Effects of Centella asiatica extracts on apoptosis of mouse spleen lymphocytes

AIM：To isolate the active compounds of Centella asiatica and to investigate their effects on the apoptosis of mouse spleen lymphocytes. METHODS：Cold soak, polar extraction, silica gel column chromatography and Sephadex LH-20 column chromatography were performed to isolate the active compounds from Centella asiatica, which were identified by the assays of scavenging activity on 1,1-diphenyl-2-picrylhydrayl radical (DPPH·) and hydroxyl radical (OH·). Flow cytometry was performed to observe the effects of Centella asiatica extracts on the apoptosis of spleen lymphocytes in mice. RESULTS：Four extracts (B1, B2, B3 and B4) were obtained by the separating procedure. Among them, the extract B4 exerted a potent scavenging effect on both DPPH· and OH·. Quercetin was identified from the extract B4 by HPLC analysis. The mouse spleen lymphocytes with extract B4 treatment showed a significant rise in the level of apoptosis compared with control group. CONCLUSION：Centella asiatica extract B4 induces apoptosis of spleen lymphocytes, and quercetin is the major substance of extract B4.     

Determination of T cell cycle and the expression of bcl- 2 in asthmatic mice and its significance

AIM: To investigate the changes of T cell cycle, the expression of bcl- 2 in allergic asthmatic mice and the effects of dexamethasone on them. METHODS: An animal model with asthma was established by means of ovalbumin sensitizing-challenging. CD3 expression in spleen and lymphocytes in bronchoalveolar lavage fluid (BALF), T cell cycle and Bcl-2 expression in spleen were detected by flow cytometry. RESULTS: In BALF lymphocytes and spleen lymphocytes, CD3 expression rate in the asthmatic group was significantly higher than that of control group. In BALF lymphocytes, CD3 expression rate in the asthma plus dexamethasone group was significantly lower than that of the asthmatic group. However, in spleen lymphocytes, CD3 expression rate in the asthma plus dexamethasone group was significantly higher than that of the asthmatic group. In spleen lymphocytes, the cell count in S phase, G₂+M phase and apoptosis rate of T cell from the asthmatic group were significantly higher than that from the control group. Cell count in S phase, G₂+M phase and apoptosis rate of T cell from the asthmaplus dexamethasone group was significantly lower than that from the asthmatic group. The Bcl-2 expression rate of T cell from the asthmatic group was significantly higher than that from the control group. CONCLUSIONS: In the allergic asthmatic mice model, T cell count, proliferation and activation of T cells, apoptosis rate of T cells in spleen lymphocytes increase, meanwhile bcl- 2 expression also increases significantly. There was no significant effect of dexamethasone on the bcl- 2 expression. The therapeutic effects of dexamethasone on asthma may be not due to the inhibition of the bcl- 2 expression in T cells.     

Isolation and purification of active components from Centella asiatica and observation of their immunosuppressive effect

AIM：To isolate and purify the active components from Centella asiatica, and to observe their effect on the proliferation and apoptosis of mouse spleen lymphocytes. METHODS：Semi-preparative high-performance liquid chromatography was performed to further isolate and purify the extracts from Centella asiatica. The effects of the active components on apoptosis and mitochondrial membrane potential of the spleen lymphocytes were assessed by flow cytometry. The structures of the active components were identified by ultraviolet spectrometry, electrospray ionization negative-ion mass spectrometry, ［1H］ nuclear magnetic resonance (NMR) and ［13C］ NMR. RESULTS：The molecular weights of the active components from Centella asiatica, named compound I and compound II, were 302 and 286, respectively. The compound I and compound II from Centella asiatica significantly inhibited the proliferation, promoted the apoptosis and reduced the mitochondrial membrane potential of mouse spleen lymphocytes. Compound I and compound II were identified as quercetin and kaempferol. CONCLUSION：The compound I and compound II from Centella asiatica show antiproliferative and immunosuppressive effects on mouse spleen lymphocytes by promoting apoptosis and reducing mitochondrial membrane potential.     

