Search

The hematological phenotype and genotype analysis of hemoglobin New York (Hb New York) combined with α or β thalassemia has been rarely reported, and whether there is any effect of Hb New York on thalassemia has not been well explored.In this study, peripheral blood samples from 346 Hb New York carriers were collected for blood cell parameter analysis. When comparing Hb New York heterozygotes, Hb New York combined with αOur study shows that the hematological characteristics of Hb New York combined with thalassemia are similar to the corresponding thalassemia, and Hb New York does not aggravate the clinical manifestations of thalassemia.

As an important transcription factor that is widely expressed in most tissues of the human body, Myc-associated zinc finger protein (MAZ) has been reported highly expressed in many malignant tumors and thought to be a promising therapeutic target for cancer treatment. In this review, we aim to offer a comprehensive understanding of MAZ regulation in malignant tumors. The carboxy terminal of MAZ protein contains six C2H2 zinc fingers, and its regulation of transcription is based on the interaction between the GC-rich DNA binding sites of target genes and its carboxy-terminal zinc finger motifs. MAZ protein has been found to activate or inhibit the transcriptional initiation process of many target genes, as well as play an important role in the transcriptional termination process of some target genes, so MAZ poses dual regulatory functions in the initiation and termination process of gene transcription. Through the transcriptional regulation of c-myc and Ras gene family, MAZ poses an important role in the occurrence and development of breast cancer, pancreatic cancer, prostate cancer, glioblastoma, neuroblastoma, and other malignant tumors. Our review shows a vital role of MAZ in many malignant tumors and provides novel insight for cancer diagnosis and treatment.

BACKGROUND In recent years, HIV infection in students has been an ongoing concern worldwide. A great number of articles have been published, however, statistical analysis of the data presented in these publications is lacking. OBJECTIVE This study aims to detect and analyze emerging trends and collaborative networks in student human immunodeficiency virus (HIV) / acquired immunodeficiency syndrome (AIDS) research. METHODS Student HIV/AIDS publications from 1985 to 2022 were collected from the Web of Science Core Collection. A topic search was used for this study, and articles in English were included. Citespace was used to generate visual networks of countries/regions, institutions, references, and keywords. Citation analysis was used to discover milestones in the field and trace the roots of the knowledge base. Keyword analysis was used to detect research hotspots and predict future trends. RESULTS A total of 2,726 publications met this criterion. Over the past 38 years, the number of annual publications has been on the rise overall. The United States had the highest number of publications (1303) and the highest centrality (0.91). The University of California System was the core institution. The main target population of the student HIV study was medical and university students. These studies focused on students' knowledge, attitudes, risk behaviors, and education about HIV/AIDS. The recent bursting keywords (gay, sexual health, adherence, barriers, mental health, HIV testing, stigma, and antiretroviral therapy) reveal research trends and public interest in this topic. CONCLUSIONS The study identified countries/regions and institutions contributing to the area of HIV/AIDS among students and reveals research hotspots and emerging trends. The field of student HIV/AIDS was growing rapidly. The United States was at the center, and the University of California system was the core institution. However, academic collaboration should be strengthened. Future research may focus on exploring gay students, sexual health, adherence, barriers, mental health, HIV testing, stigma, and antiretroviral therapy. CLINICALTRIAL

Aims: The aim of this study was to examine the RNA and protein expression levels and clinical significance of the pore membrane protein 121 kDa (POM121) in lung cancer. Materials and Methods: Paire...

BACKGROUND Nearly one-third of new HIV infections occurred among youth in 2019 worldwide. Previous studies suggested that student youths living with HIV and nonstudent youths living with HIV might differ in some risk factors, transmission routes, HIV care, and disease outcomes. OBJECTIVE This study aimed to compare the HIV epidemic, disease outcomes, and access to care among student and nonstudent youths living with HIV aged 16 to 25 years in Guangxi, China. METHODS We performed a historical cohort study by extracting data on all HIV or AIDS cases aged 16 to 25 years in Guangxi, China, during 1996-2019 from the Chinese Comprehensive Response Information Management System of HIV or AIDS. We conducted analyses to assess possible differences in demographic and behavioral characteristics, HIV care, and disease outcomes between student and nonstudent youths living with HIV. Multivariate Cox regression was used to assess differences in mortality and virologic failure between student and nonstudent cases. RESULTS A total of 13,839 youths aged 16 to 25 years were infected with HIV during 1996-2019. Among them, 10,202 cases were infected through sexual contact, most of whom were men (n=5507, 54%); 868 (8.5%) were students, and 9334 (91.5%) were not students. The number of student youths living with HIV was lower before 2006 but gradually increased from 2007 to 2019. In contrast, the nonstudent cases increased rapidly in 2005, then gradually declined after 2012. Student cases were mainly infected through homosexual contact (n=614, 70.7% vs n=1447, 15.5%; PPPPP=.008). The virologic failure rate was 2.3 and 2.6 per 100 person-years among student and nonstudent youths living with HIV, respectively. Nonstudent cases had double the risk of virologic failure compared to student cases (AHR 1.9, 95% CI 1.3-2.6; P CONCLUSIONS Nonstudent youths living with HIV might face a low CD4 count at the time of HIV diagnosis, delayed ART initiation, and increased risk of death and virologic failure. Thus, HIV prevention and interventions should target youths who dropped out of school early to encourage safe sex and HIV screening, remove barriers to HIV care, and promote early ART initiation to curb the HIV epidemic among youths.

