Inhibition of GLUD1 mediated by LASP1 and SYVN1 contributes to hepatitis B virus X protein-induced hepatocarcinogenesis.

Glutamate dehydrogenase 1 (GLUD1) is implicated in oncogenesis. However, little is known about the relationship between GLUD1 and hepatocellular carcinoma (HCC). In the present study, we demonstrated that the expression levels of GLUD1 significantly decreased in tumors, which was relevant to the poor prognosis of HCC. Functionally, GLUD1 silencing enhanced the growth and migration of HCC cells. Mechanistically, the upregulation of interleukin-32 through AKT activation contributes to GLUD1 silencing-facilitated hepatocarcinogenesis. The interaction between GLUD1 and AKT, as well as α-ketoglutarate regulated by GLUD1, can suppress AKT activation. In addition, LIM and SH3 protein 1 (LASP1) interacts with GLUD1 and induces GLUD1 degradation via the ubiquitin-proteasome pathway, which relies on the E3 ubiquitin ligase synoviolin (SYVN1), whose interaction with GLUD1 is enhanced by LASP1. In hepatitis B virus (HBV)-related HCC, the HBV X protein (HBX) can suppress GLUD1 with the participation of LASP1 and SYVN1. Collectively, our data suggest that GLUD1 silencing is significantly associated with HCC development, and LASP1 and SYVN1 mediate the inhibition of GLUD1 in HCC, especially in HBV-related tumors.

Hepatitis B virus core protein stabilizes RANGAP1 to upregulate KDM2A and facilitate hepatocarcinogenesis.

PURPOSE: As a vital component of the hepatitis B virus (HBV) nucleocapsid, HBV core protein (HBC) contributes to hepatocarcinogenesis. Here, we aimed to assess the effects of RANGAP1 and KDM2A on tumorigenesis induced by HBC. METHODS: Co-immunoprecipitation (Co-IP) combined with mass spectrometry were utilized to identify the proteins with the capacity to interact with HBC. The gene and protein levels of RANGAP1 and KDM2A in hepatocellular carcinoma (HCC) and HBV-positive HCC tissues were evaluated using different cohorts. The roles of RANGAP1 and KDM2A in HCC cells mediated by HBC were investigated in vitro and in vivo. Co-IP and western blot were used to estimate the interaction of HBC with RANGAP1 and KDM2A and assess RANGAP1 stabilization regulated by HBC. RESULTS: We discovered that HBC could interact with RANGAP1 and KDM2A, the levels of which were markedly elevated in HCC tissues. Relying on RANGAP1 and KDM2A, HBC facilitated HCC cell growth and migration. The increased stabilization of RANGAP1 mediated by HBC was relevant to the disruption of the interaction between RANGAP1 and an E3 ligase SYVN1. RANGAP1 interacted with KDM2A, and it further promoted KDM2A stabilization by disturbing the interaction between KDM2A and SYVN1. HBC enhanced the interaction of KDM2A with RANGAP1 and upregulated the expression of KDM2A via RANGAP1 in HCC cells. CONCLUSIONS: These findings demonstrate a novel mechanism by which HBC facilitates hepatocarcinogenesis. RANGAP1 and KDM2A could act as potential molecular targets for treating HBV-associated malignancy.

Quantitation of 5α-androstanedione in normal women and women with PCOS.

In vitro studies show that 5α-androstane-3,17-dione (5α-A) is an important intermediate in the formation of dihydrotestosterone (DHT) from androstenedione (A) in women and men. Many studies involving hyperandrogenism, hirsutism, and polycystic ovary syndrome (PCOS) have measured A, testosterone (T), and DHT, but not 5α-A due to lack of a readily available assay to quantify this androgen. We have developed a specific and sensitive radioimmunoassay to measure 5α-A levels, together with A, T, and DHT, in both serum and genital skin. The present study involves 2 cohorts. Cohort 1 included 23 mostly postmenopausal women who provided both serum and genital skin to measure those androgens. In cohort 2, serum androgen levels were compared between women with PCOS and non-PCOS controls. Tissue-to-serum ratios were significantly higher for 5α-A and DHT as compared to A and T. None of the androgens showed a significant correlation between serum and genital tissue. In serum, 5α-A was significantly correlated with A, T, and DHT. In cohort 2, A, T, and DHT were significantly higher in the PCOS group compared to the control group. In contrast, 5α-A levels were similar between the 2 groups. Our findings support the view that 5α-A is an important intermediate in DHT formation in genital skin. Also, the relatively low levels of 5α-A in PCOS women suggest that it may play a more important intermediate role in the conversion of A to androsterone glucuronide.

