Metastasis-associated in coIon cancer 1(MACC1)is a recentIy discovered gene which is cIoseIy associated with coIorectaI cancer metastasis,and aIso pIay an important roIe in metastasis of other tumors. Some ceII signaIing pathways or bioIogicaI moIecuIes may be invoIved in the reguIation of MACC1 expression and reIevant mechanism of MACC1 promoting tumor invasion and metastasis. However,the reguIation mechanism and pathways of MACC1 expression are currentIy not compIeteIy known. This articIe reviewed the roIe and mechanism of reguIation of MACC1 expression in the deveIopment and progression of tumor.

AIM To investigate the effect of aspirin on the proliferation and NOS expression in astrocytoma cell line, and probe into its mechanism. METHOD The effect of aspirin on the growth of astrocytoma cells was evaluated by MTT assay; NOS protein levels were determined by immunocytochemistry, NO and CEA concentration in the medium were determined by Griess assay and lepton catch immunising method respectively. RESULTS Aspirin inhibited the growth of astrocytoma cells, induced the expression of iNOS, increased the concentration of NO in the medium. The effects of these were centratoin dependent. Moreover, aspirin reduced the concentration of CEA in the medium. CONCLUSION Aspirin inhibits the growth of astrocytoma cell line. Up regulated iNOS expression resulting a increase of NO concentration are ascribed to mechanism of antiproliferation activity of aspirin. CEA is a good indicator in monitoring curative effect of astrocytoma.

Objective To investigate the expression of sphingosine kinase 1(SphK1)and NF-κB in colon carcinoma tissues and their correlation with clinicopathologic features.Methods Sixty-six paraffinembedded colon carcinoma samples and 66 fresh colon carcinoma samples were tested using immunohistochemistry,RT-PCR and Western blot,respectively.Results In 66 fresh colon carcinoma samples,the positive rate of SphK1 and NF-κB mRNA expression were 84.85％(56/66)and 74.24％(49/66),while the positive rate of SphK1 and NF-κB protein detected by Western blot were 78.79％(52/66)and 69.70％(46/66).The positive rates were higher than those in the adjacent tissues[mRNA:63.64％(42/66),48.49％(32/66);protein:57.58％(38/66),45.45％(30/66)]and the normal mucosa [mRNA:42.42％(28/66),25.76％(17/66); protein:36.36％(24/66),24.24％(16/66)],with statistical significances(all P values ＜ 0.05).The mean expressive levels of SphK1 and NF-kB mRNA and protein in colon carcinoma were both significantly higher than those in the adjacent tissues and the normal mucosa(mRNA:0.55±0.06 vs0.35 ±0.05 vs0.25±0.05,0.75 ±0.06 vs0.43±0.05 vs0.30±0.04 ; protein:0.77 ± 0.05 vs 0.38 ± 0.06 vs 0.12 ± 0.03,0.45 ± 0.08 vs 0.23 ± 0.05 vs 0.13 ± 0.03 ;all P values ＜ 0.05).There was a close correlation between SphK1 and NF-kB expression levels (r =0.459,P =0.036).The results of immunohistochemistry were similar to those of RT-PCR and Western blot.Overexpression of SphK1 and NF-κB in colon carcinoma was related with depth of invasion,distant and lymph node metastasis and Dukes'stages(all P values ＜0.05).The expression of SphK1 was also related with differentiation(P ＜ 0.05).Conclusions Overexpression of SphK1 and NF-κB may be involved in the pathogenesis and progression of colon carcinoma.Moreover,SphK1 and NF-κB may be correlated with the invasion and metastasis of colon carcinoma.

Objective To evaluate the therapeutic effect of endoscopic management of plastic stents of post-liver transplantation anastomotic biliary stricture. Methods From January 2010 to October 2015, clinical data of patients with post-liver transplantation anastomotic biliary stricture and received endoscopic retrograde cholangiopancreatog﹣raphy and plastic stents management was collected. The technical success rate, ERCP-related complications, clinical remission rate and long-term complications were main outcome measurements to compare the efficacy and safety of different number of stents in managing post-liver transplantation anastomotic biliary stricture. Results Among the 18 patients (0.5 ~ 60.0 months) with post-liver transplantation ABSs, seven patients received less plastic stents treat﹣ment (< 3 stents), nine patients with persistent anastomotic or recurrent stricture received multiple plastic stents treatment (≥ 3 stents), two patients received multiple plastic stents treatment once suffered with post-liver trans﹣plantation ABSs. The endoscopic technical success rate was seventy-six over eighty (95.0 %). Among the seven pa﹣tients received less plastic stents treatment, one loss to follow-up, two were still under treatment, one died of acute hepatic failure, one died of septic stock, one combined with biliary fistula resulted in treatment failure, one achieved clinical remission, the clinical remission rate was one third (33.3 %). Among the eleven patients received multiple plastic stents treatment, two loss to follow-up, one was still under treatment, two received surgery because of failed treatment, six achieved clinical remission, the clinical remission rate was 75.0 % (6/8). The average diameters and stent durations of management of 1 stent, 2 stents, 3 stents, 4 stents, 5 stents, 7 stents were 8.5 F, 17.0 F, 24.0 F, 28.0 F, 36.0 F, 50.0 F. Among the six early postoperative complications, five cases occurred in less stent manage﹣ment and one occurred in MPSs management, the early postoperative complication rate was 7.5 %(6/80). No severe ERCP-related complications and procedure-related deaths. Conclusions Endoscopic management of plastic stents is safe and effective for post-liver transplantation ABSs. Providing larger biliary support, the multiple plastic stents treatment was superior to less plastic stents treatment in view of clinical remission rate, especially for refractory one. Multiple plastic stents did not increase the incidence of complications, it could be used as the first-line treatment of post-liver transplantation duct-to-duct biliary anastomosis for its safety and effectivity.

