Zingerone induced caspase-dependent apoptosis in MCF-7 cells and prevents 7,12-dimethylbenz(a)anthracene-induced mammary carcinogenesis in experimental rats.

Breast cancer is a prevalent of tumoregenesis in women and reports for the maximum mortality and morbidity in the global. Ginger (Zingiber officinale) is the mainly widespread spice and herbal remedies used in the world. Since antique periods, ginger has been used in Greece, India and China for the curing of upset stomach, nausea, diarrhea, colds, and headaches. The current work was planned to explore the anticancer properties of zingerone (ZO) toward 7,12-dimethylbenz(a)anthracene (DMBA)-treated mammary carcinogenesis in Sprague-Dawley (SD) rats and MCF-7 mammary cancer cells. The mammary carcinogenesis was produced through a single dosage of DMBA (20 mg/kg bwt) mixed in soya oil (1 mL) administrated intragastrically with a gavage. We found improved concentrations of lipid peroxidation (LOOH and TBARS), carcinoembryonic antigen, lowered levels of enzymatic (CAT, GPx, and SOD), and nonenzymatic (vitamin E, GSH, and vitamin C) antioxidant in mammary tissues and plasma of DMBA-induced cancer bearing animals. Moreover, augmented concentrations of phase I (Cyt-b5 and CYP450 ) and reduced levels of phase II (GR and GST) detoxification microsomal proteins in mammary tissues were noticed. ZO administrations significantly reverted back to all these parameters in this way, showing efficient of anticancer effect. Furthermore, our in vitro study also supported the anticancer effect of the treatment of ZO were noticed loss of cell viability, improved reactive oxygen species formation, and reduced MMP. Furthermore, the status of apoptosis proteins such as Bcl-2, Bax, and Bid expressions was determined by using Western blot analysis techniques. Overall, these results proposed the anticancer effect of ZO toward DMBA-induced mammary cancer in SD animals and Michigan cancer foundation-7 mammary cancer cells.

Perineural dexamethasone does not enhance the analgesic efficacy of ultrasound-guided subcostal transversus abdominis plane block during laparoscopic cholecystectomy.

BACKGROUND: Ultrasound-guided transversus abdominis plane (TAP) block is an adjunct therapy to provide effective postoperative analgesia in abdominal surgical procedures. Dexamethasone is a supplement agent that can improve the efficacy of local anesthesia. However, information about its additive effect is limited. This study aimed to compare the analgesic efficiency using ultrasound-guided TAP block with and without perineural dexamethasone for patients who underwent laparoscopic cholecystectomy. METHODS: Sixty patients who underwent laparoscopic cholecystectomy were randomly divided into three groups: group I, controls; group II, TAP; and group III, TAP+perineural dexamethasone supplement. The requirement of additional analgesia and the first-time request of rescue-analgesia were recorded after operation and the numerical rating scale was evaluated at specific intervals. RESULTS: Compared to group I, the first-time requirement of rescue-analgesia in groups II and III was significantly delayed (403.0+/-230.9, 436.0+/-225.3 vs 152.3+/-124.7, P<0.01). Compared with those in group I, patients in groups II and III were associated with lower numerical rating scale pain scores (P<0.01) and less postoperative analgesic consumption (P<0.01). There was no significant difference in the variables mentioned above between groups II and III (P>0.05). CONCLUSION: Perineural dexamethasone has no additive/synergistic effect with subcostal TAP block on analgesic efficacy for the patients undergoing laparoscopic cholecystectomy.

CPEB4-Promoted Paclitaxel Resistance in Ovarian Cancer In Vitro Relies on Translational Regulation of CSAG2.

