Abstract.It is well known that local anesthetics have a broad spectrum of pharmacological actions, acting as nerve blocks, and treating pain and cardiac arrhythmias via blocking of the sodium channel. The use of local anesthetics could reduce the possibility of cancer metastasis and recurrence following surgical tumor excision. The purpose of the present study was to investigate the inhibitory effect of lidocaine upon the invasion and migration of transient receptor potential cation channel subfamily V member 6 (TRPV6)-expressing cancer cells. Human breast cancer MDA-MB-231 cells, prostatic cancer PC-3 cells and ovarian cancer ES-2 cells were treated with lidocaine. Cell viability was quantitatively determined by MTT assay. The migration of the cells was evaluated using the wound healing assay, and the invasion of the cells was assessed using a Transwell assay. Calcium (Ca 2+ ) measurements were performed using a Fluo-3 AM fluorescence kit. The expression of TRPV6 mRNA and protein in the cells was determined by quantitative-polymerase chain reaction and western blot analysis, respectively. The results suggested that lidocaine inhibits the cell invasion and migration of MDA-MB-231, PC-3 and ES-2 cells at lower than clinical concentrations. The inhibitory effect of lidocaine on TRPV6-expressing cancer cells was associated with a reduced rate of calcium influx, and could occur partly as a result of the downregulation of TRPV6 expression. The use of appropriate local anesthetics may confer potential benefits in clinical practice for the treatment of patients with TRPV6-expressing cancer.

Pulsed electromagnetic field (PEMF) has been suggested as a promising method alternative to drug-based therapies for treating osteoporosis (OP), but the role of PEMF in GIOP animal models still remains unknown. This study was performed to investigate the effect of PEMF on bone formation and lipid metabolism and further explored the several important components and targets of canonical Wnt signaling pathway in GIOP rats. After 12 weeks of intervention, bone mineral density (BMD) level of the whole body increased significantly, serum lipid levels decreased significantly, and trabeculae were thicker in GIOP rats of PEMF group. PEMF stimulation upregulated the mRNA and protein expression of Wnt10b, LRP5, β-catenin, OPG, and Runx2 and downregulated Axin2, PPAR-γ, C/EBPα, FABP4, and Dkk-1. The results of this study suggested that PEMF stimulation can prevent bone loss and improve lipid metabolism disorders in GIOP rats. Canonical Wnt signaling pathway plays an important role in bone formation and lipid metabolism during PEMF stimulation.

Abstract. Dopamine receptor 2 (DR2) may be a biomarker for various types of cancer. Ovarian cancer cells overexpress DR2; therefore, blocking DR2 may be a novel treatment strategy for ovarian cancer. Thioridazine, a DR2 blocker, has antineoplastic activity in a variety of cancer cells. In view of the requirement for novel therapeutic agents in ovarian cancer, the present study aimed to determine the potential effects of thioridazine in vitro and in vivo. It was revealed that the DR2 blocker thioridazine induced cell death in a dose-dependent manner in ovarian cancer cells. Thioridazine treatment induced apoptosis and autophagy, which may be attributed to an increased level of reactive oxygen species and associated DNA damage. Additionally, the expression of various proteins increased with oxidative stress, including nuclear factor E2-related factor 2, which is a pivotal transcriptional factor involved in cellular responses to oxidative stress. Heme oxygenase 1, NAPDH quinone dehydrogenase 1 and hypoxia inducible factor-1α and phosphorylated (p)-protein kinase B expression was significantly decreased, and the expression level of p-extracellular signal-related kinases and p-P38 was increased. Using 3-methyl adenine to inhibit autophagy caused the rate of apoptosis to increase. Thioridazine inhibited the growth of SKOV3 xenografts in nude mice. The present study demonstrated that the DR2 blocker thioridazine exhibited anticancer effects in vitro and in vivo, suggesting that thioridazine may be used as a potential drug in ovarian cancer therapy. IntroductionEpithelial ovarian cancer is the leading cause of mortality among gynecological types of cancer. Surgical debulking combined with chemotherapy is the standard therapeutic strategy. However, the relapse rate is high, primarily due to the development of chemotherapy resistance (1), therefore, novel modalities must be explored.Dopamine receptor (DR) expression may be associated with the development of various types of cancer. Patients with schizophrenia who receive DR antagonists have a reduced incidence of cancer of the rectum, colon, prostate and uterine cervix (2,3). Patients with Parkinson's disease, which functionally similar to disease-induced DR antagonism, also have a lower incidence of cancer. It was hypothesized that DR may be a biomarker for cancer (4). Knockdown/blocking of DR2 inhibited the proliferation of cancer cells, including cancer stem cells (5). This suggested that DR2 may be a treatment target for types of cancer that expresses dopamine receptor 2.Thioridazine is a DR2 antagonist and has been clinically approved to treat schizophrenia and other psychotic disorders (6). Of note, thioridazine exhibits anticancer action in breast cancer, leukemia, hepatoma and cervical carcinoma (5,7-9). Ovarian cancer cells express a number of DRs, with the exception of DR3 (10), suggesting that thioridazine may be used to treat ovarian cancer. In the present study, the effects of thioridazine on ovarian cancer were explored in vitro and in vivo. The findings sug...

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, the authors have realized that Fig. 4D also featured the incorrect placement of a data panel; essentially, the data panel shown for the A2780, thioridazine experiment was a duplicate of the SKOV3, thioridazine data panel. The corrected version of Fig. 4, featuring the correct data for the A2780, thioridazine experiment, is shown on the next page. All the authors agree to this Corrigendum. Note that the revisions made to these figures do not adversely affect the results reported in the paper, or the conclusions stated therein.