Clinical value of ultrasonic indicators in predicting the outcome of caesarean scar pregnancy after pregnancy termination.

BACKGROUND: To investigate the predictive value of ultrasound indicators in early pregnancy for the outcome of caesarean scar pregnancy (CSP) after pregnancy termination. METHODS: This study retrospectively analysed the ultrasound images of 98 CSP patients who underwent transabdominal ultrasound-guided hysteroscopic curettage during early pregnancy at Changsha Hospital for Maternal and Child Health Care between January 2017 and October 2021. Patients were equally divided into a case group and a control group. The case group included 49 CSP patients with postoperative complications, such as intraoperative blood loss ≥ 200 ml or retained products of conception (RPOC). The remaining 49 CSP patients, with similar age and gestational age and with good postoperative outcomes, such as intraoperative blood loss ≤ 50 ml and no RPOC, were included in the control group. CSP was classified into three types according to the location of the gestational sac (GS) relative to the uterine cavity line (UCL) and serosal contour. Differences in ultrasound indicators between the case and control group were compared. RESULTS: There were significant differences between the case and control groups in the mean gestational sac diameter (MGSD), residual myometrium thickness (RMT) between the GS and the bladder, blood flow around the GS at the site of the previous caesarean incision, and types of CSP (P < 0.05). The rs of each ultrasound indicator were as follows: 0.258, -0.485, 0.369, 0.350. The optimal threshold for predicting good postoperative outcomes, such as intraoperative blood loss ≤ 50 ml and no RPOC, by receiver operating characteristic (ROC) curve analysis of the RMT was 2.3 mm. CONCLUSION: Our findings show that the RMT, blood flow around the GS at the site of the previous caesarean incision, and types of CSP have a low correlation with postoperative complications, such as intraoperative blood loss ≥ 200 ml or RPOC, of early pregnancy termination in patients with CSP. To some extent, this study may be helpful for clinical prognostic prediction of patients with CSP and formulation of treatment strategies. Given the low correlation between these three indicators and postoperative complications, further studies are needed to identify indicators that can better reflect the postoperative outcomes of CSP patients.

Linc01133 promotes proliferation and metastasis of human renal cell carcinoma through sponging miR-760.

Renal cell carcinoma (RCC) is one of the most frequent human tumors and has brought great threats to the health of the people around the globe. It was reported that linc01133, a long non-coding RNA (lncRNA), was involved in the pathogenesis and development of several human cancer. But the biological role of linc01133 in RCC is still not understood. The present study aimed to investigate the biological functions of linc01133 in RCC. We did some biological experiments in this study, including quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, MTT assay, wound healing assay, Transwell invasion assay and xenograft tumor assay. In this study, we found the expression levels of linc01133 markedly increased in the RCC tissues compared with the normal tissues. And we found that the over-expressing of linc01133 promoted cell proliferation, migration and invasion, the interfering of linc01133 inhibited cell proliferation, migration and invasion. Furthermore, we found that the interfering of linc01133 inhibited tumor growth in murine xenograft models. Additionally, we found that linc01133 promotes RCC cell proliferation, migration and invasion through sponging miR-760. Collectively, our work preliminarily illuminated the tumor-promoting role of linc01133 in RCC and the potential molecular mechanism. Thus, our study may provide some evidence for the treatment of RCC.

Transient tracer gas measurements: Development and evaluation of a fast-response SF6 measuring system based on quartz-enhanced photoacoustic spectroscopy.