Hepatitis B virus X protein promotes MAN1B1 expression by enhancing stability of GRP78 via TRIM25 to facilitate hepatocarcinogenesis.

BACKGROUND: GRP78 has been implicated in hepatocarcinogenesis. However, the clinical relevance, biological functions and related regulatory mechanisms of GRP78 in hepatitis B virus (HBV)-associated hepatoma carcinoma (HCC) remain elusive. METHODS: The association between GRP78 expression and HBV-related HCC was investigated. The effects of HBV X protein (HBX) on GRP78 and MAN1B1 expression, biological functions of GRP78 and MAN1B1 in HBX-mediated HCC cells and mechanisms related to TRIM25 on GRP78 upregulation to induce MAN1B1 expression in HBX-related HCC cells were examined. RESULTS: GRP78 expression was correlated with poor prognosis in HBV-positive HCC. HBX increased MAN1B1 protein expression depending on GRP78, and HBX enhanced the levels of MAN1B1 to promote proliferation, migration and PI3-K/mTOR signalling pathway activation in HCC cells. GRP78 activates Smad4 via its interaction with Smad4 to increase MAN1B1 expression in HBX-expressing HCC cells. TRIM25 enhanced the stability of GRP78 by inhibiting its ubiquitination. HBX binds to GRP78 and TRIM25 and accelerates their interaction of GRP78 and TRIM25, leading to an increase in GRP78 expression. CONCLUSIONS: HBX enhances the stability of GRP78 through TRIM25 to increase the expression of MAN1B1 to facilitate tumorigenesis, and we provide new insights into the molecular mechanisms underlying HBV-induced malignancy.

Xinfuli granule alleviates metabolic remodeling through inhibition of endoplasmic reticulum stress and mitochondrial injury in heart failure.

ETHNOPHARMACOLOGICAL RELEVANCE: "Qi deficiency-blood stasis-water retention syndrome" was the most frequent syndrome among heart failure(HF) patients according to Traditional Chinese Medicine (TCM) theory. Xinfuli Granule (XG) was constructed on the basis of classical formula "Baoyuan decoction" to enhance the function of nourishing Qi, activating blood and removing water retention. XG treatment has obtained clinical effect on HF patients. AIM OF THE STUDY: The regulation of XG on energy metabolism of HF was investigated with special focus on endoplasmic reticulum stress (ERS) and mitochondrial function. MATERIALS AND METHODS: Components of XG was acquired by UPLC/Q-TOF-MS Analysis, left anterior descending ligation(LAD)-induced HF rats model and hypoxia-ischemia(H-I)-induced H9c2 cells model were constructed to evaluate the effect of XG treatment. Cardiac function was evaluated by echocardiographic parameters, energy metabolism was evaluated by metabolites and ATP/ADP/AMP levels in blood samples, cardiomyocyte morphology and myocardial fibrosis were assessed by HE staining and Masson staining, mitochondrial ultrastructure was observed under Transmission Electron Microscope, viability and apoptosis rate of H9c2 cells was detected by cell counting kit-8 reaction and flow cytometry analysis, respectively. Mitochondrial membrane potential (MMP) of H9c2 cells was observed by JC-1 kit under fluorescent microscope, expression of peroxisome-proliferator-activated receptor (PPAR)-coactivator (PGC1α), ERS-related genes and RHOA/ROCK pathway were analysed by Quantitative Real-time PCR (RT-qPCR) and Western Blot. RESULTS: Here, we showed that XG alleviated cardiac metabolic remodeling and stimulated ATP production through elevated expression of PGC1α in HF rats. XG also helped recover mitochondrial deformation and decrease apoptosis rate accompanied by an increase of the Bcl2/Bax ratio and the mitochondrial membrane potential in hypoxia-ischemia (H-I) H9c2 cells. In addition, we found that XG downregulated ERS-related proteins ATF4, CHOP, Phospho-eIF2α, and Phospho-PERK, and suppressed the RHOA/ROCK pathway, which served as a potential mediator of ERS. CONCLUSIONS: we found that XG improved energy production by alleviating mitochondrial injury and inhibiting ERS in heart failures mediated by the RHOA/ROCK pathway.