mTOR kinase inhibitor CC-223 suppresses human breast cancer cell viability

AIM: To investigate the inhibitory effect of CC-223, an inhibitor of mammalian target of rapamycin (mTOR) kinase, on the viability of human breast cancer cells and its mechanism. METHODS: The inhibitory effect of CC-223 on the viability of MCF-7 cells and MDA-MB-231 cells was measured by CCK-8 assay. The cell cycle distribution of breast cancer cells was examined by flow cytometry. The expression of cell cycle-related proteins and oncoproteins c-Myc and survivin was analyzed by Western blot. RESULTS: CC-223 significantly inhibited the viability of both MCF-7 and MDA-MB-231 cells (P<0.05). CC-223 induced cell cycle arrest in both G₁ phase and G₂/M phase in the MCF-7 cells (P<0.05). However, low concentration of CC-223 treatment resulted in the accumulation of MDA-MB-231 cell cycle in the G₂/M phase, and the cell number in G₁ phase was unaffected. Treatment with CC-223 for 24 h clearly inhibited the protein levels of cyclin B1, cyclin D1 and phosphorylated cell division cycle protein 2 in the breast cancer cells (P<0.05). CC-223 suppressed the expression of c-Myc and survivin in both MCF-7 cells and MDA-MB-231 cells (P<0.05). CONCLUSION: CC-223 inhibits cell viability by blocking cell cycle progression and down-regulating expression of c-Myc and survivin in both MCF-7 and MDA-MB-231 cells.     

Effect of ginsenoside Rh2 on cultured PC-3M cells in vitro

AIM:To explore the influence of ginsenoside Rh₂ on cultured PC-3M cell cycle in vitro. METHODS:DNA content was measured using [³H]-TdR incorporation assay. To analysis the cycle changes of PC-3M cells, flow cytometry was used in the experiment.RESULTS:The results indicated that the rate of [³H]-TdR incorporation was lower in Rh₂-treated cells than the control in a dose-dependent manner. Flow cytometry demonstrated that the pecent of G₁ phase treated with Rh₂ was higher than that of control. CONCLUSION:These results suggested that PC-3M cells cultured with Rh₂ for 24 h were blocked at G₁ phase, and Rh₂ inhibited the growth of PC-3M cells in vitro.     

Effects of edible-medicinal fungus crude extracts on vascular endothelial cells with high glucose-induced injury

AIM: To investigate the effects of crude extracts of Cordyceps gunnii (CGE), Lepista lentinus (LLE), Cordyceps sinensis (CSE) and Lentinus striguellus (LSE) on the proliferation of high glucose-treated human umbilical vein endothelial cells (HUVECs). METHODS: The cultured HUVECs were divided into normal control group (treated with M199 culture medium alone), high glucose group (treated with M199 culture medium containing 33 mmol/L glucose) and 4 crude extracts of edible-medicinal fungi (CGE, LLE, CSE and LSE) intervention groups (treated with the crude extract of edible-medicinal fungus at concentrations of 12.5, 25, 50, 100 mg/L in high glucose M199 culture medium). The cell proliferation was evaluated by MTT assay. The cell cycle and ROS level were measured by flow cytometry. RESULTS: Compared with normal control group, the MTT absorbance value and the percentage of G₀/G₁ stage of the HUVECs in high glucose group were significantly decreased (P<0.05), while the percentage of S+G₂/M and ROS level were significantly increased (P<0.05). Compared with high glucose group, treatment with the crude extracts of Lepista lentinus and Lentinus striguellus decreased the cell absorbance value (P<0.05), and the inhibitory effect was enhanced in a dose-dependent manner. However, Cordyceps gunnii had no effect (P>0.05). The crude extracts of Cordyceps sinensis (12.5~50 mg/L) significantly enhanced the proliferative activity of HUVECs, decreased the percentage of G₀/G₁ stage of HUVECs, increased the percentage of S+G₂/M of HUVECs, and reduced the intercellular ROS level (P<0.05). CONCLUSION: Only Cordyceps sinensis crude extract effectively protects the HUVECs in high glucose-induced injury, which might be due to promoting more cells to enter to the cell cycle and down-regulating oxidative stress.     