This study aims to develop a fast-response sulfur hexafluoride (SF6 ) measuring system, and evaluate its performance in tracer gas measurements for studying transient airborne contaminant transport. The new system is based on a quartz-enhanced photoacoustic spectroscopy (QEPAS) sensor using a quantum cascade laser. Transient SF6 tracer gas measurements were carried out in an environmental chamber with an instantaneous source using both the QEPAS system and a traditional commercial instrument. Real-time SF6 concentrations, peak SF6 concentrations and average SF6 concentrations for one room time constant under two air change rates obtained by the two instruments were compared. The results show that the QEPAS system, which features a 0.4 s data acquisition interval, can provide detailed real-time SF6 concentrations even when the concentration is changing rapidly. The QEPAS system successfully captured the peak SF6 concentrations for all the studies cases, while commercial instrument failed in most studied cases. In most of the cases, the two instruments obtained similar average SF6 concentrations for one room time constant. However, when the concentration was in rapid change, the two systems would report significantly different results. The QEPAS system can be potentially applied in transient tracer gas measurements under complex scenarios.

Grafting Polymer Brushes by ATRP from Functionalized Poly(ether ether ketone) Microparticles.

Poly(ether ether ketone) (PEEK) is a semi-crystalline thermoplastic with excellent mechanical and chemical properties. PEEK exhibits a high degree of resistance to thermal, chemical, and bio-degradation. PEEK is used as biomaterial in the field of orthopaedic and dental implants; however, due to its intrinsic hydrophobicity and inert surface, PEEK does not effectively support bone growth. Therefore, new methods to modify PEEK's surface to improve osseointegration are key to next generation polymer implant materials. Unfortunately, PEEK is a challenging material to both modify and subsequently characterize thus stymieing efforts to improve PEEK osseointegration. In this manuscript, we demonstrate how surface-initiated atom transfer radical polymerization (SI-ATRP) can be used to modify novel PEEK microparticles (PMP). The hard core-soft shell microparticles were synthesized and characterized by DLS, ATR-IR, XPS and TEM, indicating the grafted materials increased solubility and stability in a range of solvents. The discovered surface grafted PMP can be used as compatibilizers for the polymer-tissue interface.

MiR-302a-3p aggravates myocardial ischemia-reperfusion injury by suppressing mitophagy via targeting FOXO3.

OBJECTIVE: This study aimed to investigate whether the protection of miR-302a-3p in myocardial ischemia-reperfusion injury (MIRI) is mediated through the suppression of mitophagy. METHODS: We constructed a mouse I/R model in vivo by the ligation of left anterior descending coronary artery for 45 min followed by 2 h reperfusion, and an in vitro model by treating mouse cardiomyocytes with hypoxia-reoxygenation (H/R). Knockdown experiments were then performed in vivo and in vitro to determine the effects of miR-302a-3p knockdown on the mitophagy, mitochondrial dysfunction and oxidative stress and apoptosis. The potential targets of miR-302a-3p were further studied by bioinformatics analysis, luciferase assays, quantitative real-time PCR and western blotting. RESULTS: MiR-302a-3p expression was significantly upregulated in mice subjected to MIRI and in H/R-treated mouse cardiomyocytes. Functional analyses demonstrated that inhibition of miR-302a-3p protected cardiac tissues against I/R-induced apoptosis and mitophagy, mitochondrial damage and mitochondrial oxidative stress. Furthermore, FOXO3 was identified as the direct target of miR-302a-3p. Mechanistically, knockdown of FOXO3 partially reversed the cardioprotective effects of miR-302a-3p inhibitor. CONCLUSION: Our study suggested that inhibition of miR-302a-3p promoted mitochondrial autophagy and inhibited oxidative stress by targeting FOXO3 to suppress myocardial apoptosis, representing a potential target for MIRI treatment.

Direct ATRP of Methacrylic Acid with Iron-Porphyrin Based Catalysts.

An iron porphyrin catalyst, derived from the active center of proteins such as horseradish peroxidase and hemoglobin, was successfully used for the atom transfer radical polymerizations (ATRP) of methacrylic acid. ATRP of methacrylic acid and other acidic monomers is challenging due to Cu complexation by carboxylates, protonation of the ligand, and displacement of the halogen chain end. A robust mesohemin-based catalyst provided controlled ATRP of methacrylic acid, yielding poly(methacrylic acid) with Mn ≥ 20000 and dispersity D < 1.5. Retention of halogen chain end was confirmed by successful chain extension of a poly-(methacrylic acid)-Br macroinitiator.

