[Retracted] microRNA­335 inhibits proliferation, cell­cycle progression, colony formation, and invasion via targeting PAX6 in breast cancer cells.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the cell cycle assay data shown in Fig. 4A, and the western blotting assay data shown in Fig. 4B, were strikingly similar to data appearing in different form in other articles by different authors; furthermore, there were other possible anomalies associated with these data. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 11: 379­385, 2015; DOI: 10.3892/mmr.2014.2684].

Six1 is negatively correlated with poor prognosis and reduces 5-fluorouracil sensitivity via attenuating the stemness of hepatocellular carcinoma cells.

The promoting roles of transcriptional factor six1 have been shown in various tumors, such as breast cancer and colorectal Cancer. However, its roles in hepatocellular carcinoma (HCC) cell stemness and chemotherapeutic sensitivity are never been revealed. In the present study, we showed that six1 expression was negatively correlated the overall survival of HCC patients and significantly increased in HCC tissues. Analysis on normal hepatic cells and HCC cells obtained the consistent result. Functional experiments revealed that six1 knockdown enhanced 5-fluorouracil (5-FU) sensitivity and reduced the stemness of HCC cells. Additionally, six1 knockdown partially reversed 5-FU resistance and attenuated the stemness in 5-FU-resistant HCC cells. Furthermore, we demonstrated that six1 directly bound to sox2 (a stemness master regulator) promoter, enhanced its transcription and expression. Overexpression of sox2 rescued the inhibitory effects of six1 knockdown on the stemness and 5-FU sensitivity of HCC cells. Thus, our work identified a novel six1/sox2 axis in regulating the stemness of HCC cells.

[Docosahexaenoic acid inhibits aflatoxin B1-induced migration and invasion in hepatocellular carcinoma cells in vitro].

OBJECTIVE: To investigate the effect of docosahexaenoic acid (DHA) on invasiveness of aflatoxin B1 (AFB1)-induced hepatocellular carcinoma cells in vitro. METHODS: HepG2.2.15 cells were exposed to different concentrations of AFB1 and DHA plus AFB1. The cell migration and invasion were assessed using wound-healing and Transwell assay, and flow cytometry was used to analyze the cell cycle changes. The ultrastructural changes of the cells were observed by transmission electron microscopy. RESULTS: Compared with the control group, the cells exposed to2 µmol/L AFB1 showed obviously enhanced migration and invasion with decreased cell ratio in G1/G1 phase and increased cell ratio in G2/M phase but no changes in S phase cells; transmission electron microscopy revealed the presence of multiple nucleoli and significantly increased mitochondria and Golgi apparatus in the exposed cells. Compared with AFB1-exposed cells, the cells treated with DHA and AFB1 showed decreased migration and invasion abilities, and the G1/G1 phase cells increased and G2/M phase cells decreased significantly; ultrastructurally, the cells contained single nucleoli with decreased mitochondria and vacuolization occurred in the cytoplasm. CONCLUSION: DHA can significantly inhibit AFB1-induced enhancement of cell migration and invasion in hepatocellular carcinoma cells in vitro.

microRNA-335 inhibits proliferation, cell-cycle progression, colony formation, and invasion via targeting PAX6 in breast cancer cells.

microRNAs (miRNAs) have been demonstrated to play crucial roles in tumorigenesis. However, the molecular mechanism underlying the roles of miRNAs in breast cancer remains largely unknown. In this study, we showed that miR-335 is downregulated in a number of breast cancer tissues and cell lines. Luciferase reporter assays identified the paired box 6 gene (PAX6) as a novel target of miR-335. Further investigation revealed that miR-335 negatively regulates the expression of PAX6 in human breast cancer MCF-7 cells. Our results further suggested that overexpression of miR-335 inhibits MCF-7 cell proliferation by inducing cell-cycle arrest at the G1 phase via targeting PAX6. Western blot analysis showed that overexpression of miR-335 promotes p27 protein expression but inhibits cyclin D1 expression in MCF-7 cells; however, overexpression of PAX6 decreased the p27 protein level but increased the cyclin D1 protein level in MCF-7 cells. Furthermore, miR-335 overexpression reduced colony formation and cellular invasion in MCF-7 cells, an effect that was reversed by PAX6 overexpression. In conclusion, this study provides novel insights into the in vitro regulatory patterns of miRNA-335 and PAX6 in breast cancer, and indicates that miRNA-335 may constitute a promising candidate for the treatment of breast cancer.