Effects of zinc on biological behavior of hepatocellular carcinoma cell line BEL-7404

AIM: To observe the effects of exogenous zinc on the biological behavior of hepatocellular carcinoma (HCC) cell line BEL-7404. METHODS: BEL-7404 cells were cultured with zinc sulfate at various concentrations. The intracellular concentration of zinc, cell viability, cell cycle, cell apoptosis and migration and invasion abilities were measured by TSQ fluorescent probe, MTT assay, DNA ploid analysis, acridine orange/ethidium bromide fluorescence staining and Transwell assay, respectively. The mRNA and protein expression levels of albumin in the BEL-7404 cells were determined by real-time PCR and Western blot, respectively. RESULTS: With the elevated concentration of zinc in culture condition, the concentration of zinc in the BEL-7404 cells was increased (P<0.05). The cell viability and migration and invasion abilities were decreased, while the apoptotic rate was increased (P<0.05). The cells in G₀/G₁ phase were decreased, while the cells in G₂/M phase were increased. Additionally, the mRNA and protein expression of albumin also increased (P<0.05). CONCLUSION: The zinc ion inhibits the cell viability as well as migration and invasion abilities, blocks the cells in G₂/M phase, and may reduce cell malignant phenotype.     

Effect of sodium selenite on proliferation of endometrial cancer cells

AIM: To investigate the effect and mechanism of sodium selenite (Na₂SeO₃) on the proliferation of endometrial cancer cells. METHODS: Endometrial cancer Ishikawa cells and HEC-1A cells were treated with Na₂SeO₃. The effect of Na₂SeO₃ on cell proliferation was determined by MTT assay. The effects of Na₂SeO₃ on cell cycle distribution and apoptosis were tested by flow cytometric analysis. The expression of cyclin A was detected by Western blotting. RESULTS: Na₂SeO₃ inhibited the proliferation of Ishikawa cells and HEC-1A cells. For Ishikawa cells, IC₅₀ was 3.26 μmol/L, and for HEC-1A cells, IC₅₀ was 4.77 μmol/L. After treated with Na₂SeO₃, the cells in G₀/G₁ phase were reduced and the cells in S phase and G₂/M phase were increased. Na₂SeO₃ also increased the percentage of apoptosis cells. The result of Western blotting showed that the expression of cyclin A was increased. CONCLUSION: Na₂SeO₃ inhibits the proliferation of endometrial cancer Ishikawa cells and HEC-1A cells via up-regulating the expression of cyclin A, arresting cell cycle and inducing apoptosis.     

Lovastatin-induced G1 phase synchronization in human endometrial cancer JEC cells

AIM: To investigate the method of inducing G₁ phase synchronization in human endometrial cancer JEC Cells by lovastatin and the cell cycle progress of JEC cells after desynchronization. METHODS: The doubling time of JEC cells was detected by Cell Counting Kit-8 (CCK-8) assay. To determine the best lovastatin concentrations for G₁ synchronization, JEC cells were treated with lovastatin at concentrations of 10, 20, 30 and 40 μmol/L for 1× doubling time, and the cell cycle was detected using flow cytometry (FCM). To determine the best period of lovastatin treatment to achieve G₁ synchronization, JEC cells were treated with lovastatin at the best concentration for 0.5× to 2× doubling time, and the cell cycle was detected every 4 h using FCM. Furthermore, the cell cycle progress of JEC cells after desynchronization was also observed. RESULTS: The doubling time of JEC cells was almost 24 h. Treatment with lovastatin at the concentration of 20 μmol/L for 24 h achieved maximum G₁ arrest in JEC cells. Minimum G₁ phase and maximum S phase were observed after desynchronization for 16 h. CONCLUSION: Maximum G₁ synchronization of JEC cells is induced by lovastatin at the concentration of 20 μmol/L for 24 h. The JEC cells show minimum G₁ phase and maximum S phase after desynchronization for 16 h.     

P53 overexpression in different subcellular location in non small cell lung cancer

AIM: Nuclear P53 localization was considered to be proof of mutation, cytoplasmic staining has also been signalled. In this study, special attention has paid to protein subcelluler localization. A different functional meaning may attributed to tumor biological characteristic and evolution. METHODS: Immunohistochemical approach and flow cytometry were used to explored the relationship between P53 overexpression pattern (nuclear and cytoplas- mic) and G₁/S checkpoint function of P53 protein in cell cycle. RESULTS: Two patterns of P53 overexpression are related to disease stage significantly. S - phase fraction (SPF) was higher and G₀-G₁ phase fraction was lower in P53 nuclear pattern than cytoplasmic (SPF, 42.42± 5.45/14. 12± 442, G₀-G₁: 53.04 ± 6.14／75.56 ± 4.46, respectively P < 0.05). No difference was found in G₂ - M phase fraction and DNA index between two patterns. CONCLUSION: Most of the cells showing cytoplasmic P53 overexpression pattern are properly arrested in G/S checking point, which may represent an early tumor cell population with low grade of neoplastic development. In contrast, inactivated product detectable at nuclear level possible carry a mutated P53 associated with tumor progression. The mechanism of P53 cytoplasmic location is not clear.     