Knockdown of long non-coding RNA linc00511 suppresses proliferation and promotes apoptosis of bladder cancer cells via suppressing Wnt/ß-catenin signaling pathway.

More and more studies have shown that long non-coding RNAs (lncRNAs) play critical roles in various biological processes of bladder cancer, including proliferation, apoptosis, migration and cell cycle arrest. LncRNA long intergenic noncoding RNA 00511 (linc00511) is one of the lncRNAs highly expressed in bladder cancer tissues and cells. However, little is known about the roles and mechanisms of linc00511 in bladder cancer. Here, we demonstrated that linc00511 was highly expressed in bladder cancer tissues and cells. Linc00511 knockdown could cause the cell proliferation suppression and cell cycle arrest, which were mediated by p18, p21, CDK4, cyclin D1 and phosphorylation Rb. Suppressed linc00511 could induce the apoptosis in T24 and BIU87 cells via activating the caspase pathway. Down-regulation of linc00511 could also suppress the migration and invasion of T24 and BIU87 cells. In addition, we found that the expression of linc00511 was negatively correlated with that of miR-15a-3p in the clinical bladder cancer samples. Further mechanistic studies showed that linc00511 knockdown induced proliferation inhibition, and apoptosis increase might be regulated through suppressing the activities of Wnt/ß-catenin signaling pathway. Thus, we revealed that knockdown of linc00511 suppressed the proliferation and promoted apoptosis of bladder cancer cells through suppressing the activities of Wnt/ß-catenin signaling pathway. Moreover, we suggested that linc00511 could be a potential therapeutic target and novel biomarker in bladder cancer.

Betulinic acid induces apoptosis and inhibits metastasis of human renal carcinoma cells in vitro and in vivo.

Betulinic acid (BA), a natural product with a broad range of biological properties, is a lupane-type pentacyclic triterpene isolated from various plants. Evidence is accumulating that BA is cytotoxic against multiple types of human cancer cells; however, its effects on renal carcinoma cells remain obscure. This study aimed to evaluate the anticancer activity of BA in human renal cancer cells in vitro and in vivo. In the current study, we found that BA inhibited renal cancer cell proliferation in a time-dependent and dose-dependent manner in vitro. Moreover, flow cytometry analysis revealed that BA affected the survival of renal cancer cells via the induction of apoptosis. Western blot analysis showed that the occurrence of apoptosis was associated with upregulation of Bcl2-associated X protein and cleaved caspase-3 and downregulation of B-cell lymphoma 2 in renal cancer cells. Additionally, BA treatment augmented the production of reactive oxygen species and induced a significant loss of mitochondrial membrane potential in renal cancer cells, suggesting that BA may trigger apoptosis via the mitochondria-mediated apoptotic pathway. Furthermore, the migrative and invasive capabilities of renal cancer cells were markedly repressed by BA treatment, which was related to upregulation of matrix metalloproteinase (MMP)2, MMP9, and vimentin, and downregulation of tissue inhibitor of metalloproteinase 2 and E-cadherin. Notably, administration of BA retarded tumor growth in 786-O-bearing mice in vivo. Taken together, our results demonstrated the anticancer potential of BA in human renal cancer cells by triggering apoptosis and suppressing migration and invasion.

Over-expression of ARHGAP18 suppressed cell proliferation, migration, invasion, and tumor growth in gastric cancer by restraining over-activation of MAPK signaling pathways.