The emerging role of DEAD/H-box helicases in hepatitis B virus infection.

DEAD/H-box helicases are an essential protein family with a conserved motif containing unique amino acid sequences (Asp-Glu-Ala-Asp/His). Current evidence indicates that DEAD/H-box helicases regulate RNA metabolism and innate immune responses. In recent years, DEAD/H-box helicases have been reported to participate in the development of a variety of diseases, including hepatitis B virus (HBV) infection, which is a significant risk factor for hepatic fibrosis, cirrhosis, and liver cancer. Furthermore, emerging evidence suggests that different DEAD/H-box helicases play vital roles in the regulation of viral replication, based on the interaction of DEAD/H-box helicases with HBV and the modulation of innate signaling pathways mediated by DEAD/H-box helicases. Besides these, HBV can alter the expression and activity of DEAD/H-box helicases to facilitate its biosynthesis. More importantly, current investigation suggests that targeting DEAD/H-box helicases with appropriate compounds is an attractive treatment strategy for the virus infection. In this review, we delineate recent advances in molecular mechanisms relevant to the interplay of DEAD/H-box helicase and HBV and the potential of targeting DEAD/H-box helicase to eliminate HBV infection.

Regulation of epithelial-mesenchymal transition by protein lysine acetylation.

The epithelial-mesenchymal transition (EMT) is a vital driver of tumor progression. It is a well-known and complex trans-differentiation process in which epithelial cells undergo morphogenetic changes with loss of apical-basal polarity, but acquire spindle-shaped mesenchymal phenotypes. Lysine acetylation is a type of protein modification that favors reversibly altering the structure and function of target molecules via the modulation of lysine acetyltransferases (KATs), as well as lysine deacetylases (KDACs). To date, research has found that histones and non-histone proteins can be acetylated to facilitate EMT. Interestingly, histone acetylation is a type of epigenetic regulation that is capable of modulating the acetylation levels of distinct histones at the promoters of EMT-related markers, EMT-inducing transcription factors (EMT-TFs), and EMT-related long non-coding RNAs to control EMT. However, non-histone acetylation is a post-translational modification, and its effect on EMT mainly relies on modulating the acetylation of EMT marker proteins, EMT-TFs, and EMT-related signal transduction molecules. In addition, several inhibitors against KATs and KDACs have been developed, some of which can suppress the development of different cancers by targeting EMT. In this review, we discuss the complex biological roles and molecular mechanisms underlying histone acetylation and non-histone protein acetylation in the control of EMT, highlighting lysine acetylation as potential strategy for the treatment of cancer through the regulation of EMT. Video Abstract.

Myosin light chain 9 promotes the proliferation, invasion, migration and angiogenesis of colorectal cancer cells by binding to Yes-associated protein 1 and regulating Hippo signaling.