Inhibitory effect of berberine on the activation and proliferation of T lymphocytes

AIM: To investigate the effect of berberine (Ber) on the activation and proliferation of T lymphocytes and its mechanism of action. METHODS: Whole peripheral blood from normal subjects was stimulated with phytohemagglutinin (PHA) or phorbol ester (PDB) plus ionomycin (Ion) and the expression levels of CD69 and CD25 were evaluated with flow cytometry after the staining with appropriate fluorescent monoclonal antibody. The distribution of cell cycles was analyzed by propidium iodide staining and dead cells by 7-aminoactinomycin live staining. RESULTS: 100 μmol/L and 50 μmol/L of Ber had significant inhibition of the expression of CD69 on T cells stimulated with PDB plus Ion or PHA, while effect of 25 μmol/L Ber was not significant. And as time of action extended, the extent of inhibition decreased. For the expression of CD25, Ber at the concentrations as above all exerted significant inhibitory effect in a dose-dependent manner. Moreover, Ber could block lymphocytes cell cycle progression from G₀/G₁ phase to S and G₂/M phase without phase specificity. Besides, live staining analysis revealed that Ber did not have significant cytotoxicity on lymphocytes. CONCLUSIONS: Ber significantly inhibits the expression of early and mid activation antigens of T cells and also blocks the progression of lymphocytes cell cycles. These results suggest that Ber exerts immunosuppression effect through inhibiting the activation and proliferation of T cells.     

Effect of 7-hydroxyisoflavone on HCT116 cells proliferation by Id1

AIM:To investigated the effect of 7-hydroxyisoflavone (7-HIF) on the proliferation, apoptosis and stem-like cell feature of colorectal cancer cells. METHODS:The effect of 7-HIF on the proliferation of HCT116 cells was detected by WST-1 assay and colony formation assay. The effects of 7-HIF on the cell cycle distribution and apoptosis in the HCT116 cells were analyzed by flow cytometry. The expression of cell-cycle related proteins and the stemness related proteins was determined by Western blot. RESULTS:After treated with 7-HIF (200 μmol/L), the viability of HCT116 cells was inhibited, and the size and number of the colony were decreased as compared with control group (P<0.05). The G₀/G₁ phase of the cell cycle was increased. The proportion of S phase was decreased and the cells were mainly arrested in G₀/G₁ phase. The apoptotic rate of HCT116 cells was 21.4%, which was significantly higher than that in the control group (1.1%). The results of Western blot revealed that the expression of inhibitor of differentiation 1(Id1) was significantly decreased (P<0.05). The expression of cell cycle markers cyclin D1 and cyclin E, the proliferative markers survivin and PCNA, and stem cell markers CD133, ALCAM and EpCAM were all down-regulated by 7-HIF treatment (P<0.05). CONCLUSION:7-HIF inhibits the proliferation and induces the apoptosis of colorectal cancer cells, and inhibits the stem-like cell feature, which may be related to Id1 inhibition.     

Effects of simvastatin on PDGF-BB and serum-induced proliferation of vascular smooth muscle cells and on the expression of tumor suppressor gene PTEN

AIM:To observe the effect of simvastatin on the proliferation of vascular smooth muscle cells(VSMCs) induced by serum and growth factor PDGF-BB and the effect of simvastatin on the expression of PTEN,a important regulator of G₁/S cell cycle transition. METHODS:The DNA synthesis was determined by [³H]-TdR incorporation, cell cycle was examined with flow cytometry, the protein level of PTEN was measured by Western blot method. RESULTS: (1)Simvastatin inhibited [³H]-TdR incorporation in a dose dependent manner. (2) Flow cytometric DNA analysis revealed that simvastatin induced significantly enhancement of G₀/G₁ phase and decrease in S phase VSMCs.(3)Simvastatin increased protein level of PTEN and mevalonate, a metabolite of HMG-COA, reversed the effect of simvastatin on PTEN protein expression. CONCLUSION:Simvastatin may inhibit proliferation of VSMCs and retarded cell cycle in G₀/G₁ phase by increasing PTEN expression through inhibiting synthesis of mevalonate.     