Globally, gastric cancer is the second-greatest cause of cancer death. ARHGAP18 belongs to the Rho family of GTPases which is involved in cellular migration, invasion, and growth phases. The aim of the present study was to investigate whether ARHGAP18 could regulate cell proliferation, migration, invasion, and related molecular mechanisms in gastric cancer. Cell Counting Kit-8 (CCK-8) assay results showed that following transfection of a recombinant plasmid, over-expression of ARHGAP18 inhibited cell viability in MGC-803 and BGC823 cells. Using in vitro transwell analysis, migration and invasion abilities were significantly inhibited in cells with high ARHGAP18 expression. Phosphorylation levels of ERK, JNK, and p38 by Western blot analysis significantly declined after transfection of cells with the ARHGAP18 plasmid. Expression levels of ROCK, MTA1, and MMP-2/9 were detected by real-time polymerase chain reaction and Western blotting, and over-expression of ARHGAP18 decreased the expression levels of ROCK, MTA1, and MMP-9. A further in vivo tumor formation study in nude mice indicated that over-expression of ARHGAP18 delayed the progress of tumor formation. These results indicate that ARHGAP18 could act as a tumor suppressor and may serve as a promising therapeutic strategy for gastric cancer.

Ror2, a Developmentally Regulated Kinase, Is Associated With Tumor Growth, Apoptosis, Migration, and Invasion in Renal Cell Carcinoma.

Renal cell carcinoma (RCC) represents one of the most resistant tumors to radiation and chemotherapy. Current therapies for RCC patients are inefficient due to the lack of diagnostic and therapeutic markers. The expression of novel tumor-associated kinases has the potential to dramatically shape tumor cell behavior. Identifying tumor-associated kinases can lend insight into patterns of tumor growth and characteristics. In the present study, we investigated the receptor tyrosine kinase-like orphan receptor 2 (Ror2), a new tumor-associated kinase, in RCC primary tumors and cell lines. Knockdown of Ror2 expression in RCC cells with specific shRNA significantly reduced cell proliferation and induced apoptosis. Using in vitro migration and Matrigel invasion assays, we found that cell migration and invasive ability were also significantly inhibited. In RCC, Ror2 expression correlated with expression of genes involved at the cell cycle and migration, including PCNA, CDK1, TWIST, and MMP-2. Furthermore, in vivo xenograft studies in nude mice revealed that administration of a Ror2 shRNA plasmid significantly inhibited tumor growth. These findings suggest a novel pathway of tumor-promoting activity by Ror2 within renal carcinomas, with significant implications for unraveling the tumorigenesis of RCC.

ß-Catenin promotes cell proliferation, migration, and invasion but induces apoptosis in renal cell carcinoma.

ß-Catenin (CTNNB1 gene coding protein) is a component of the Wnt signaling pathway that has been shown to play an important role in the formation of certain cancers. Abnormal accumulation of CTNNB1 contributes to most cancers. This research studied the involvement of ß-catenin in renal cell carcinoma (RCC) cell proliferation, apoptosis, migration, and invasion. Proliferation, cell cycle, and apoptosis were analyzed by using Cell Counting Kit-8 and by flow cytometry. Migration and invasion assays were measured by transwell analysis. Real-time polymerase chain reaction and Western blot analysis were used to detect the expression of CTNNB1, ICAM-1, VCAM-1, CXCR4, and CCL18 in RCC cell lines. It was found that CTNNB1 knockdown inhibited cell proliferation, migration, and invasion and induced apoptosis of A-498 cells. CTNNB1 overexpression promoted cell proliferation, migration, and invasion and inhibited apoptosis of 786-O cells. Moreover, knockdown of CTNNB1 decreased the levels of ICAM-1, VCAM-1, CXCR4, and CCL18 expression, but CTNNB1 overexpression increased the expression of ICAM-1, VCAM-1, CXCR4, and CCL18. Further in vivo tumor formation study in nude mice indicated that inhibition of CTNNB1 delayed the progress of tumor formation through inhibiting PCNA and Ki67 expression. These results indicate that CTNNB1 could act as an oncogene and may serve as a promising therapeutic strategy for RCC.

Knockdown of Cyclin-Dependent Kinase Inhibitor 3 Inhibits Proliferation and Invasion in Human Gastric Cancer Cells.