Objective To observe after the NIBP (NIK and IKK beta binding protein) gene transfected into colon cancer cell lines HT29, the migration of cells and expression of p65, MMP2, MMP9 mRNA and proteins. Methods The experimental group: divided into without transfection HT29 cell (HT29 group) and transfection no-load HT29 cell (HT29-NC group) and transfection NIBP HT29 cell (HT29-NIBP steady group). Using the Transwell test to detect cell migration ability. Q-PCR method to detect the mRNA expressions of NIBP , p65, MMP2, MMP9. Western Blot method to detect the expressions of NIBP, p65, phosphorylation p65 (p-p65) proteins. The method of ELISA was used to detect the secretion of matrix metalloproteinase (MMP)-2, MMP-9. Results The high expression of NIBP may enhance the migration ability of colon cancer cell lines HT29 , increasing the expression of p-p65, MMP2, MMP9 mRNA and proteins (P < 0.05). Conclusion NIBP potently enhances colon cancer HT29 cell migration and invasion. Activation of NF-κB signaling pathways resulted in up-regulation of MMP-2 and MMP-9 maybe one of its molecular mechanisms.

[ ABSTRACT] AIM:To investigate the effects of sphingosine kinase l ( SphK1) and focal adhesion kinase ( FAK) on the epithelial-mesenchymal transition ( EMT) of human colon cancer HCT 116 cells.METHODS:Human colon cancer HCT116 cells were divided into 3 groups.N, N-dimethylsphingosine (DMS) was used to suppress the activity of SphK1. PF573228 was used to suppress the activation of FAK .The cells treated with equal volume of culture medium severed as control group.The cell viability was measured by MTT assay .The protein expression of SphK1, FAK and the EMT relative protein E-cadherin, N-cadherin, vimentin and matrix metalloproteinase (MMP) 2 was analyzed by Western blot.The mR-NA expression of SphK1, sphingosine-1-phosphate (S1P), FAK, E-cadherin and vimentin was detected by real-time PCR. The ability of tumor cell migration was measured by wound-healing assay.RESULTS:The cell viability of HCT116 cells was suppressed by DMS and PF 573228 in dose and time dependent manners .DMS significantly suppressed the expression of SphK1, FAK, N-cadherin, vimentin and MMP2, meanwhile enhanced the expression of E-cadherin.PF573228 reduced the expression of FAK , SphK1, N-cadherin, vimentin and MMP2, meanwhile increased the expression of E-cadherin (P<0.01).In addition, the migration ability of HCT116 cells was significantly decreased by treating with DMS and PF573228 (P<0.01).Compared with control group , the mRNA expression of FAK, SphK1, S1P and vimentin was de-creased, while the expression of E-cadherin was increased significantly in PF573228 group and DMS group (P<0.05). CONCLUSION:SphK1 and FAK signaling pathways may play an important role in the occurrence of EMT in the colon cancer HCT116 cells.

Acute pancreatitis (AP) is a severe disease with an increasing incidence rate in clinical practice. Although most patients have mild pancreatitis, the fatality rate of severe pancreatitis remains at a relatively high level, and therefore, early-stage, simple, and accurate clinical scoring systems are urgently needed to determine the severity of AP, so as to facilitate effective disease management and symptomatic treatment and reduce the fatality rate of patients. At present, a large number of studies have demonstrated that the scoring systems such as Ranson score, APACHE Ⅱ score, BISAP score, CTSI score, and some serological markers have been used to evaluate the severity and prognosis of AP, but all of them have certain limitations. This article reviews the research advances in the existing scoring systems, single serological markers, and related modified scoring systems in recent years. Through a literature review, it is concluded that there is no a single scoring system or a single indicator that can cover the whole process of AP diagnosis and treatment and accurately judge the severity of AP, and therefore, it is necessary to develop a new scoring system or combine various indicators for comprehensive evaluation.

[Abstract] Objective: To investigate the effect of sphingosine kinase 1 (SphK1) knockdown on the proliferation and migration of colon cancer RKO cells induced by mesenchymal stem cells (MSCs). Methods: RKO cells were treated with MSCs conditioned medium (MSC-CM) or control medium (Control-CM), respectively. Cell proliferation was detected by CCK-8 assay. Cell migration ability was tested by Transwell chamber assay. The proteins expression of Ki-67, MMP-2/9, CD44 and CD133 was detected by Western blotting. Then, the expression of SphK1 in RKO cells was suppressed by targeted gene lentivirus shRNA vector transfection. The effects of SphK1 knockdown on the proliferation, migration and protein expressions of Ki-67, MMP-2/9, CD44 and CD133 of RKO cells induced by MSC-CM were observed. Results: The RKO cells proliferation was promoted by MSC-CM in a time-dependent manner; moreover (P<0.05), the migration ability of cells was significantly enhanced after being treated with MSC-CM(P<0.01). In addition, MSC-CM significantly increased the protein expressions of Ki-67, MMP-2/9, CD44 and CD133(all P<0.05 or P<0.01). Lentiviral ShRNA vector transfection could significantly inhibit the expression of SphK1. Down-regulation of SphK1 significantly inhibited the proliferation, migration and protein expressions of Ki-67, MMP-2/9, CD44 and CD133 of RKO cells induced by MSC-CM(all P<0.05 or P<0.01). Conclusion: MSC-CM promotes the proliferation and migration of colon cancer RKO cells. Down-regulation of SphK1 reverses the cell proliferation and migration induced by MSC-CM via inhibiting the expression of MMP-2/9, CD44 and CD133.