Effects of human growth arrest-specific homeobox gene delivery on proliferation,migration and cell cycle distribution of vascular smooth muscle cells

AIM: To explore a new gene therapeutic strategy for vein graft restenosis by investigating the effects of adenovirus-mediated human growth arrest-specific homeobox (Ad5-hGax) gene delivery on the proliferation, migration and cell cycle distribution of serum-induced rabbit vascular smooth muscle cells (VSMCs). METHODS: The recombinant adenovirus vector containing hGax gene was constructed and transfected into rabbit VSMCs. The expression of hGax in VSMCs was detected by RT-PCR and immunofluorescent staining. Methyl thiazolyl tetrazolium (MTT) assay was used to assess the effect of hGax over-expression on serum-induced proliferation of VSMCs. Wound healing method was applied to examine the distance of serum-induce VSMCs migration. Flow cytometry was employed to analyze the cell cycle distribution. RESULTS: The recombinant adenovirus vector Ad5-hGax was successfully constructed. The results of RT-PCR and immunofluorescent staining revealed that the hGax -transfected cells contained a 174 bp specific fragment of hGax gene and target protein 48 h after transfection. The proliferation of serum-induced VSMCs was significantly inhibited by overexpression of hGax gene as compared with control group. The migration of serum-induced VSMCs was inhibited after hGax gene delivery. Flow cytometry showed that 72 h after serum induction, the cells in G₀/G₁ phase in Ad5-hGax group were significantly increased, whereas the cells in G₂/M+S phase were significantly decreased. CONCLUSION: Overexpression of hGax gene inhibits the proliferation and migration of serum-induced rabbit VSMCs, and arrests the cells in G₀/G₁ phase. It is likely that hGax gene is a potential target for the gene therapy of vein graft restenosis.     

Effect of calcitonin gene-related peptide on proliferation of vascular smooth muscle cells

AIM: To elucidate the effect of calcitonin gene-related peptide (CCRP) in the therapy of atherosclerosis.METHODS:Effect of CGRP on cell cycle kinetics of cultured vascular smooth muscle cells(HA-VSMC) was investigated by flow cytometry. The expression of cyclins D₁ and E required for initiation of S phase were also studied by immunochemistry method. RESULT: CGRP was shown to arrest VSMC in the G₀/G₁ phase of cell cycle and reduced expression of cyclins D₁ and E. CONCLUSION:CGRP inhibits proliferation of HA-VSMC by arresting cells in G₁ phase via limiting accumulation of cyclin D₁ and E. It might play a role in the therapy of atherosclerosis.     

Effect of HMBA on proliferation and expression of KLF6 and related proteins in human tongue carcinoma Tca8113 cells

AIM: To study the effect of hexamethylene bisacetamide(HMBA) on the proliferation and expression of KLF6 and related proteins in human tongue carcinoma Tca8113 cells. METHODS: After cultured with HMBA, the growth of the Tca8113 cells was assayed by MTT method, and the morphology of the cells was observed under microscope. The cell cycle was determined by flow cytometry. The mRNA expression of KLF6 was detected by RT-PCR. The protein levels of KLF6, p53, cyclin D1 and c-Jun were measured by the method of immunohistochemistry. RESULTS: The number of adherent cells obviously decreased along with the concentration of HMBA, and the growth inhibition of Tca8113 cells was in a concentration/time-effect relationship after treated with HMBA. Some reversal features of the Tca8113 cells developed to normal cells in morphology after induced by HMBA. The proportion of the cells in G₁ phase was (52.00?0.02)% before treating with HMBA. The proportion of the cells in S phase was (34.00?0.08)%, and (14.00?0.10)% of G₂ phase cells. After treated with HMBA, the cell number in G₁ phase significantly increased with the exposure time going on, while the cell number in S phase significantly reduced, so did the cell number in G₂ phase. The cell cycle was significantly arrested in G₁ phase (P<0.05). The apoptosis peak also appeared. The mRNA expression of KLF6 significantly increased after induced by HMBA (P<0.05), so did the protein levels of KLF6 and p53 (P<0.05), while the expression of cyclin D1 and c-Jun was significantly decreased (P<0.05). CONCLUSION: HMBA inhibits the proliferation of Tca8113 cells by arresting the cell cycle in G₀/G₁ phase and resuming Tca8113 cells to normal and apoptosis at last.     