Cyclin-dependent kinase inhibitor 3 (CDKN3) has been reported to promote tumorigenesis. Since it is unclear whether CDKN3 participates in the development of human gastric cancer, this study assessed the association between CDKN3 expression and cell biological function and demonstrated the clinical significance and prognosis of CDKN3 in human gastric cancer. In this study, we found that CDKN3 showed a high expression in 35 paired human gastric cancer tissues and was correlated with poor patient survival, AJCC clinical staging, and recurrence. Silencing of CDKN3 in human gastric cancer cells can significantly reduce proliferation, migration, invasion, and adhesion abilities. Also, silencing of CDKN3 in human gastric cancer cells can induce G0-G1 cell cycle arrest and apoptosis. Detection of cell cycle marker expression showed that CDKN3 knockdown promotes cell cycle arrest by decreasing the expression of CDK2, CDC25A, CCNB1, and CCNB2 in human gastric cancer cells. The results of this study will help elucidate the oncogene function of CDKN3 in human gastric cancer.

Inhibition of MDM2 Re-Sensitizes Rapamycin Resistant Renal Cancer Cells via the Activation of p53.

BACKGROUND/AIMS: Rapamycin is a potential anti-cancer agent, which modulates the activity of mTOR, a key regulator of cell growth and proliferation. However, several types of cancer cells are resistant to the anti-proliferative effects of rapamycin. In this study, we report a MDM2/p53-mediated rapamycin resistance in human renal cancer cells. METHODS: Trypan blue exclusion tests were used to determine the cell viability. Changes in mRNA and protein expression were measured using real-time PCR and western blot, respectively. Xenograft models were established to evaluate the in vivo effects of rapamycin combined with a MDM2 inhibitor. RESULTS: Rapamycin treatment suppresses the expression of MDM2 and exogenous overexpression of MDM2 in A498 cells contributes to rapamycin resistance. By establishing a rapamycin resistant cell line, we observed that MDM2 was significantly upregulated in rapamycin resistant cells than that in rapamycin sensitive cells. Importantly, the rapamycin resistant cells demonstrated attenuated accumulation of p53 in the nucleus in response to rapamycin treatment. Moreover, the inhibition of MDM2 by siMDM2 sensitizes A498 cells to rapamycin through the activation of p53. In both in vitro and in vivo models, the combination of rapamycin with the MDM2 inhibitor, MI-319, demonstrated a synergistic inhibitory effect on rapamycin resistant cells. CONCLUSION: Our study reports a novel mechanism for rapamycin resistance in human renal cancer and provides a new perspective for the development of anti-cancer drugs.

Synergistic effects of snail and quercetin on renal cell carcinoma Caki-2 by altering AKT/mTOR/ERK1/2 signaling pathways.

Renal cell carcinoma has become the most common subtype of kidney cancer, and has the highest propensity to manifest as metastatic disease. Because of lack of knowledge in events that correlated with tumor cell migration and invasion, few therapeutic options are available. Therefore, in current study, we explore the anti-tumoral effect of a potential chemopreventive natural product, quercetin, combined with anti-sense oligo gene therapy (inhibiting Snail gene). We found that either one of them had the remarkable effects in suppressing cell proliferation and migration, inducing cell cycle arrest and apoptosis in a ccRCC cell line, Caki-2 cells. The combination of both means provides even strong suppressive effects toward these ccRCC cells. Our study, for the first time, provides the possibility of using a novel treatment for renal cancer, by combining natural product and gene therapy.

[Change and clinical significance of peripheral blood T-lymphocyte functional subsets in acute graft-versus-host disease].

