a) on apoptosis of human gastric cancer SGC-7901 cells and the underluing mechanism. METHODS: miR-146a mimic (up-regulated miR-146a expression) and miR-146a inhibitor (down-regulated miR-146a expression) were transfected into the SGC-7901 cells by liposome method. At the same time, miRNA nonsense sequence transfection group as the negative control group (NC group) was set up. RT-qPCR was used to evaluate the levels of miR-146a in the SGC-7901 cells after transfection. The effects of miR-146a on the cell apoptosis and growth were assessed by flow cytometry analysis and CCK-8 assay, respectively. The effect of over-expression or knockdown of miR-146a on transforming growth factor-β-activated kinase 1 (TAK1)/nuclear factor-kappa B (NF-κB) signaling was evaluated by RT-qPCR and Western blot. RESULTS: miR-146a modulated apoptosis of SGC-7901 cells. Over-expression of miR-146a significantly increased apoptosis, whereas knockdown of miR-146a inhibited the apoptosis of SGC-7901 cells. The expression of TAK1 at mRNA and protein levels was significantly decreased when miR-146a mimic was transfected into the SGC-7901 cells (P<0.05). On the contrast, the expression of TAK1 at mRNA and protein were significantly higher in miR-146a inhibitor transfection group than that in NC group (P<0.05), suggesting that miR-146a negatively regulated TAK1 expression. Moreover, knockdown of TAK1 enhanced the apoptosis of SGC-7901 cells (P<0.01), while over-expression of TAK1 inhibited the apoptosis of SGC-7901 cells(P<0.01). Additionally, both over-expression of miR-146a and knockdown of TAK1 led to a prominent increase in the expression of NF-κB inhibitor protein alpha (IκBα) and a significat decrease in B cell lymphoma-2 (Bcl-2) level in the SGC-7901 cells. CONCLUSION: miR-146a significantly promotes apoptosis of SGC-7901 cells by inhibition of NF-κB pathway via targeting TAK1.     

Emodin inhibits proliferation and blocks cell cycle of human breast cancer MCF-7 cells

AIM：To investigate the effects of emodin on the proliferation of human breast cancer MCF-7 cells and its mechanisms. METHODS：MTT assay was used to observe the viability of MCF-7 cells. The cell cycle distribution and apoptosis of MCF-7 cells was analyzed by flow cytometry. The membrane surface morphology and three-dimensional ultrastructure of MCF-7 cells were observed under atomic force microscope (AFM). RESULTS：MTT assay showed that emodin could inhibit MCF-7 cell proliferation in a dose-dependent manner. Flow cytometric analysis demonstrated that emodin induced cell cycle arrest at G0/G1 phase. Annexin V/PI double staining confirmed that emodin had no effect on cell apoptosis. AFM images revealed that the cell nuclear area was full and the surface of cell membrane was flat and smooth in control group. Compared with control group, the cell nuclear area collapsed and shrank in emodin group at 48 h. The cell membrane ultrastructure showed that the particles in emo-din group had an intensive distribution. The height of cell nuclear area was decreased, and the surface average roughness (Ra) and root mean square roughness (Rq) were elevated in emo-din group compared with control group. CONCLUSION: Emodin has cytotoxicity on MCF-7 cells via cell cycle arrest at G0/G1 phase and ultrastructural changes.     

Effects of GOLPH3 gene silencing mediated by lentivirus on proliferation,invasion and metastasis of human gastric cancer cell line SGC-7901

AIM：To investigate the effect of Golgi phosphoprotein 3 (GOLPH3) gene silencing on the proliferation, invasion and metastasis of human gastric cancer SGC-7901 cell in vitro. METHODS：SGC-7901 cells were transfected with lentiviral vector carrying GOLPH3 shRNA to construct a stable GOLPH3-silencing cell line LV-GOLPH3-RNAi. The expression of GOLPH3 at mRNA and protein levelss were detected by real-time PCR and Western blotting, respectively. The cell proliferation was analyzed by MTT assay. Transwell migration and invasion experiments were performed to measure the migration and invasion abilities, respectively. RESULTS：The stable GOLPH3-silencing cell line was successfully established. The expression of GOLPH3 at mRNA and protein levels was reduced significantly (P<0.05), leading to the inhibition of cell proliferation in LV-GOLPH3-RNAi group compared with scrambled group and blank control group, as well as the capacities of migration (56.7±1.5 vs 186.0±3.4 and 183.3±4.2, P<0.05) and invasion (33.5±3.0 vs 85.0±3.9 and 83.1±4.4, P<0.05). CONCLUSION：GOLPH3 silencing suppresses the capacities of proliferation, migration and invasion of human gastric cancer SGC-7901 cells, suggesting that GOLPH3 may be a potential tumor marker and independent prognostic factor.     

Effect of over-expression of transcription factor CDX2 on proliferation and cell cycle of human gastric cancer cell line SGC-7901

AIM: To study the effect and the molecular mechanism of CDX2 over-expression on the proliferation, growth and cell cycle of human gastric cancer cell line SGC-7901. METHODS: The SGC-7901 cells in LV-CDX2-GFP group were transfected with the recombinant lentivirus vector LV-CDX2-GFP, the cells in LV-GFP group were transfected with the negative control lentiviral vector for the negative control, and the cells in blank control group were without any treatment. The cell proliferation was detected by CCK-8 assay. The cell cycle distribution was analyzed by flow cytometry. The expression of CDX2, Bax, Bcl-2, cyclin D1 and survivin was determined by semi-quantitative RT-PCR and Wes-tern blotting. RESULTS: Compared with LV-GFP group and blank control group, the proliferation activity of the SGC-7901 cells was significantly lower (P<0.05), the G0/G1 phase proportion increased (P<0.05), the mRNA and protein levels of Bcl-2, cyclin D1 and survivin were reduced (P<0.05), and the mRNA and protein levels of Bax were up-regulated (P<0.05) in LV-CDX2-GFP group. No statistically significant difference of the above indexes was observed (P>0.05) between LV-GFP group and blank control group. CONCLUSION: Over-expression of CDX2 mediated by lentivirus inhibits the proliferation and growth of human gastric cancer SGC-7901 cells and arrestes the cell cycle at G0/G1 phase, which may be related to down-regulation of Bcl-2, cyclin D1 and survivin and up-regulation of Bax.     

