Objective To systematically evaluate the efficiency of laparoscopic hepatectomy（LH） and conventionalopen hepatectomy （OH）in patients with hepatocellular carcinoma （HCC）. Methods The literatures about the therap-eutic effect of LH and OH on hepatocellular carcinoma were collected from PubMed， Chinese Journal Full-text Database （CJFD）， Wanfang Database， China Doctor/Master Dissertations Full-text Database （CDMD）， and China Proceedings of Conference Full-text Database （CPCD）from 2000 to 2011. RevMan 5.0 software was used for data analysis. Results Eleven controlled clinical trials were included in this analysis. These studies included a total of 781 patients：325 treated with LH and 456 treated with OH. The results of meta-analysis showed that LH group had shorter operation time〔WMD=-20.85， 95% CI （-29.54， -12.16）， P＜0.000 01〕， less operative blood loss 〔SMD=-0.42，95% CI（-0.65，-0.19）， P=0.000 4〕， a lower postoperative morbidity rate 〔OR=0.43，95% CI （0.28，0.65），P＜0.000 1〕， and shorter hospitalization days 〔WMD=-4.32，95％ CI （-6.29，-2.34），P＜0.000 1〕 than OH group. There was no significant difference in postoperative recurrence （P=0.80）， overall survival in 1-year （P=0.98）， 3-year （P=0.41）， and 5-year （P=0.12）， and in disease-free survival in 1-year （P=0.15）， 3-year （P=0.62）， and 5-year （P=0.99）between the two groups. Conclusions For the patients with hepatocellular carcinoma localized to the CouinaudⅡ，Ⅲ，Ⅳ，Ⅴ，and Ⅵ segments with a maximum lesion size of 5cm， as well as the tumor has no effect on the exposure of blood vessel of the first and second hepatic portal， and the liver functions are classified as Child B or A high grade， the laparoscopic liver resection is priority considered in the conditions allow.
Objective To realize the research progress of regulating the endoplasmic reticulum stress response to inhibit autophagy in tumor cells. Method The literatures about regulating the endoplasmic reticulum stress response to inhibit autophagy in tumor cells were reviewed. Result In the endoplasmic reticulum stress response induced by the release of calcium and accumulation of unfolded proteins, autophagy can be activated by several pathways, and to regulate physiological and pathological processes. Conclusion Further research about the endoplasmic reticulum stress response in tumor cells need to be done to regulate the response factors to inhibit autophagy.
Objective To investigate the effects and mechanism of 3-methyladenine （3-MA， an autophagy inhib-itor） on the apoptosis of hepatocellular carcinoma cell line SMMC7721 induced by 5-fluorouracil （5-FU）. Methods The autophagy was observed using fluorescent microscope by monodansyicadaverin （MDC） staining. The viability of SMMC-7721 cell induced by 5-FU was measured using CCK8 assay before and after autophagy inhibited by 3-MA， meanwhile the apoptosis of SMMC7721 cell was determined via AnnexinⅤ/PI assay. The light chain 3 protein （LC3， the autophagy specific protein） and caspase-3， PARP protein were detected by Western blot. Results The autophagy of SMMC7721 cell could be induced by 5-FU after treatment for 48 h， the cell survival rate was （60.73±2.65）%， and the apoptosis rate was （40.42±2.34）%. Compared with the group of 5-FU treatment， the survival rate of SMMC7721 cell in the combination of 5-FU and 3-MA after treatment for 48 h decreased to （42.31±1.32）% （P＜0.01）， and the apoptosis rate increased to （60.92±2.99）% （P＜0.01）， meanwhile the expressions of LC3-Ⅱ， activation fragment of caspase-3， and cleavage frag-ment of PARP significantly increased （P＜0.01）. Conclusions Autophagy is a protective phenomenon during the SMMC7721 cell line apoptosis induced by 5-FU， and autophagy inhibition may enhance the sensitivity of SMMC7721 cell line to 5-FU treatment， which is probably associated with the activation of caspase-3 and cleavage of PARP. Therefore， autophagy inhibition could be a promising strategy for adjuvant chemotherapy in hepatocellular carcinoma.