Chronic inflammation has been demonstrated closely related to the tumor progression.Tumorassociated macrophage,as the most abundant immune cells in the tumor microenvironment,is a key element that links inflammation and cancer.Recently,studies found that the phenomenon and function of tumor-associated macrophage almost tend to M2 type macrophage.As an important indicator,tumor-associated macrophage usually predicts the poor progress with the cancer development.In China,Most of patients with hepatocellular carcinoma are associated with chronic viral infection.A large number of macrophages in the liver infiltrated in chronic inflammation,which are differentiated by variety of mechanisms under the chronic inflammatory stimulation,promote the development of liver cancer.In this paper,we will review the tumor-associated macrophages and the development of liver cancer.

Purpose:To investigate the effects of octreotide on TGF-? autocrine in human hepatocellular carcinoma cells SMMC-7721 and TGF-?-induced cells proliferation. Methods:The expression of TGF-?in SMMC-7721 was determined by radioimmunoassay and reverse-transcriptase polymerase chain reaction(RT-PCR). The expression of epidermal growth factor receptor (EGFR) in the cells was determined by immunohistochemistry method and RT-PCR. The proliferative activity of the cells was evaluated by flow cytometry and colony-forming assay. Results:The content of TGF-?was significantly attenuated by octreotide and the inhibitor rate was 15.0%~26.7%. TGF-?mRNA index was decreased by octreotide.TGF-?increased the expression of EGFR both in mRNA and protein level,while octreotide inhibited the expression induced by TGF-?. Proliferative index (PI) and colony-forming rates were obviously lower in octreotide and TGF-?-treated cells than those in TGF-?-treated cells. Conclusions:There exists a TGF-? autocrine loop in human hepatocellular carcinoma cells SMMC-7721. octreotide could inhibit TGF-? autocrine in the cells, and consequently exerts an inhibitory effect on cell proliferation.

ObjectiveTo summarize the complications after precise hepatectomy for primary liver cancer and explore the prevention experiences.MethodsThe clinical data of 120 primary liver cancer patients who underwent precise hepatectomy in Anhui Provincial Hospital from August 2008 to October 2011 were retrospectively analyzed.The common complications after hepatectomy and the management measures of the complications were studied.Results Related complications were found in 19 cases,including 7 cases of pleuraI effusion,3 cases of pneumonia,1 case of intra- abdominal hemorrhage,2 cases of up gastrointestinal bleeding,1 case of abdominal abscess,1 case of hepatic failure,1 case of bile leakage,2 cases of would infection,1 case of urinary tract infection.ConclusionsPrecise hepatectomy has characteristics of preoperative accurate assessment,intraoperative fine operation and postoperative excellent management,which reduce the incidence of postoperative complications.

Hepatectomy for huge hepatocellular carcinoma (HCC) is difficult due to its huge size and the compression and invasion to the surrounding tissues as well as the important vascular systems.Surgical resection of huge carcinoma in the caudate lobe is a big challenge for hepatobiliary surgeons because of its special location and complex anatomical structure.As the improvement of surgical techniques in recent years,especially the promotion of the concept of precision liver surgery,many surgeons begin to take the challenge of resection of huge HCC in the caudate lobe in a variety of ways.In April 2014,a male patient aged 58 years with huge HCC in the caudate lobe was admitted to the Anhui Provincial Hospital.Precision right hemihepatectomy combined with caudate lobectomy was performed on this patient without occlusion of the hepatic inflow,and the efficacy was satisfactory.The key techniques involved in this procedure were discussed in this article.

Ischemia reperfusion injury is an important factor which has been affected the recuperation of hepatic function after hepatectomy and liver transplantation,and is a complex course in pathophysiology with many factors.With the development of research on ischemia reperfusion injury,effective prevention measures of ischemia reperfusion injury also have made new progress.And this will greatly improve the prognosis of hepatic surgery.The mechanism and its prevention measure of hepatic ischemia reperfusion injury were reviewed in this paper.