Colorectal cancer is a common type of cancer with high incidence and poor prognosis. Increased expression of myosin light chain 9 (MYL9) has been reported in early-stage and recurrent colorectal cancer tissues. This study aimed to investigate the precise role of MYL9 on the progression of colorectal cancer. MYL9 expression in several colorectal cancer cell lines was detected by Western blotting and RT-qPCR. Following MYL9 overexpression or knockdown, MYL9 expression was determined via RT-qPCR. Cell proliferation was detected with Cell Counting Kit-8 assay. Cell invasion, migration and angiogenesis were, respectively, examined with transwell, wound healing and tube formation assays. The binding between MYL9 and Yes-associated protein 1 (YAP1) was verified by a co-immunoprecipitation assay. The expression of YAP1, connective tissue growth factor and cysteine-rich angiogenic inducer 61 was examined by Western blotting. Subsequently, YAP1 silencing or Hippo antagonist was performed to clarify the regulatory mechanisms of MYL9 in colorectal cancer progression. Experimental results showed that MYL9 expression was elevated in colorectal cancer cell lines. MYL9 overexpression promoted cell proliferation, invasion, migration and angiogenesis, while silencing of MYL9 exerted the opposite effects. Results of co-immunoprecipitation assay indicated that MYL9 could bind to YAP1. Further experiments revealed that MYL9 affected the expression of YAP1 and its downstream signaling proteins. Afterward, YAP1 knockdown or the addition of Hippo antagonist inhibited the proliferation, invasion, migration and angiogenesis of colorectal cancer cells. Overall, MYL9 promotes the proliferation, invasion, migration and angiogenesis of colorectal cancer cells by binding to YAP1 and thereby activating Hippo signaling.

Simple and accurate visual detection of single nucleotide polymorphism based on colloidal gold nucleic acid strip biosensor and primer-specific PCR.

Single nucleotide polymorphism (SNP) was associated with many human diseases, therefore, SNP detection was important for early diagnosis and clinical prognosis. Herein, a simple and accurate method for visual detection SNP sites (A/A, G/G, A/G) in CYP1A1 gene related to cancers based on colloidal gold nucleic acid strip biosensor and primer-specific polymerase chain reaction (PCR) was established. This method could directly distinguish SNP sites on strip biosensor by introducing twice PCR amplifications. The second PCR (primer-specific PCR) was performed using specific product of the first PCR as template, thus this twice PCR could reduce non-specific amplification greatly and obtain target product. In addition, single-strand or double-strand DNA (ssDNA or dsDNA) was accurately produced by introducing mismatched base at the 3' end of forward primers in primer-specific PCR. The designed strip biosensor could only combine with the ssDNA, thus visual detection of SNP could be achieved within 10 min by color difference of a pair of strips. 61 human blood samples by this method were identical with those of pyrosequencing. This method had the advantages of rapid, visual and low-cost and was expected to be applied in medical diagnosis.

Oncogene Lin28B increases chemosensitivity of colon cancer cells in a let-7-independent manner.

Lin-28 homolog B (Lin28B) is a RNA binding protein conserved between Caenorhabditis elegans and humans, and it has important roles in regulating development. The overexpression of Lin28B has been observed in various human malignant tumors and the upregulation of Lin28B predicts tumor progression and/or poor prognosis. The majority of studies suggested that Lin28B is an oncogene that promotes the proliferation and metastasis of cancer cells. However, few studies have focused on the function of Lin28B in chemotherapy. In the present study, the role of Lin28B in the chemosensitivity of colon cancer cells to 5-fluorouracil (5-FU) was detected by establishing a Lin28B over-expressing HCT116 (EGFP-Lin28B-HCT116) cell line. In accordance with the immunohistochemistry results, Lin28B-GFP expression was predominantly distributed in the cytoplasm, and the overexpression of Lin28B was confirmed using quantitative polymerase chain reaction and western blot analysis. The control EGFP-HCT116 and Lin28B over-expressing EGFP-Lin28B-HCT116 cells were then exposed to various concentrations of 5-FU for 48 h. A luminescence-based cell viability assay was used to detect the effect of Lin28B on the chemotherapeutic sensitivity of colon cancer cells. It was demonstrated that overexpression of Lin28B improved the chemotherapeutic sensitivity of colon cancer cells to 5-FU. Additional investigation revealed that Lin28B enhanced the chemosensitivity of colon cancer cells by promoting cell apoptosis induced by 5-FU; however, this effect was independent of Lin28B inhibiting the biogenesis of let-7, the well-known target of Lin28B. The mechanism of this effect of Lin28B on the chemosensitivity of cells requires additional investigation. The present study suggested that Lin28B may act as a biomarker for predicting chemotherapy sensitivity in patients with colon cancer.