Effect of cardiopulmonary bypass for 30 min on structure and mechanical properties of erythrocyte membrane surface

AIM: To observe and analyze the effect of cardiopulmonary bypass(CPB) for 30 min on surface ultra-structure and mechanical properties of the erythrocyte membrane by atomic force microscopy(AFM).METHODS: Ten cases of elective patients in cardiac surgery were selected in the study and divided into control(CON) group and CPB group. The central venous blood(2 mL) before surgery and 30 min after CPB was collected with heparin anticoagulation. The non-circular red blood cells were counted under a stand fluorescence microscope. AFM was used to examine the ultrastructure of the membrane surface and measure the force curve of the erythrocytes.RESULTS: The percentage of non-circular red blood cells in CPB group showed no statistically significant differences as compared with CON group. AFM images showed that the significant differences of membrane surface concave and convex, evenness, particle distribution, the surface average roughness(Ra), the surface root mean square roughness(Rq) and cell membrane adhesion between CPB group and CON group were observed. However, the membrane deformation resilience and curve slope had no significant difference between the 2 groups.CONCLUSION: Cardiopulmonary bypass for 30 min changes the morphology and ultrastructure of the erythrocyte membrane surface, and increases the adhesion between cells.     

Effects of diterpenoid C from ether extract of Radix Curcumae on nuclear factor-κB activity in LPS-induced human gastric adenocarcinoma SGC7901 cells

AIM: To observe the effects of diterpenoid C from ether extract of Radix Curcumae (RC) on the activity of nuclear factor-κB in human gastric adenocarcinoma SGC7901 cells stimulated with lipopolysaccharide (LPS). METHODS: SGC7901 cells were normally cultured, induced by LPS, or treated with LPS plus RC. The protein expression of IKKα, IKKβ, p65, phosphorylated p65 and phosphorylated IκBα was assayed by Western blotting. NF-κB DNA binding activity was determined by electrophoretic mobility shift assay. RESULTS: RC reduced the protein expression of IKKα, IKKβ, p65, phosphorylated p65 and phosphorylated IκBα induced by LPS. NF-κB DNA binding activity increased much greatly by LPS stimulation, while RC resisted the action of LPS. CONCLUSION: RC may attenuate the secretion of inflammatory cytokines by inhibiting the activation of NF-κB signaling pathway.     

Effects of RARG on viability and migration ability of gastric cancer cells

AIM:To investigate the effect of retinoic acid receptor gamma (RARG) on the viability and migration ability of gastric cancer cells. METHODS:The expression of RARG in gastric cancer and normal gastric tissues and its correlation with the overall survival rate of gastric cancer patients were analyzed by bioinformatics. The expression of RARG was promoted and inhibited by over-expression plasmid transfection and RNA interference technique in gastric can-cer cells in vitro, respectively. MTT and Transwell assays were used to detect the effect of RARG on the viability and migration ability of gastric cancer cells. The effect of RARG on regulating the Wnt/β-catenin signaling pathway was evaluated by Western blot and TOP/FOP dual-luciferase reporter assay. The protein interaction of RARG and β-catenin was determined by co-immunoprecipitation and immunofluorescence co-localization assay. RESULTS:Over-expression of RARG enhanced the viability and migration ability of gastric cancer SGC7901 cells (P<0.05). Knockdown of RARG attenuated the viability and migration ability of gastric cancer MGC-803 cells (P<0.05). At the same time, RARG over-expression increased the protein expression levels of β-catenin, c-Myc, cyclin D1, Twist and Snail (P<0.05), and the activity of TOP/FOP dual-luciferase reporter gene (P<0.05). In addition, RARG interacted with β-catenin protein in the gastric cancer cells. CONCLUSION:RARG promotes the viability and migration ability of gastric cancer cells via activating the Wnt/β-catenin signaling pathway, thus playing an important role in the development of gastric cancer.     

Effects of all-trans retinoic acid on sensitivity of gastric cancer cells to radiotherapy

AIM: To investigate the effect of all-trans retinoic acid (ATRA) on the viability of gastric cancer cell SGC-7901 and the sensitivity to radiotherapy. METHODS: MTT assay was used to examine the cell viability. Radio-sensitivity and cell cycle were determined by colony formation assay and flow cytometry, respectively. The mRNA levels of Bax, Bcl-2, survivin and NF-κB in the cells were measured by RT-qPCR. RESULTS: ATRA inhibited the viability of SGC-7901 cells in a concentration-dependent manner. The maximal inhibition was at concentration of 8 μmol/L. Colony formation assay revealed that the combination of ATRA with X-ray treatment significantly reduced the values of D0 and Dq, and shifted down the fitting survival curve, as compared with radiotherapy alone. Moreover, ATAR markedly decreased the percentage of G₂/M phase in the SGC-7901 cells (P<0.05). In addition, following ATRA treatment, the mRNA levels of Bcl-2 and survivin were decreased (P<0.05), whereas the mRNA levels of Bax and NF-κB were increased (P<0.05). CONCLUSION: ATRA enhances the sensitivity of SGC-7901 cells to radiotherapy, inhibits G₂/M arrest and regulates the mRNA expression of Bax, Bcl-2, survivin and NF-κB.