OBJECTIVE: This study was aimed to detect the change of T-lymphocyte functional subsets marked by CCR7 and CD45RA in the aGVHD within 100 days after allo-HSCT and to explore its clinical significance. METHODS: The peripheral blood of 42 patients after allo-HSCT was collected every two weeks since hematopoietic reconstitution. The expression of CD3, CD4, CD8, CCR7 and CD45RA-marked T-lymphocytes was detected by flow cytometry, the relationship between their expression and the prognosis of aGVHD was analyzed. RESULTS: The percentage and the absolute count of CCR7(+) T lymphocyte were significantly reduced in aGVHD. The percentage of T(naïve), T(CM), T(EM) and the absolute count of T(naïve), T(EM), TTD were sharply reduced in aGVHD, moreover has changed correspondingly with outcome of aGVHD. The percentage of CD3, CD4, CD8-marked T-lymphocyte subsets did not significantly changed. CONCLUSION: T-lymphocyte functional subsets marked by CCR7 and CD45RA are a valuable indicator to monitor early immune reconstruction for patients with the aGVHD after allo-HSCT.

Bufalin Induces Mitochondria-Dependent Apoptosis in Pancreatic and Oral Cancer Cells by Downregulating hTERT Expression via Activation of the JNK/p38 Pathway.

Bufalin, a digoxin-like active component of the traditional Chinese medicine Chan Su, exhibits potent antitumor activities in many human cancers. Bufalin induces mitochondria-dependent apoptosis in cancer cells, but the detailed molecular mechanisms are largely unknown. hTERT, the catalytic subunit of telomerase, protects against mitochondrial damage by binding to mitochondrial DNA and reducing mitochondrial ROS production. In the present study, we investigated the effects of bufalin on the cell viability, ROS production, DNA damage, and apoptosis of CAPAN-2 human pancreatic and CAL-27 human oral cancer cells. Bufalin reduced CAPAN-2 and CAL-27 cell viability with IC50 values of 159.2 nM and 122.6 nM, respectively. The reduced cell viability was accompanied by increased ROS production, DNA damage, and apoptosis and decreased expression of hTERT. hTERT silencing in CAPAN-2 and CAL-27 cells by siRNA resulted in increased caspase-9/-3 cleavage and DNA damage and decreased cell viability. Collectively, these data suggest that bufalin downregulates hTERT to induce mitochondria-dependent apoptosis in CAPAN-2 and CAL-27 cells. Moreover, bufalin increased the phosphorylation of JNK and p38-MAPK in CAPAN-2 and CAL-27 cells, and blocking the JNK/p38-MAPK pathway using the JNK inhibitor SP600125 or the p38-MAPK inhibitor SB203580 reversed bufalin-induced hTERT downregulation. Thus, the JNK/p38 pathway is involved in bufalin-induced hTERT downregulation and subsequent induction of apoptosis by the mitochondrial pathway.

Identification of TGF-ß-activated kinase 1 as a possible novel target for renal cell carcinoma intervention.

Renal cell carcinoma (RCC) is common renal malignancy within poor prognosis. TGF-ß-activated kinase 1 (TAK1) plays vital roles in cell survival, apoptosis-resistance and carcinogenesis through regulating nuclear factor-κB (NF-κB) and other cancer-related pathways. Here we found that TAK1 inhibitors (LYTAK1, 5Z-7-oxozeanol (5Z) and NG-25) suppressed NF-κB activation and RCC cell (786-O and A489 lines) survival. TAK1 inhibitors induced apoptotic cytotoxicity against RCC cells, which was largely inhibited by the broad or specific caspase inhibitors. Further, shRNA-mediated partial depletion of TAK1 reduced 786-O cell viability whiling activating apoptosis. Significantly, TAK1 was over-expressed in human RCC tissues, and its level was correlated with phosphorylated NF-κB. Finally, kinase inhibition or genetic depletion of TAK1 enhanced the activity of vinblastine sulfate (VLB) in RCC cells. Together, these results suggest that TAK1 may be an important oncogene or an effective target for RCC intervention.

Stable knockdown of protein kinase CK2-alpha (CK2α) inhibits migration and invasion and induces inactivation of hedgehog signaling pathway in hepatocellular carcinoma Hep G2 cells.

