OBJECTIVETo evaluate the oncologic safety and short-term outcomes of laparoscopic surgery in early and advanced rectal cancers.

METHODSClinical and follow-up data of 186 cases with rectal cancer undergoing laparoscopic radical resection from June 2009 to December 2013 were analyzed retrospectively, including 48 early rectal cancer (stage 0-I) and 138 advanced cancer (stage II-III). Thirty-seven cases with early rectal cancer and 275 with advanced cancer undergoing open radical surgery were selected as control group. Surgical safety, oncologic safety and short-term outcomes were compared between two groups.

RESULTSAs for either early or advanced rectal cancer, there were no significant differences in the number of harvested lymph nodes, length of distal resection margin, complication morbidity, rate of local recurrence, distant metastasis, and 3-year survival rate between the two groups (all P>0.05). Although the operation time was longer in laparoscopic group, the laparoscopic group presented less intra-operative blood loss, faster recovery of bowel function, and shorter postoperative hospital stay (all P<0.05). As for advanced rectal cancer, laparoscopic radical surgery tended to achieve less lymph nodes dissected (mean, 13.5 vs. 15.0) and develop more anastomotic leakage (8.0% vs. 5.5%) compared to open surgery, although neither reached statistical significance (P=0.112, P=0.221). Moreover, the conversion rate in patients with advanced rectal cancer was significantly higher than that in those with early cancer (10.9% vs 2.1%, P=0.048).

CONCLUSIONSLaparoscopic surgery can obtain the same oncologic and surgical safety for early rectal cancer as compared to open surgery. However, due to higher conversion rate, potential risk of decreased number of harvested lymph nodes and increased anastomotic leakage, laparoscopic surgery for advanced rectal cancer should be carried out prudently, especially in some hospitals with less laparoscopic experience.

Digestive System Surgical Procedures ; Humans ; Laparoscopy ; Lymph Nodes ; Neoplasm Staging ; Operative Time ; Rectal Neoplasms ; Retrospective Studies ; Safety ; Survival Rate

OBJECTIVETo investigate the effect of ASCT2 gene (glutamine transporter) knock-down by shRNA on biological behaviors of colorectal cancer cells.

METHODSshRNA was transfected into colorectal cancer cells Lovo and SW480 to knockdown ASCT2 mediated by Lipofectamine 2000. Reverse transcription-PCR and Western blot were used to examine the mRNA and protein expression of ASCT2. MTT and transwell assay were used to determine the proliferation and invasiveness of Lovo and SW480 cells. Radioactive-tracer was used to detect the uptake of glutamine.

RESULTSASCT2 mRNA and protein levels were significantly down-regulated by shRNA in Lovo and SW480 cells(P<0.01). MTT and transwell assays showed that ASCT2 knock-down could significantly inhibit the proliferation of Lovo and SW480 cells (A490) and decrease the number of invasive Lovo and SW480 cells from the membrane (both P<0.01). The number of membrane Lovo cells in shASCT group and control group was 46.3±5.9 and 197.7±9.1, respectively while the number of membrane SW480 cells in shASCT group and control group was 29.7±3.8 and 139.0±9.5, respectively. Radioactive-tracer showed that shASCT2 transfection could significantly reduce the uptake of glutamine, with an inhibition rate of 79.15% in Lovo and 67.22% in SW480 cells (both P<0.01).

CONCLUSIONSASCT2 plays an oncogenic role in colonic cancer, and its promotion mechanism may be associated with glutamine metabolism. ASCT2 may be a novel therapeutic target of colonic cancer.

Amino Acid Transport System ASC ; drug effects ; genetics ; physiology ; Cell Line, Tumor ; physiology ; Cell Proliferation ; genetics ; Colorectal Neoplasms ; genetics ; physiopathology ; Down-Regulation ; drug effects ; Gene Knockdown Techniques ; methods ; Glutamine ; drug effects ; genetics ; physiology ; Humans ; Minor Histocompatibility Antigens ; drug effects ; genetics ; physiology ; Neoplasm Invasiveness ; genetics ; physiopathology ; Oncogenes ; drug effects ; genetics ; RNA, Messenger ; physiology ; RNA, Small Interfering ; pharmacology ; Transfection