Objective To observe vasculogenic mimicry formation difference in human hepatocellular carcinoma cell lines MHCC97-H/L with different metastatic potentials under three-dimensional culture condition,and to study extracellular matrix and adhesion molecules-related mechanism of vasculogenic mimicry.Methods Three-dimensional cell culture system of MHCC97-H/L was established to observe tubelike structures by inverted microscope.Human umbilical vein endothelial cell(HUVEC),human hepatocellular carcinoma cell line Hep3B with non-metastatic potentials and normal human hepatic cell line HL-7702 were taken as control.Gene expression profiles of MHCC97-H and MHCC97-L were detected by Oligo extracellular matrix and adhesion molecules microarray analysis.Two differentially expressed genes were verified with semi-quantitative reverse transcriptionpolymerase chain reaction(RT-PCR)and Western blot.All data were analyzed using two sample t test.Results After a 24-hour three-dimensional culture,the length of tubelike structures was(474 ± 16)mm/cm2 in MHCC97-H,which were significantly longer than(320 ±41)mm/cm2 in MHCC97-L(t =6.119,P ＜0.05).Hep3B and HL-7702 could not form tubelike structures.Compared with MHCC97-L,the expression of 7 genes were up-regulated and the expression of 3 genes were down-regulated among a total of 113 angiogenesis genes in MHCC97-H.Two of the genes with differential expressions including tenascin C and extracellular matrix protein 1 were further validated by RT-PCR and Western blot.Conclusion MHCC97-H has stronger ability to form vasculogenic mimicry than MHCC97-L,and this perhaps correlates with the differential expression of certain extracellular matrix and adhesion molecules-related genes in MHCC97-H.

Objective To evaluate the role of nodal gene modulating malignancy of a hepatocellular carcinoma cell lines SMMC7721. Methods To silence the expression of nodal gene in human hepatocellular carcinoma cells by RNA interference ( RNAi),and to observe the effect on cells biological behaviour and vasculogenic mimicry.4 expression vectors of nodal gene targeting small interference RNA were constructed and transfected into SMMC-7721 cells.Real-time quantitive PCR and Western blot were used to examine nodal gene expression. The effects of nodal gene RNA interference on proliferation,apoptosis,infestation,migration and vasculogenic mimicry of SMMC-7721 were studed. Results The expression of nodal gene was suppressed in SMMC-7721 cells by RNA interference.In the first 4,5,6 days of proliferation experiment,the proliferation of interference group was significantly lower than the control group(separately F =17 098.922,18 135.107,32 641.075,all P ＜ 0.05 ); 48 h after transfection,the apoptosis rate of interference group was significantly higher than the control group (F =1136.452,P ＜0.05); In the infestation and migration experiments,the cells through the transwell chamber in the interference group were less than the control group( separately F =83.6,1126.857,all P ＜ 0.05 ) ; 24 h and 48 h after transfection,the vasculogenic mimicry in the interference group did not form which was significantly different from the control group. Conclusions Interfering the expression of nodal gene inhibits the malignant biological behaviour and the formation of vasculogenic mimicry in human hepatocellular carcinoma cells.

Objective To detect the expression of Mortalin in human hepatoma-derived cell lines and explore its effect on epithelial-mesenchymal transition in hepatocellular carcinoma (HCC) cell lines.Methods Six HCC cell lines and 1 normal liver cell line (L02) were chosen.The expression of Mortalin was detected using Western blot and real-time quantitative PCR (qPCR).The endogenous gene expression of Mortalin was inhibited by RNA interference (shRNA).Cell viability was detected using MTT assay and flow cytometry.The expression of Mortalin,E-cadherin and Vimentin were detected by Western blot and qPCR.The experiment was divided into three groups; blank,control,and shRNA.Results Mortalin was detected in Hep3B,MHCC97H,HepG2,and HCCLM3,but not in MHCC97L and L02.After 24 h transfection,GFP fluorescence showed that plasmid Mortalin shRNA was successfully transfected into MHCC97H cells.MTT assay indicated that cytotoxicity was 0％,2.5％,and 3.5％ in the blank,control,and shRNA group respectively.Similarly,flow cytometric showed that early apoptosis rates were 0.8％,4.5％,and 9.2％ in the blank,control,and shRNA group respectively.These results indicated that transfection did not cause severe cell damage.After 48 h of interference,Western blot and qPCR analysis showed that shRNA significantly inhibited the expression of Mortalin.Moreover,cells were collected after 24 h,48 h,72 h and 96 h of interference and analyzed for the relationship between Mortalin,E-cadherin and Vimentin by Western blot and qPCR.It was found that decreased expression of Mortalin was accompanied by elevated E-cadherin expression and reduced Vimentin expression.Conclusion Overexpression of Mortalin correlated with the metastatic phenotype of HCC cells and could promote epithelial-mesenchymal transition.