Effect of ClC-3 siRNA on cell cycle of HeLa cells

AIM: To investigate the roles of ClC-3 chloride channels in the regulation of cell cycle and the relationship between ClC-3 chloride channels and the cell cycle regulators, such as cyclin D1, cyclin-dependent kinase (CDK)4, CDK6, P21 and P27 in the HeLa cells.METHODS: ClC-3 genes were silenced by the siRNA technique in the HeLa cells. The transfection efficiency of ClC-3 siRNA was detected by real-time PCR. The cell cycle distribution was analyzed by the flow cytometry. The protein expression of ClC-3, P21, P27, CDK4, CDK6 and cyclin D1 was determined by Western blot.RESULTS: ClC-3 was knocked down by ClC-3 siRNA in the HeLa cells. Transfection of the cells with ClC-3 siRNA arrested the cells at G₀/G₁ phases, decreased the expression of cyclin D1, CDK4 and CDK6, and increased the expression of P21 and P27.CONCLUSION: ClC-3 plays an important role in the cell cycle of HeLa cells through the G₁-S transition point. ClC-3 may regulate the cell cycle progression by up-regulation of cyclin D1, CDK4 and CDK6 expression and/or by down-regulation of P21 and P27 expression.     

Berberine enhances mitomycin C-induced cell cycle arrest and apoptosis of T24 bladder cancer cells

AIM: To observe the effects of the combination of berberin (Ber) and mitomycin C (MMC) on the cell cycle arrest and apoptosis of T24 bladder cancer cells and the underlying mechanisms. METHODS: The T24 cells were exposed to MMC in the presence or absence of difference concentrations of Ber. The viability of the T24 cells was determined by CCK-8 assay. The cell cycle distribution was detected by flow cytometry. The apoptosis was analyzed by flow cytometry with Annexin V-FITC/PI staining, and the protein expression levels of cyclin D1, survivin, CDK2, CDK4, p21 and p27 were determined by Western blot. RESULTS: CCK-8 experiments showed that Ber enhanced the inhibitory effect of MMC on the viability of T24 cells. The results of flow cytometry showed that Ber also enhanced the blockade effect of MMC on T24 cells in G₀/G₁ phase (P<0.05). Compared with the MMC group, Ber increased the expression of p21 and p27 up-regulated by MMC, and decreased the expression of cynlin D1, CDK2 and CDK4 (P<0.05). Meanwhile, Ber promoted MMC to inhibit the expression of survivin (P<0.05). Ber increased the apoptosis of T24 cells induced by MMC (P<0.05). CONCLUSION: Ber significantly enhances the inhibitory effect of MMC on the viability of T24 cells. The mechanism may be related to up-regulation of p21 and p27, thereby inhibiting the expression of cyclin D1, CDK-2 and CDK-4. At the same time, Ber inhibits the protein expression of survivin, which eventually leads to cell arrest in G₀/G₁ phase and promotes apoptosis.     

Effect of oncogenic microRNA-106a on growth of normal gastric mucous epithelial cells and gastric cancer cells

AIM: To investigate the oncogenic effect of microRNA-106a (miR-106a) on normal gastric mucous epithelial cells and gastric cancer cells.METHODS: The miR-106a mimic was transfected into normal gastric mucous epithelial cell line GES-1 using liposome. The change of cell growth was measured by MTT assay. The miR-106a inhibitor was transfected into gastric cancer cell lines MGC-803 and SGC-7901 using liposome, and the changes of cell cycle distribution and cell cycle-related protein expression were measured by flow cytometry and Western blotting,respectively. The growth of gastric cancer was also observed using nude mouse xenograft model. RESULTS: The miR-106a mimic increased the growth of GES-1 cells in a dose-dependent manner. By decreasing the expression of cyclin-dependent kinase (CDK) 1 and CDK2, the miR-106a inhibitor arrested MGC-803 cells at G₀/G₁ and G₂/M phases. The miR-106a inhibitor also arrested SGC-7901 cells at G₂/M phase by decreasing the expression of CDK1. The results of animal experiments showed that the miR-106a inhibitor significantly suppressed the tumor growth in a dose-dependent manner.CONCLUSION: miR-106a may play an important role in the development of gastric cancer.