Objective To explore the inhibition effect and the possible mechanism of resveratrol on human hepatocellular carcinoma cell line Bel-7402 both in vitro and vivo.Methods Four Res drugs in the experiment group,the final concentrations were 12.5,25,50,100μmol/L,the control group at the same time set not containing Res drugs,MTT assay was used to measure the inhibition of resveratrol on Bel-7402.The expression of Bcl-2 was detected by RT-PCR and Western Blot.The levels of IL-2,IL-6,IL-12 and TNF-αwere detected by ELISA.Results Resveratrol inhibited Bel-7402 cell proliferation in dose and time manner,and influenced the expression of Bcl-2 mRNA and protein.At the same time,resveratrol inhibited the growth of tumor and improved the levels of IL-2,IL-6,IL-12 and TNF-α.Conclusion Resveratrol could inhibit Bel-7402 cell proliferation both in vitro and vivo, the possible mechanism may be that resveratrol could low down the expression of Bcl-2 and improve the levels of IL-2,IL-6,IL-12 and TNF-α.

Objective To study the efficacy of CPT-11 TACE in the treatment of unresectable HCC.Methods A retrospective review was undertaken on unresectable HCC patients receiving doxorubicin transarterial chemoembolization (59 cases) and irinotecan(CPT-11) in 24 cases from May 2003 to November 2011.Survival analysis was performed with Kaplan-Meier statistics.Differences in survival between the two groups were assessed for statistical significance with the log-rank test.Results Overall survival time was significantly longer in patients treated with CPT-11 compared with doxorubicin treated group (21.7 vs 14.5 months,P =0.042).There was no significant difference in time to progression between the two groups,but time to progression was longer in CPT-11 group than doxorubicin treated group (11.42 vs 9.46 months,P =0.091).Subgroup analysis showed that for intermediate-stage HCC,CPT-11 resulted in a significantly longer time to progression and overall survival compared with doxorubicin treated group (P =0.029 and P =0.014,respectively).There were no significant differences in adverse events among the two groups (P ＞ 0.05).Conclusions Chemotherapeutic agent CPT-11 in the form of TACE significantly improved overall survival when compared with doxorubicin for the treatment of unresectable HCC.

Objective To evaluate the efficacy of chemoradiotherapy in patients with unresectable pancreatic cancer who were previously treated with PTCD.Methods From September 2005 to December 2012,47 unresectable pancreatic cancer patients with obstructive jaundice were enrolled in this study.They were divided into two groups.21 patients received after PTCD chemotherapy or radiation,or chemoradiotherapy.26 patients in support care group received only nutrition,analgesia and other related support treatment.Survival analysis was performed with Kaplan-Meier statistics.Differences in survival between the groups were assessed for statistical significance with the log-rank test.Results The median overall survival time of patients after PTCD was 7.19 months.The median overall survival time of chemoradiation group was 9.07 months,which was higher than that of support care group (5.52 months),P=0.017.12 patients received single therapy (either chemo or radiation),and 9 patients received chemoradiotherapy.The median overall survival times were 8.31 months and 11.15 months,respectively (P =0.325).Conclusions Post PTCD chemoradiotherapy helps prolong the survival time in unresectable pancreatic cancer patients.

Objective To investigate the expression of far upstream element binding protein 1 (FUBP1) gene in gastric cancer,and analyze its effect on proliferation and invasion of gastricc cancer cells.Methods The expression of FUBP1 in gastric cancer tissues was detected by real-time PCR.The relationship between FUBP1 expression and clinic pathological factors of gastricc cancer was analyzed by one-way ANOVA.The silence vector for FUBP1 was constructed and transfected into gastricc cancer SGC7901 cells,and the transfected effects were then detected by real-time PCR.The influence of FUBP1 silence on cell proliferation and invasion in SGC7901 cells were detected by CCK8 method and Transwell assay.Results FUBP1 expression was increased markedly in gastricc cancer tissues.Following the depressing of differentiation and the increase of invasion depth and metastatic lymph nodes,the FUBP1 expression was up-regulated in primary gastric carcinoma significantly.The pS-FUBP1 vector could silence the FUBP1 expression in SGC7901 cells.FUBP1 silence inhibited SGC7901 cell proliferation amd invasion.Conclusion FUBP1 was high-expressed in gastricc cancer,and related with genesis and progress of gastric cancer,silence of FUBP1 expression can inhibit the cell proliferation and invasion in gastric cancer cells.

As a novel and promising antitumor target, AXL plays an important role in tumor growth, metastasis, immunosuppression and drug resistance of various malignancies, which has attracted extensive research interest in recent years. In this study, by employing the structure-based drug design and bioisosterism strategies, we designed and synthesized in total 54 novel AXL inhibitors featuring a fused-pyrazolone carboxamide scaffold, of which up to 20 compounds exhibited excellent AXL kinase and BaF3/TEL-AXL cell viability inhibitions. Notably, compound 59 showed a desirable AXL kinase inhibitory activity (IC₅₀: 3.5 nmol/L) as well as good kinase selectivity, and it effectively blocked the cellular AXL signaling. In turn, compound 59 could potently inhibit BaF3/TEL-AXL cell viability (IC₅₀: 1.5 nmol/L) and significantly suppress GAS6/AXL-mediated cancer cell invasion, migration and wound healing at the nanomolar level. More importantly, compound 59 oral administration showed good pharmacokinetic profile and in vivo antitumor efficiency, in which we observed significant AXL phosphorylation suppression, and its antitumor efficacy at 20 mg/kg (qd) was comparable to that of BGB324 at 50 mg/kg (bid), the most advanced AXL inhibitor. Taken together, this work provided a valuable lead compound as a potential AXL inhibitor for the further antitumor drug development.