[Application of "modified double pocket suture" pancreatoenterostomy in laparoscopic pancreatoduodenectomy].

Objective: The purpose of this study was to explore the value of the "improved double purse-string suture method" for pancreatojejunostomy in laparoscopic pancreaticoduodene-ctomy. Methods: The clinical data of 273 patients who underwent laparoscopic pancreaticoduode-nectomy in the Department of Hepatobiliary and Pancreatic Surgery of the First Hospital of Jilin University from January 2021 to May 2022 were retrospectively analyzed. According to the method of pancreaticoenteric anastomosis, the patients were divided into two groups: the "improved double purse-string suture method" group and the "Hong's one-stitch method" group. Results: The "improved double purse-string suture method" for pancreaticoenteric anastomosis was performed in a total of 189 patients, including 107 males and 82 females, with a mean age of (59.6±10.2) years. The "Hong's one-stitch method" group" was performed in a group of 84 patients, including 52 males and 32 females, with a mean age of (60.8±9.3) years.The results showed that the "improved double purse-string suture method" group had a lower incidence of postoperative pancreatic fistula (6.88% vs 8.33% for grade B fistula, and 1.58% vs 2.38% for grade C fistula) and a shorter anastomosis time [(25.25±4.73) min vs (25.76±6.71) min] than the "Hong's one-stitch method" group. There was no statistically significant difference between the two groups in terms of postoperative biliary fistula, abdominal bleeding, delayed gastric emptying, and other complications (P>0.05). Conclusion: The "improved double purse-string suture method" for pancreatojejunostomy is safe and feasible in laparoscopic pancreaticoduodenectomy.

Retraction Note: Combination therapy with metformin and IL-12 to inhibit the growth of hepatic carcinoma by promoting apoptosis and autophagy in HepG2-bearing mice.

The article "Combination therapy with metformin and IL-12 to inhibit the growth of hepatic carcinoma by promoting apoptosis and autophagy in HepG2-bearing mice, by Z. Jin, B.-X. Jia, L.-D. Tan, Q.-M. Chen, Y.-H. Liu, published in Eur Rev Med Pharmacol Sci 2020; 24 (23): 12368-12379-DOI: 10.26355/eurrev_202012_24031-PMID: 33336757" has been retracted by the authors as they cannot ensure the reliability of the manuscript due to inaccuracies in the conclusions and in the experiment (the cell migration and invasion assay along with the cell cycle arrest assay are missing). The Publisher apologizes for any inconvenience this may cause https://www.europeanreview.org/article/24031.

Combination therapy with metformin and IL-12 to inhibit the growth of hepatic carcinoma by promoting apoptosis and autophagy in HepG2-bearing mice.

OBJECTIVE: To investigate the effects and mechanism of metformin (Met) combined the interleukin-12 (IL-12) on inhibiting hepatoma HepG2 cell proliferation via in vitro and in vivo assays. MATERIALS AND METHODS: MTT assay was used to detect inhibitory effects of Met, IL-12 alone or combination on HepG2 cells proliferation. Half inhibitory concentration (IC50) and combination index (CI) were also calculated. Anti-tumor effects of combination or monotherapy on the HepG2-bearing mice were investigated and protein expression levels of apoptosis, as well as the Akt/mTOR/STAT3 signaling pathway-related factors were detected by Western blot. RESULTS: MTT results showed that the inhibitory effect of Met combined with IL-12 on HepG2 cell proliferation was significantly enhanced (both p<0.01) compared with monomer therapy group with a significant synergistic effect (CI<1). The apoptosis rate of HepG2 cells treated with Met combined with IL-12 were 88.12±7.15% and significantly higher than the others (all p<0.01). Moreover, combination treatment significantly suppressed hepatoma growth and increased the survival rate of HepG2-bearing mice without evident body weight loss. Western blot analysis showed that Met combined with IL-12 significantly increased the expression of autophagy-related marker proteins, downregulated the protein expression levels of Bcl-2, p-Akt, p-mTOR, p-STAT3, upregulated the expression level of BAX in both HepG2 cells and tumor tissues. CONCLUSIONS: Met combined with IL-12 exhibited a synergistic antitumor effect on hepatoma HepG2 cells, and the mechanism may be related to its common inhibition of Akt/mTOR/STAT3 signaling pathway and increase of autophagy in HepG2-bearing mice.

Cancer-associated fibroblasts induce epithelial-mesenchymal transition of breast cancer cells through paracrine TGF-ß signalling.

BACKGROUND: Cancer-associated fibroblasts (CAFs) activated by tumour cells are the predominant type of stromal cells in breast cancer tissue. The reciprocal effect of CAFs on breast cancer cells and the underlying molecular mechanisms are not fully characterised. METHODS: Stromal fibroblasts were isolated from invasive breast cancer tissues and the conditioned medium of cultured CAFs (CAF-CM) was collected to culture the breast cancer cell lines MCF-7, T47D and MDA-MB-231. Neutralising antibody and small-molecule inhibitor were used to block the transforming growth factor-ß (TGF-ß) signalling derived from CAF-CM, which effect on breast cancer cells. RESULTS: The stromal fibroblasts isolated from breast cancer tissues showed CAF characteristics with high expression levels of α-smooth muscle actin and SDF1/CXCL12. The CAF-CM transformed breast cancer cell lines into more aggressive phenotypes, including enhanced cell-extracellular matrix adhesion, migration and invasion, and promoted epithelial-mesenchymal transition (EMT). Cancer-associated fibroblasts secreted more TGF-ß1 than TGF-ß2 and TGF-ß3, and activated the TGF-ß/Smad signalling pathway in breast cancer cells. The EMT phenotype of breast cancer cells induced by CAF-CM was reversed by blocking TGF-ß1 signalling. CONCLUSION: Cancer-associated fibroblasts promoted aggressive phenotypes of breast cancer cells through EMT induced by paracrine TGF-ß1. This might be a common mechanism for acquiring metastatic potential in breast cancer cells with different biological characteristics.