[Construction of recombinant lentiviral vectors containing Rheb gene and its mutant Rheb'D60K gene and their expression in human liver cancer cells].

OBJECTIVE: To construct recombinant lentiviral vectors carrying Rheb gene and its mutant Rheb'D60K gene, and examine their expression in human liver cancer cells. METHODS: Rheb gene was amplified by PCR to construct the recombinant plasmid LV31-Rheb-WT and LV31-Rheb-D60K. HEK-293 FT cells were contransfected with the recombinant lentiviral vector together with a lentiviral package plasmid to produce the lentiviral particles. The expression of PS6 protein was detected in the lentivirus-infected MCF-7 cells. The apoptosis of SK-HEP-1 cells transfected with LV31-Rheb-WT or LV31-Rheb-D60K was observed. RESULTS: The recombinant LV31-Rheb-WT and LV31-Rheb-D60K vectors were confirmed by PCR and DNA sequencing. Western blotting showed that PS6 protein expression was increased in LV31-Rheb-WT-transfected cells while decreased in LV31-Rheb-D60K-transfected cells. LV31-Rheb-D60K-transfected SK-HEP-1 cells showed more obvious apoptosis after starvation than LV31-Rheb-WT-transfected cells. CONCLUSION: Lentiviral vectors carrying Rheb gene and its mutant has been successfully constructed, which can be useful in further investigation of the role of Rheb gene in cancer cells.

[Application of Ligasure vessel sealing instrument in laparoscopic hepatectomy for liver cancer].

OBJECTIVE: To investigate the indication and effect of the application of Ligasure vessel sealing instrument in laparoscopic hepatectomy for liver cancer. METHODS: Eleven patients with liver cancer undergoing laparoscopic hepatectomy were analyzed for the tumor size and location, operation time, volume of intraoperative bleeding, postoperative hospital stay and short-term clinical outcomes. RESULTS: All the operations were performed successfully in the 11 cases. All the tumors were less than 7 cm in diameter, locating at the segments II, III, V, VI and VII. The mean operation time was 91 min (80-126 min), and the intraoperative blood loss averaged 82 ml (20-200 ml). The average postoperative hospital stay of the patients was 8 days (7-9 days). No complications were observed in these cases. CONCLUSION: Ligasure vessel sealing instrument in laparoscopic hepatectomy is applicable in cases of perimeter liver cancer. This instrument can decrease the operation time, reduce the intraoperative blood loss and postoperative hospital stay with good safety and minimal invasiveness.

[Wound healing after pancreaticojejunostomy in piglets: a comparison between two anastomotic methods].

OBJECTIVE: To evaluate wound healing after types of pancreaticojejunostomy. METHODS: After resection of the pancreatic head, 38 domestic piglets were divided into two groups according to the types of anastomoses: group I: binding pancreaticojejunostomy, a new technique designed and advocated by professor Peng Shuyou; group II: end-to-end pancreaticojejunal invagination. Anastomotic strength in vivo and histopathological findings were assessed on operative day and postoperative day 5 and 10. RESULTS: Bursting pressure was 139.7 +/- 8.0, 178.7 +/- 9.7 and 268.8 +/- 12.8 mm Hg in group I on day 0, 5 and 10, whereas 67.3 +/- 7.9, 96.2 +/- 10.4 and 130.6 +/- 9.3 mm Hg in group II. The gain on day 0 to 5 and 5 to 10 was 27.9% and 50.5% in group I and 42.9% and 35.7% in group II, respectively. A significant difference was observed between group I and group II, and between 5 and 10 day after anastomoses (P < 0.01). Breaking strength was 4.5 +/- 0.4, 6.6 +/- 0.4 and 10.0 +/- 0.6 N in group I on day 0, 5 and 10 and 4.6 +/- 0.6, 5.8 +/- 0.5 and 7.1 +/- 0.6 N in group II. Although a similar value was shown in both types of anastomoses on day 0, a rapider gain was demonstrated on day 0 to 5 and 5 to 10 in group I (44.8% and 52.9%) than in group II (25.4% and 22.0%). A significant difference was found on day 5 and 10 between the two types of anastomoses (P < 0.05 and P < 0.01). Anastomotic site was well repaired by connective tissue and the cut surface of pancreatic stump was covered by mucosal epithelium in group I on day 10, but the cut surface was incompletely repaired by granulation tissue and no, regeneration of the epithelium was found in group II. CONCLUSION: Anastomotic strength of binding pancreaticojejunostomy was stronger than end-to-end pancreaticojejunal invagination and the healing was better and rapid.