Background: Drug resistance is a major obstacle in chemotherapy for ovarian cancer, wherein the up regulation of drug-resistant genes plays an important role. The cytoplasmic polyadenylation element binding protein 4 (CPEB4) is an RNA binding protein that controls mRNA cytoplasmic polyadenylation and translation. Methods: The expression of CPEB4 in paclitaxel-resistant ovarian cancer cell lines and recurrent ovarian tumors relative to counterparts was determined by qRT-PCR, Western blotting and immunohistochemistry. The response to paclitaxel treatment was evaluated by cellular viability test and colony formation assay. RNA immunoprecipitation and poly(A) tail test were applied to examine the levels of RNA binding and cytoplasmic polyadenylation. Results: CPEB4 is elevated in paclitaxel-resistant ovarian cancer cells and recurrent ovarian tumors treated with paclitaxel-based chemotherapy. In addition, CPEB4 overexpression promotes paclitaxel resistance in ovarian cancer cells in vitro, and vice versa, CPEB4 knockdown restores paclitaxel sensitivity, indicating that CPEB4 confers paclitaxel resistance in ovarian cancer cells. Mechanistically, CPEB4 binds with the taxol (paclitaxel)-resistance-associated gene-3 (TRAG-3/CSAG2) mRNAs and induces its expression at a translational level. Moreover, CSAG2 expression is upregulated in paclitaxel-resistant ovarian carcinoma and cancer cell lines, and more importantly, siRNA-mediated CSAG2 knockdown overtly attenuates CPEB4-mediated paclitaxel resistance. Conclusion: This study suggests that the drug-resistant protein CSAG2 is translationally induced by CPEB4, which underlies CPEB4-promoted paclitaxel resistance in ovarian cancer in vitro. Thus, interfering CPEB4/CSAG2 axis might be of benefit to overcome paclitaxel-resistant ovarian cancer.

Systematic Review and Meta-analysis of Endostar Combined With Transcatheter Arterial Chemoembolization (TACE) Versus TACE Alone for Hepatocellular Carcinoma.

Many studies have investigated the efficacy of Endostar combined with transcatheter arterial chemoembolization (TACE) versus TACE alone for hepatocellular carcinoma (HCC). A systematic review was conducted to evaluate the efficacy of Endostar. PubMed, Embase, and other databases were searched, and meta-analysis was performed using RevMan 5.3 software. Nine studies, all of which were clinical randomized controlled trials, involving 411 participants were included. The overall response rate, disease control rate and α-fetoprotein negative conversion ratio, and the 6- and 12-month survival rate of HCC patients treated with combined Endostar and TACE were higher than those treated with TACE alone ( P < .01). Furthermore, the incidence of tumor progression was low after Endostar treatment ( P = .005). The incidence of adverse effects (leukocytopenia, liver function damage, and vomiting) was similar in Endostar with TACE and in TACE alone ( P > .05). However, large studies and more randomized trials are necessary to determine the effects of Endostar on HCC.

Synergistic Apoptotic Effect of D-Fraction From Grifola frondosa and Vitamin C on Hepatocellular Carcinoma SMMC-7721 Cells.

The aim of this study was to investigate the anticancer effect of a combination of D-fraction polysaccharide from Grifola frondosa (DFP) and vitamin C (VC) on hepatocellular carcinoma in vitro. DFP is a bioactive extract from the maitake mushroom. Anticancer activity was demonstrated using various concentrations of DFP alone or in combination with VC against the human hepatocarcinoma SMMC-7721 cell line. To investigate the anticancer mechanism, studies designed to detect cell apoptosis were conducted. Results from the MTT assay indicated that a combination of DFP (0.2 mg/mL) and VC (0.3 mmol/L) led to a 70% reduction in cell viability. Flow cytometry results indicated that DFP/VC treatment induced apoptosis in approximately 65% SMMC-7721 cells. Cell cycle analysis identified cell cycle arrest at the G2/M phase following DFP/VC treatment for 48 hours. In addition, cellular morphological changes were observed using transmission electron microscopy. Western blot analysis revealed that the upregulation of BAX, downregulation of Bcl-2, activation of poly-(ADP-ribose)-polymerase (PARP), and the release of cytochrome c were observed in cells treated with the combination of DFP/VC, which showed that the mechanism of anticancer activity in the SMMC-7721 hepatocarcinoma cells involved induction of apoptosis.