Objective To assess the value of indocyanine green excretion test in predicting hepatic failure after hepatectomy. Methods The retention rate of indocyanine green at 15 minutes (ICG R15), effective hepatic blood flow (EHBF) and clinical and biochemical parameters of 128 patients who received hepatectomy at the Affiliated Provincial Hospital of Anhui Medical University from June 2007 to June 2008 were detected by pulse dye densitometry. All patients were divided into non-hepatic failure group (n = 110) and hepatic failure group (n =18). ICG R15, EHBF, Child's score, histology activity index (HAI) score, clinical and biochemical parameters and other indexes were analyzed to predict hepatic failure by the t test, chi-square test, linear regression analysis or regression model. The relationship between positive predictive indexes and HAI score was studied. Results Eighteen patients suffered from hepatic failure after operation. ICG R15, Child's score, HAI score of patients without hepatic failure were 9% ±4%, 5.6 ±0.7, 3.8 ±0.5, which were significantly lower than 15% ±6%,6.1 ± 0. 8, 5.0 ± 0. 8 of patients with hepatic failure (t = 11. 121,2. 356, 3. 915, P ＜ 0.05). EHBF of patients without hepatic failure was (1.2 ±0.2) L/min, which was significantly higher than (1.0 ±0.2) L/min of patients with hepatic failure (t = 2. 802, P ＜ 0. 05). In a logistic regression model, age ≥ 65 years, ICG R15 ≥ 14% and EHBF ＜ 1.0 L/min were risk factors of postoperative hepatic failure (x2 = 4. 758, 9.709, 5. 362, P ＜ 0.05).ICG R15 was negatively correlated with EHBF (r =-0. 527, P ＜0.05). HAI score was positively correlated with ICG R15 (r =0. 638, P ＜0.05), while it was negatively correlated with EHBF (r =-0. 445, P ＜0. 05).Conclusions ICG R15 and EHBF are good predictive indicators for hepatic failure after hepatectomy. Patients with ICG R15≥14% and EHBF ＜ 1.0 L/min are prone to have postoperative hepatic failure.

Objective To assess the effects of gonadectomy on carcinogenesis and development of hepatocellular carcinoma (HCC) induced by chemical substances in rat model. Methods Fifty male and 50 female Sprague-Dawley rats (age of 5-6 weeks) were equally divided into four groups: male experimental (surgical castration) and control groups and female experimental (surgical castration)and control groups. The HCC model was induced by diethylnitrosamine (DEN) and Nnitrosomorpholine (NMOR) in SD rats. The effects of gonadectomy on occurring and development of HCC were observed. Results The incidence of HCC in female experimental group was higher than that in female control group (11/11 vs 5/14, P=0. 001), while it was lower in male experimental group than that in male control group (3/10 vs 12/12, P=0. 001). It was demonstrated that gonadectomy could increase the growth of HCC (P=0. 013) and tumor metastasis (P=0. 036) in female rats, but not in male rats. The formation of liver cirrhosis and HCC was found at 8 and 16 weeks in male experimental group, at 12 and 20 weeks in male control group, at 16 and 20 weeks in female experimental group and at 12 and 16 weeks in female control group. These findings showed that gonadectomy could improve the development of carcinogenesis in female rats and delay the carcinogenesis in male rats. Conclusion Sex hormones, especially estrogens, may be involved in development and metastasis of rats HCC.