Paracrine effect of bone marrow mesenchymal stem cells on proliferation, apoptosis, and alpha-actin-2 expression in hepatic stellate cells.

We investigated the paracrine effects of bone marrow mesenchymal stem cells (BMSCs) on the proliferation, apoptosis, and alpha-actin-2 (ACTA2) expression of hepatic stellate cells (HSCs), and explored the possible mechanisms of hepatocyte growth factor (HGF). We established a co-culture system by culturing BMSCs on the upper layer and HSCs on the lower layer of a 6-well Transwell plate. Normal HSCs were cultured alone as a control. Cell apoptosis was determined by flow cytometry. We detected the expression of ACTA2 mRNA and ACTA2 protein in HSC using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting, respectively. ACTA2 in HSCs was detected by fluorescent staining, and HGF in the co-culture supernatant was detected by enzyme-linked immunosorbent assay (ELISA). The apoptotic rate of HSCs in the experiment group was 2.6 times that in the control group (P < 0.05). The expression levels of ACTA2 mRNA and ACTA2 protein were significantly inhibited in HSCs compared with the control group (P < 0.05). HGF concentration in the co-culture supernatant was 0.43 ± 0.47 mM in the experimental group, which was significantly higher than in the control group (0.16 ± 0.43 mM) (P < 0.05). The paracrine effect of BMSCs, which was caused by the suppression of ACTA2 and HGF expression, induced HSC apoptosis.

Retraction RETRACTION of "Methylation of the RASSFIA promoter in breast cancer" by Y. Ji, H.H. Jin, M.D. Wang, W.X. Cao, J.L. Bao - Genet. Mol. Res. 15 (2): gmr.15028261 (2016) - DOI: 10.4238/gmr.15028261.

The retracted article is: Ji Y, Jin HH, Wang MD, Cao WX, et al. (2016). Methylation of the RASSFIA promoter in breast cancer. Genet. Mol. Res. 15: gmr.15028261. There are significant parts of this article (particularly, in the discussion section) that are copied from "Methylation of HIN-1, RASSF1A, RIL and CDH13 in breast cancer is associated with clinical characteristics, but only RASSF1A methylation is associated with outcome", by Jia Xu, Priya B Shetty, Weiwei Feng, Carol Chenault, Robert C Bast Jr, Jean-Pierre J Issa, Susan G Hilsenbeck and Yinhua Yu, published in BMC Cancer 2012; 12: 243. DOI: 10.1186/1471-2407-12-243. The first paragraphs of both discussions are identical. This is concerning. The abstract and introduction sections have much of their text plagiarized. Overall, there is high plagiarism detected. The GMR editorial staff was alerted and after a thorough investigation, we have strong reason to believe that the peer review process was failure and, after review and contacting the authors, the editors of Genetics and Molecular Research decided to retract the article in accordance with the recommendations of the Committee on Publication Ethics (COPE). The authors and their institutions were advised of this serious breach of ethics.

Methylation of the RASSFIA promoter in breast cancer.

Tumor suppressor genes are the key targets of hypermethylation in breast cancer and may therefore lead to malignancy by deregulation of cell growth and division. Our previous pilot study with pairs of malignant and normal breast tissues identified a correlation between RASSFIA gene methylation and breast cancer. To determine the relationship between RASSFIA methylation and breast cancer, we conducted a larger study. We took samples from 108 patients with breast cancer, 28 patients with benign breast tumors, and 33 subjects with normal breast tissues at the Second Affiliated Hospital of Nanjing Medical University at Wuxi between July 2013 and September 2015. We used the samples to investigate methylation levels of the RASSF1A gene for associations with breast cancer. Quantitative real-time polymerase chain reaction (PCR) and methylation-specific PCR were used to investigate the levels of RASSF1A mRNA expression and RASSF1A methylation, respectively. RASSFIA was not expressed in 22 of the 108 breast cancer tissue samples (20.37%), and there was no statistically significant difference (P > 0.05); however, RASSFIA expression was significantly lower than that in the normal breast tissue samples (P < 0.05). Moreover, the methylation rate of the RASSFIA gene promoter was significantly higher in the breast cancer tissues (64.81%) than in the normal breast tissues (18.18%) and benign breast tumors (17.86%) (P < 0.05). High methylation of the RASSF1A gene promoter was an important reason for its downregulation, and the gene played a critical regulated role in the incidence and development of breast cancer.