Separation and determination of peptide metabolite of Bacillus licheniformis in a microbial fuel cell by high-speed capillary micellar electrokinetic chromatography.

A method using high-speed capillary micellar electrokinetic chromatography and a microbial fuel cell was applied to determine the metabolite of the peptides released by Bacillus licheniformis. Two peptides, l-carnosine and l-alanyl-l-glutamine were used as the substrate to feed Bacillus licheniformis in a microbial fuel cell. The metabolism process of the bacterium was monitored by analyzing the voltage outputs of the microbial fuel cell. A home-made spontaneous injection device was applied to perform high-speed capillary micellar electrokinetic chromatography. Under the optimized conditions, tryptophan, glycine, valine, tyrosine and the two peptides could be rapidly separated within 2.5 min with micellar electrokinetic chromatography mode. Then the method was applied to analyze the solutions sampled from the microbial fuel cell. After 92 h running, valine, as the metabolite, was successfully detected with concentration 3.90 × 10-5 M. The results demonstrated that Bacillus licheniformis could convert l-carnosine and l-alanyl-l-glutamine into valine. The method employed in this work was proved to have great potential in analysis of metabolites, such as amino acids, for microorganisms.

Clinical characteristics and outcomes of left ventricular pseudoaneurysm: A retrospective study in a single-center of China.

Left ventricular (LV) pseudoaneurysm is a fatal and rare condition with a high risk of rupture. The symptoms are nonspecific and diagnosis is often delayed. The purpose of this study is to analysis a series of cases in our institution.Between March 2009 and April 2016, 10 patients (5 males and 5 females) with LV pseudoaneurysm were retrospectively enrolled. Clinical information, diagnostic imaging modalities, treatment, and outcomes were evaluated.The mean age was 58.2 ±â€Š11.0 years (28-71 years). The common symptoms were chest pain (3 cases), dyspnea (3 cases), and syncope (2 cases). All patients had nonspecific abnormalities on the electrocardiogram, and 7 patients had chest X-ray abnormalities. Three etiologies including myocardial infarction (6 cases), mitral valve replacement (3 cases), and suspected endocarditis (1 case) were identified. LV pseudoanerysm was diagnosed in 8 patients by transthoracic echocardiography, and the other 2 patients were diagnosed by computed tomography angiogram. Posterior (4 cases) and lateral (4 cases) of the left ventricle were the most common positions of the rupture orifice. Eight patients accepted surgery repair and 2 patients were treated conservatively. In 2 patients, residual apical aneurysm was found, 1 patient was detected with a residual LV pseudoaneurysm, and 1 patient had myocardial infarction at 61 months' follow-up.Myocardial infarction was the most common etiology of patients with LV pseudoaneurysm. The most frequently ruptured orifices were lateral and posterior walls of the left ventricle. Surgery is recommended as the first option, and conservative therapy can be considered for appropriate patients.

Pulmonary ground-glass opacity: computed tomography features, histopathology and molecular pathology.

The incidence of pulmonary ground-glass opacity (GGO) lesions is increasing as a result of the widespread use of multislice spiral computed tomography (CT) and the low-dose CT screening for lung cancer detection. Besides benign lesions, GGOs can be a specific type of lung adenocarcinomas or their preinvasive lesions. Evaluation of pulmonary GGO and investigation of the correlation between CT imaging features and lung adenocarcinoma subtypes or driver genes can be helpful in confirming the diagnosis and in guiding the clinical management. Our review focuses on the pathologic characteristics of GGO detected at CT, involving histopathology and molecular pathology.

Quantitative phase imaging for medical diagnosis.

