Retraction Note: Inhibition effects of acridone on the growth of breast cancer cells in vivo.

The article "Inhibition effects of acridone on the growth of breast cancer cells in vivo", by Y.-F. Xia, H.-J. Chu, G.-F. Kuang, G.-J. Jiang, Y.-C. Che, published in Eur Rev Med Pharmacol Sci 2018; 22 (8): 2356-2363-DOI: 10.26355/eurrev_201804_14827-PMID: 29762857 has been retracted by the Editor in Chief for the following reasons. Following some concerns raised on PubPeer regarding a possible overlap in Figure 2, the Editor in Chief has started an investigation to assess the validity of the results as well as possible figure manipulation. The journal investigation revealed a duplication between Figures 2B and 2C. Consequently, the Editor in Chief mistrusts the results presented and has decided to retract the article. The authors have been informed about the journal's investigation but remained unresponsive. This article has been retracted. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/14827.

Inhibition effects of acridone on the growth of breast cancer cells in vivo.

OBJECTIVE: To investigate the anti-tumor effect of acridone against breast cancer in vivo and provide a therapeutic agent for treatment of breast cancer. MATERIALS AND METHODS: The nude mice xenografted tumor model was established by MCF-7 cells. The mice were randomly divided into four groups. The mice in each group (n=6) were intraperitoneally injected with 0.1 mg/kg saline (low-dose), 0.5 mg/kg (middle-dose) and 1.0 mg/kg (high-dose) of acridone for 21 days, respectively. At the end of the animal experiment, the weight of tumors was recorded to calculate the tumor inhibition rate. The serum hormone levels in peripheral blood were determined using ELISA. Hematoxylin and eosin (HE) staining was used to analyze the histopathological changes. The expression of ABCG2 protein and mRNA were determined by Western blot and RT-PCR, respectively. RESULTS: The inhibition rates of tumor growth in the high-dose, middle-dose, and low-dose groups were 29.18%, 17.21%, and 4.27%, respectively. Compared with control and low-dose group, the tumors growth rate in high-dose and middle-dose groups were decreased significantly. Histologically, the tumors were inhibited in the growth rate, the tissue structure was broken. Estrogen in all groups with acridone treatment decreased, the progesterone in high-dose and middle-dose groups increased remarkably. The expression of ABCG2 protein and ABCG2 mRNA decreased after treatment with acridone. CONCLUSIONS: We showed that acridone could induce cell apoptosis, inhibited ABCG2 (ATP-binding cassette sub-family G member 2) protein and adjusted hormone level. The results suggested that acridone could serve as a chemotherapeutic agent for treatment of breast cancer in vivo.

Expression of claudin-3 and claudin-4 in normal, hyperplastic, and malignant endometrial tissue.

To clarify the roles of claudins in endometrial tumorigenesis, we determined levels of protein and messengerRNA (mRNA) expression of claudin-3 and claudin-4 in human endometrial tissue (proliferative phase [PE, n= 25]; secretory phase [SE, n= 25]; simple hyperplasia [SH, n= 20]; complex hyperplasia [CH, n= 12]; atypical hyperplasia [AH, n= 15]; endometrioid adenocarcinoma [EEC, n= 30]) using immunohistochemistry, western blotting, and real-time polymerase chain reaction, respectively. Morphologic changes of tight junctions (TJs) were also observed in normal, hyperplastic, and malignant endometrial tissue. Absence or weak staining for claudin-3 and claudin-4 was observed in PE, SE, SH, and CH, while medium to intense staining was detected in AH and EEC. Staining of claudin-3 and claudin-4 was predominantly localized to the glandular epithelial cell membrane. Expression of claudin-3 and claudin-4 was significantly increased in the groups of AH and EEC in comparison with the groups of CH, SH, and normal cyclic endometrium at both protein and mRNA levels. The highest expression was observed in EEC. Although no relevance was found with regard to FIGO stage and histologic grade, overexpression of claudin-3 and claudin-4, especially claudin-4, significantly correlated with myometrial invasion. Transmission electron microscopy analysis indicated morphologic disruptions of TJs may lag behind the increase of claudins expression. These results demonstrate that claudin-3 and claudin-4 are strongly expressed in AH and EEC, but less frequently in normal endometrium. The upregulation of claudins expression during endometrial carcinogenesis suggests their potential utility as diagnostic and prognostic biomarkers.