Objective: The study aims to explore the prognostic significance of zona pellucida glycoprotein 3 (ZP3) in hepatocellular carcinoma (HCC) tissues. Methods: The expression of ZP3 protein in HCC tissues was detected by immunohistochemistry (IHC) to study its effects on the clinicopathological characteristics and prognosis of HCC patients. The Cancer Genome Atlas (TCGA) database was used to confirm the expression of ZP3 in HCC tissues and Gene set enrichment analysis (GSEA) was performed to obtain potential ZP3-related pathways in HCC. Results: IHC detection found that ZP3 had a high expression in HCC tissues and was associated with cirrhosis, and hepatitis B virus infection of HCC patients (P Conclusion: High expression of ZP3 in HCC tissues shows an important role in HCC development and prognosis.

Background Human chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family (CMTM) is implicated in the pathogenesis of immune, reproductive systems and various cancers. However, the expression and clinical significance of CMTM4 in lung cancer have not been identified. Methods We performed immunohistochemistry to detect the expression of CMTM4 in 75 paired lung adenocarcinoma and non-tumor lung tissues. The correlation between CMTM4 expression and clinical significance of lung cancer patients was analyzed by Chi-square test. Kaplan-Meier method and Log-Rank test were used to calculate the survival time of lung cancer patients. Results We found that CMTM4 was positively expressed in 34/75 (45.3%) cases of lung adenocarcinoma tissues, while positively expressed in 59/75 (78.6%) cases of non-tumor lung tissues, suggesting a lower expression of CMTM4 in lung adenocarcinoma tissues than non-tumor lung tissues (P

As a specific inhibitor of serine/threonine protein phosphatases, okadaic acid (OA) has been found to be a tumor promoter. However, whether OA plays a role in metastasis of hepatocellular carcinoma (HCC) has not been well elucidated. In this study, Hep3B and HepG2 cells were treated with different doses of OA and the cell viability was determined by CCK8 test. As a result, Hep3B and HepG2 cells showed no obvious cytotoxicity after OA treatment below 20 or 25 nM for 12 or 24 hours. However, wound healing, invasion, and migration abilities of HCC cells were significantly enhanced in the OA-treated groups than those of the control group (P < .05), measured by cell scratching and BD transwell assays. Moreover, we found that the expression of epithelial-mesenchymal transition (EMT)-related key factors was changed upon OA treatment in a dose-dependent manner. In addition, the activity of protein phosphatase 2A (PP2A) in OA-treated cells was also decreased significantly compared with the control cells (P < .05). Interfering of PP2A subunit A or C caused a similar expression change of EMT-related key factors as the OA treatment in HCC cells. Our results suggest that OA promotes the EMT process of HCC cells by inhibiting the activity of PP2A.

Background Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide, especially in China, with high metastasis and poor prognosis. Recently, as the core component of the polycomb repressive complexes 1 (PRC1), chromobox protein homolog 8 (CBX8) is considered as an oncogene and prognostic marker in HCC. Methods A tissue microarray of 166 paired HCC and adjacent non-tumor samples were collected to identify the relationship between CBX8 and epithelial mesenchymal transition (EMT) associated proteins by Spearman correlation analysis. Knock-down of CBX8 in HCC cells was conducted to detect the biologic functions of CBX8 in HCC metastasis. Results We found out that CBX8 was over-expressed in HCC and its expression was closely related to the metastasis of HCC patients. In addition, knock-down of CBX8 was found to inhibit the invasion and migration ability of HCC cells. Moreover, there was a significant relationship between expression of CBX8 and EMT associated proteins both in HCC cells and tumor tissues. Conclusions Our results indicate that CBX8 promotes metastasis of HCC by inducing EMT process.

