Growth Modulatory Role of Zinc in Prostate Cancer and Application to Cancer Therapeutics.

Zinc is a group IIB heavy metal. It is an important regulator of major cell signaling pathways in most mammalian cells, functions as an antioxidant and plays a role in maintaining genomic stability. Zinc deficiency leads to severe diseases in the brain, pancreas, liver, kidneys and reproductive organs. Zinc loss occurs during tumor development in a variety of cancers. The prostate normally contains abundant intracellular zinc and zinc loss is a hallmark of the development of prostate cancer development. The underlying mechanism of this loss is not clearly understood. The knowledge that excess zinc prevents the growth of prostate cancers suggests that zinc-mediated therapeutics could be an effective approach for cancer prevention and treatment, although challenges remain. This review summarizes the specific roles of zinc in several cancer types focusing on prostate cancer. The relationship between prostate cancer and the dysregulation of zinc homeostasis is examined in detail in an effort to understand the role of zinc in prostate cancer.

Effectiveness of pulsed electromagnetic field for pain caused by placement of initial orthodontic wire in female orthodontic patients: A preliminary single-blind randomized clinical trial.

INTRODUCTION: The purpose of this 2-arm parallel trial was to assess the effects of pulsed electromagnetic field (PEMF) on the reduction of pain caused by initial orthodontic tooth movement. METHODS: Thirty-three female patients (mean age, 16.8 ± 3.8 years) who began orthodontic treatment using fixed appliances were examined. In the pilot study, male patients were less likely to use the PEMF device (epatchQ; Speed Dental, Seoul, Korea) and answer a survey consistently, so eligibility criteria were female patients who were periodontally and systemically healthy at the initiation of treatment and had no history of dental pain in the prior 2 weeks or who used no medications (anti-inflammatory or analgesic drugs) during the experiment period. Each patient had brackets bonded on the maxillary teeth, and a 0.014-in nickel-titanium archwire was tied with elastomeric rings. Their maxillary arches were randomly divided into left and right sides in a split-mouth design: a normal PEMF device (experimental group) was used on 1 side, and a PEMF device with an inversely inserted battery (placebo group) was used on the opposite side of the arch for 7 hours on 3 consecutive nights. A Google survey link was sent to the patients' mobile phones via text message, and they were instructed to record their current pain on the survey. The survey was sent a total of 6 times after insertion of the initial archwire at 0 (T0), 2 (T1), 6 (T2), 24 (T3), 48 (T4), and 72 (T5) hours. Patients recorded the degree of pain in resting and clenching states using a numeric rating scale (NRS) from 1 (no pain) to 10 (worst pain). PEMF devices were used after T2. Generalized linear mixed models, along with ancillary pairwise analyses, were used to model and evaluate the differences in pain reported over 72 hours. RESULTS: The NRS scores did not differ across the groups during the before-PEMF phase for resting (mean difference, -0.07; 95% confidence interval [CI], -0.73 to 0.59; P = 0.842) and clenching (mean difference, -0.28; 95% CI, -1.11 to 0.56, P = 0.513). During the after-PEMF phase, NRS scores in the experimental group were significantly lower than those in the placebo group during both resting (mean difference, -1.46; 95% CI, -2.06 to -0.85; P = <0.001) and clenching (mean difference, -1.88; 95% CI, -2.74 to -1.02, P = <0.001). The NRS scores did not differ across the groups during the before-PEMF phase for either state but were significantly lower in the experimental group than in the placebo group at T3, T4, and T5 (P <0.01). The average NRS score in the clenching state was significantly greater than in the resting state. CONCLUSIONS: PEMF was effective in reducing orthodontic pain caused by initial archwire placement. REGISTRATION: The trial was not registered. PROTOCOL: The protocol was not published before trial commencement.

Effects of herbal Epimedium on the improvement of bone metabolic disorder through the induction of osteogenic differentiation from bone marrow-derived mesenchymal stem cells.

Herbal Epimedium (HE) has been commonly used as a tonic, antirheumatic agent and in the treatment of bone­associated diseases including osteoporosis. Treatment for osteoporosis is important to increase bone mass density and maintain to balance of bone remodeling. The present study was performed to investigate the effects of HE on mouse bone marrow mesenchymal stem cell (mBMMSC) proliferation and osteogenic differentiation, using MTT assays, proliferating cell nuclear antigen (PCNA) detection and apoptosis and differentiation assays. HE was demonstrated to inhibit the proliferation of mBMMSCs up to 45.43±3.33% and to decrease the level of PCNA expression compared with untreated cells. HE also induced late apoptosis at 24 and 48 h after treatment up to 71.93 and 67.03%, respectively, while only 14.93% of untreated cells exhibited apoptosis. By contrast, HE induced differentiation of mBMMSCs into an osteogenic lineage at the beginning of three weeks after commencement of treatment. This suggested that HE is a candidate as an inducer of osteogenesis from bone marrow mesenchymal stem cells, and additionally has potential for use in the treatment of bone metabolic disorders such as osteoporosis.

Licochalcone A, a natural chalconoid isolated from Glycyrrhiza inflata root, induces apoptosis via Sp1 and Sp1 regulatory proteins in oral squamous cell carcinoma.

Licochalcone A (LCA), a chalconoid derived from root of Glycyrrhiza inflata, has been known to possess a wide range of biological functions such as antitumor, anti-angiogenesis, antiparasitic, anti-oxidant, antibacterial and anti-inflammatory effects. However, the anticancer effects of LCA on oral squamous cell carcinoma (OSCC) have not been reported. Our data showed that LCA inhibited OSCC cell (HN22 and HSC4) growth in a concentration- and time-dependent manner. Mechanistically, it was mediated via downregulation of specificity protein 1 (Sp1) expression and subsequent regulation of Sp1 downstream proteins such as p27, p21, cyclin D1, Mcl-1 and survivin. Here, we found that LCA caused apoptotic cell death in HSC4 and HN22 cells, as characterized by sub-G1 population, nuclear condensation, Annexin V staining, and multi-caspase activity and apoptotic regulatory proteins such as Bax, Bid, Bcl(-xl), caspase-3 and PARP. Consequently, this study strongly suggests that LCA induces apoptotic cell death of OSCC cells via downregulation of Sp1 expression, prompting its potential use for the treatment of human OSCC.