Optical microscopy is an indispensable diagnostic tool in modern healthcare. As a prime example, pathologists rely exclusively on light microscopy to investigate tissue morphology in order to make a diagnosis. While advances in light microscopy and contrast markers allow pathologists to visualize cells and tissues in unprecedented detail, the interpretation of these images remains largely subjective, leading to inter- and intra-observer discrepancy. Furthermore, conventional microscopy images capture qualitative information which makes it difficult to automate the process, reducing the throughput achievable in the diagnostic workflow. Quantitative Phase Imaging (QPI) techniques have been advanced in recent years to address these two challenges. By quantifying physical parameters of cells and tissues, these systems remove subjectivity from the disease diagnosis process and allow for easier automation to increase throughput. In addition to providing quantitative information, QPI systems are also label-free and can be easily assimilated into the current diagnostic workflow in the clinic. In this paper we review the advances made in disease diagnosis by QPI techniques. We focus on the areas of hematological diagnosis and cancer pathology, which are the areas where most significant advances have been made to date. [Image adapted from Y. Park, M. Diez-Silva, G. Popescu, G. Lykotrafitis, W. Choi, M. S. Feld, and S. Suresh, Proc. Natl. Acad. Sci. 105, 13730-13735 (2008).].

Chloroquine inhibits tumor growth and angiogenesis in malignant pleural effusion.

Malignant pleural effusion (MPE) is associated with a poor prognosis in lung cancer. Currently, no effective cure exists for MPE. Chloroquine (CQ) has been demonstrated to induce vascular normalization and inhibit tumor growth. The aim of this study was to assess whether CQ affects MPE. The xenografts mice were divided into normal saline (NS), CQ, or bevacizumab (BE) group. Tumor growth and microvascular density (MVD) were monitored. We explored the effect of CQ on the proliferation, survival, and proangiogenic signaling of tumor cells in vitro. We further evaluated the effects of CQ on the viability, migration, and tube formation of human umbilical vein endothelial cells (HUVECs). A chicken chorioallantoic membrane (CAM) model was used to elucidate the effects of CQ on angiogenesis. Finally, an MPE mouse model were treated by CQ, BE, or NS. The volume of pleural effusion, tumor foci, and MVD was evaluated. CQ therapy group exhibited decreased tumor volume, tumor weight, and MVD in the mouse xenografts. CQ inhibited the proliferation of the tumor cells. However, the expression of vascular endothelial growth factor was not affected. Additionally, CQ inhibited the proliferation, migration, and tube formation of HUVECs and also restrained angiogenesis in the CAM. Western blot showed that CQ might suppress angiogenesis by downregulating p-Akt, Jagged1, and Ang2 in HUVECs. In MPE mice, the volume of the pleural effusion, the number of pleural tumor foci, and the MVD were significantly reduced in the CQ group. Our work demonstrated that CQ played the role of an efficient treatment for MPE.

Prognostic value of the expression of estrogen receptor ß in patients with non-small cell lung cancer: a meta-analysis.

BACKGROUND: Lung cancer remains the leading cause of cancer-related deaths in men and the second leading cause in women worldwide. It is becoming increasingly clear that estrogen and estrogen receptors are involved in the pathogenesis and development of lung cancer. However, observational studies on the prognostic role of estrogen receptor ß (ERß) in non-small cell lung cancer (NSCLC) are controversial. METHODS: To clarify the impact of ERß in NSCLC survival, we performed this meta-analysis that included eligible studies. The combined hazard ratios (HR) and their corresponding 95% confidence intervals (CIs) were calculated in terms of overall survival. RESULTS: A total of eleven studies with 3,300 patients were evaluable for this meta-analysis. Our results suggested that ERß overexpression had no relationship on survival of patients with NSCLC, the HR (95% CI) was 1.000 (0.954-1.047) overall. Moreover, there was no heterogeneity between the studies. CONCLUSIONS: ERß overexpression indicates no relationship of prognosis for patients with NSCLC.

Separation and detection of amino acid metabolites of Escherichia coli in microbial fuel cell with CE.

In this work, CE-LIF was employed to investigate the amino acid metabolites produced by Escherichia coli (E. coli) in microbial fuel cell (MFC). Two peptides, l-carnosine and l-alanyl-glycine, together with six amino acids, cystine, alanine, lysine, methionine, tyrosine, arginine were separated and detected in advance by a CE-LIF system coupled with a homemade spontaneous injection device. The injection device was devised to alleviate the effect of electrical discrimination for analytes during sample injection. All analytes could be completely separated within 8 min with detection limits of 20-300 nmol/L. Then this method was applied to analyze the substrate solution containing amino acid metabolites produced by E. coli. l-carnosine, l-alanyl-glycine, and cystine were used as the carbon, nitrogen, and sulfur source for the E. coli culture in the MFC to investigate the amino acid metabolites during metabolism. Two MFCs were used to compare the activity of metabolism of the bacteria. In the sample collected at the running time 200 h of MFC, the amino acid methionine was discovered as the metabolite with the concentrations 23.3 µg/L.