Protein kinase CK2-alpha (CK2α), one isoform of the catalytic subunits of serine/threonine kinase CK2, has been indicated to participate in tumorigenesis of various malignancies, including hepatocellular carcinoma (HCC). In the present study, in order to explore the potential role of CK2α in human HCC, we employed short hairpin RNA (shRNA)-mediated RNA interference (RNAi) technology to inhibit the endogenous CK2α expression in HCC cells and established a Hep G2 cell line with stable knockdown of CK2α. Results from wound healing and transwell invasion assays indicated that stable knockdown of CK2α markedly inhibited Hep G2 cell migration and invasion as compared with those transfected with a negative control plasmid. This alteration was accompanied with expression down-regulation of matrix metalloproteinase (MMP)-2, MMP-9, Snail, Slug, Vimentin, and up-regulation of epithelial cadherin (E-cadherin). Moreover, CK2α silencing also induced inactivation of Hedgehog signaling pathway by inhibiting Gli1 and Patched homolog 1 (PTCH1) expressions in HCC cells. Collectively, these results demonstrate that knockdown of CK2α can suppress cell migration and invasion, reduces expression of MMPs, inhibits epithelial-mesenchymal transition (EMT) process and induces inactivation of Hedgehog pathway in HCC cells in vitro. Our study provides in vitro evidence to demonstrate that the pathogenesis of human HCC may be correlated with the high expression of CK2α.

Suppression of tumor necrosis factor receptor-associated protein 1 expression induces inhibition of cell proliferation and tumor growth in human esophageal cancer cells.

Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a molecular chaperone involved in multidrug resistance and antiapoptosis in some human tumors, but its regulatory mechanisms have not been revealed in esophageal squamous cell carcinoma (ESCC). In this study, 138 specimens of ESCC were analyzed. TRAP1 was overexpressed in ESCC, particularly in poorly differentiated tumors. To further explore the molecular regulatory mechanism, we constructed specific small interfering RNA-expressing vectors targeting Trap1, and knocked down Trap1 expression in the esophageal cancer cell lines ECA109 and EC9706. Knockdown of Trap1 induced increases in reactive oxygen species and mitochondrial depolarization, which have been proposed as critical regulators of apoptosis. The cell cycle was arrested in G2/M phase, and in vitro inhibition of cell proliferation was confirmed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide and bromodeoxyuridine assays. Furthermore, re-expression of TRAP1 in Trap1 small interfering RNA-transfected ESCC cells restored cell proliferation and cell apoptosis. Bioluminescence of subcutaneously xenografted ESCC tumor cells demonstrated significant inhibition of in vivo tumor growth by Trap1 knockdown. This study shows that TRAP1 was overexpressed in most patients with ESCC, and caused an increase in antiapoptosis potency. TRAP1 may be regarded as a target in ESCC biotherapy.

The association between VDR polymorphisms and renal cell carcinoma susceptibility: a meta-analysis.

Vitamin D receptor (VDR) gene polymorphisms have previously been associated with susceptibility to renal cell carcinoma, although the findings are inconsistent. This study therefore evaluated the association of three single nucleotide polymorphisms (SNPs) in VDR (FokI, BsmI, and TaqI) with the risk of renal cell carcinoma in five previous studies of a total of 1,510 cases and 2,101 controls identified from PubMed, Web of Science, Embase, and Wanfang databases. Pooled odds ratios (ORs) and corresponding 95 % confidence intervals (CIs) were calculated, and stratified analysis by ethnicity was conducted for further estimation. All statistical analyses were conducted using STATA software. Obvious heterogeneity was noted among the five studies. The VDR BsmI polymorphism was not found to be associated with renal cell carcinoma risk, although subgroup analysis revealed a significant association with renal cell carcinoma risk in Asians (b vs B OR=1.479, 95 % CI=1.171-1.869, P OR=0.001 and bb vs BB OR=2.608, 95 % CI=1.529-4.449, P OR=0.001). No significant association was found between renal cell carcinoma risk and either FokI or TaqI polymorphisms in different models and populations. Further large-scale studies are required to confirm these conclusions.