MiR-1271 Inhibits Ovarian Cancer Growth by Targeting Cyclin G1.

BACKGROUND: Ovarian cancer is the most lethal gynecological malignant cancer in the female genital system. The dysfunction of miRNA contributes to ovarian cancer development. MATERIAL AND METHODS: The miR-1271 level in ovarian cancer tissues and cells was assayed by qRT-PCR. The miR-1271 expression in cells was overexpressed by miRNA-mimic transfection and reduced by miRNA-antisense-oligonucleotide (ASO) transfection. Cell proliferation was analyzed by an MTT assay. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. The protein level was assayed by Western blotting. RESULTS: The ovarian cancer tissue and cell lines showed low levels of miR-1271. Low levels of miR-1271 in ovarian cancer tissues were correlated with a low rate of patient survival, and the overexpression of miR-1271 inhibited the proliferation of ovarian cancer cells. The 3' UTR of cyclin G1 (CCNG1) was targeted by miR-1271. CONCLUSIONS: Low levels of miR-1271 in ovarian cancer tissues promoted cancer cell growth. MiR-1271 may be a new predictor of prognosis in ovarian cancer. MiR-1271 exerted its role by targeting CCNG1.

Analyzing large-scale samples highlights significant association between rs10411210 polymorphism and colorectal cancer.

Colorectal cancer (CRC) is the third most common form of cancer and the second leading cause of cancer-related death in the Western countries. In order to detect common CRC genetic variants, genome-wide association studies (GWAS) have been performed and reported some novel CRC susceptibility variants. RHPN2 is located on 9q13.11, which encodes a member of the rhophilin family of Ras-homologous (Rho)-GTPase binding proteins. RHPN2 gene rs10411210 polymorphism was identified to be significantly associated with CRC in European ancestry. GWAS and candidate studies investigate whether rs10411210 polymorphism is associated with CRC risk in European, Asian and American populations. However, most studies reported no association. Evidence shows that RHPN2 rs10411210 variant may be a prognostic biomarker for patients with surgically resected CRC. Here we reevaluated this association using large-scale samples from 15 studies (131580 samples including 53564 CRC cases and 78016 controls) using meta-analysis method by searching the PubMed and Google Scholar databases. We did not identify significant heterogeneity among these 15 studies (P=0.4201 and I(2)=2.8%). Our results showed significant association between rs10411210 and CRC (P=9.17E-14, odds ratio (OR)=1.10, 95% confidence interval (CI) 1.07-1.13). In subgroup analysis, we found significant association between rs10411210 and CRC in European population with P=5.70E-09, OR=1.14, 95% CI 1.10-1.20 and Asian population with P=3.36E-07, OR=1.11, 95% CI 1.07-1.16, but not American population with P=0.0576, OR=1.05, 95% CI 1.00-1.09. Collectively, our analysis further highlights significant association between rs10411210 polymorphism and colorectal cancer.

[A medical image semantic modeling based on hierarchical Bayesian networks].

A semantic modeling approach for medical image semantic retrieval based on hierarchical Bayesian networks was proposed, in allusion to characters of medical images. It used GMM (Gaussian mixture models) to map low-level image features into object semantics with probabilities, then it captured high-level semantics through fusing these object semantics using a Bayesian network, so that it built a multi-layer medical image semantic model, aiming to enable automatic image annotation and semantic retrieval by using various keywords at different semantic levels. As for the validity of this method, we have built a multi-level semantic model from a small set of astrocytoma MRI (magnetic resonance imaging) samples, in order to extract semantics of astrocytoma in malignant degree. Experiment results show that this is a superior approach.