Background. The chromobox (CBX) proteins CBX2, CBX4, CBX6, CBX7, and CBX8, also known as Polycomb (Pc) proteins, are canonical components of the Polycomb repressive complex 1 (PRC1). Abundant evidence indicates that abnormal expression of Pc proteins is associated with a variety of tumors, but their role in the pathogenesis of hepatocellular carcinoma (HCC) has not been fully elucidated. In the present study, we performed a case-control study to investigate the relationship between single nucleotide polymorphisms (SNPs) ofCBXgenes and HCC.Methods. Nine SNPs onCBXgenes (rs7217395, rs2036316 ofCBX2; rs3764374, rs1285251, rs2289728 ofCBX4; rs7292074 ofCBX6; and rs710190, rs139394, rs5750753 ofCBX7) were screened and genotyped using MassARRAY technology in 334 HCC cases and 321 controls. The association between SNPs and their corresponding gene expressions was analyzed through bioinformatics methods using the Ensembl database and Blood eQTL browser online tools.Results. The results indicated that rs2289728 (G>A) ofCBX4(P= 0.03, OR = 0.56, 95% CI: 0.33-0.94) and rs139394 (C>A) ofCBX7(P= 0.02, OR = 0.55, 95% CI: 0.33-0.90) decreased the risk of HCC. Interaction between rs2036316 and HBsAg increased the risk of HCC (P= 0.02, OR = 6.88, 95% CI: 5.20-9.11), whereas SNP-SNP interaction between rs710190 and rs139394 reduced the risk of HCC (P= 0.03, OR = 0.33, 95% CI: 0.12-0.91). Gene expression analyses showed that the rs2289728 A allele and the rs139394 A allele significantly reducedCBX4andCBX7expression, respectively.Conclusion. Our findings suggest thatCBX4rs2289728 andCBX7rs139394 are protective SNPs against HCC. The two SNPs may reduce the risk of HCC while suppressing the expression ofCBX4andCBX7.

The purpose of this study was to investigate the expression and clinical significance of N6-methyladenosine demethylase FTO in thyroid cancer. Bioinformatic analysis showed that FTO expression was downregulated in thyroid cancer tissues and correlated with lymph node metastasis in thyroid cancer patients. We conducted experimental verification by collecting Asian samples. The results of quantitative reverse transcription-PCR showed that the mRNA expression of FTO in the blood of 30 thyroid cancer patients was lower than that of the control population. At the same time, we found that FTO expression was negative in tissues of 16/56 (28.57%) thyroid cancer cases and 4/40 (10.00%) nontumor thyroid cases through the immunohistochemical method, indicating a lower FTO expression in thyroid cancer tissues than nontumor thyroid tissues (

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide, especially in China, with high metastasis and poor prognosis. Recently, as the core component of the polycomb repressive complexes 1 (PRC1), chromobox protein homolog 8 (CBX8) is considered as an oncogene and prognostic marker in HCC. A tissue microarray of 166 paired HCC and adjacent non-tumor samples were collected to identify the relationship between CBX8 and epithelial mesenchymal transition (EMT) associated proteins by Spearman correlation analysis. Knock-down of CBX8 in HCC cells was conducted to detect the biologic functions of CBX8 in HCC metastasis. We found out that CBX8 was over-expressed in HCC and its expression was closely related to the metastasis of HCC patients. In addition, knock-down of CBX8 was found to inhibit the invasion and migration ability of HCC cells. Moreover, there was a significant relationship between expression of CBX8 and EMT associated proteins both in HCC cells and tumor tissues. Our results indicate that CBX8 promotes metastasis of HCC by inducing EMT process.

Background Human chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family (CMTM) members are found deregulated in various cancers and play a role in cancer development. Recent studies showed that CMTM7 was down-regulated in liver cancer and functioned as a tumor suppressor. Methods The expression of CMTM7 in hepatocellular carcinoma (HCC) tissues was measured by bioinformatics analysis, Western blot, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR). CCK8 and cell colony formation assays were conducted to detect the cell proliferation. Cell invasion and migration ability was assessed by wound healing and Transwell assays. Results We identified a decreased expression of CMTM7 in HCC tissues was closely related to the metastasis and prognosis of HCC patients. To explore the effect of CMTM7 on the biological function of HCC cells, we over-expressed CMTM7 in two HCC cell lines, SK-Hep-1 and Bel-7402 cells. Cell proliferation was reduced significantly after exogenous expression of CMTM7, detected by both CCK8 and colony formation assay. Moreover, the invasion and migration ability of HCC cells were also inhibited by exogenous expression of CMTM7 in wound healing and Transwell assay. Furthermore, there was a significantly positive correlation between CMTM7 and CMTM3 both in HCC cells and tumor tissues. Conclusions Our results suggest that down-regulated CMTM7 promotes metastasis of HCC through inducing the expression of its family member CMTM3.

This study aimed to investigate the expression and clinical significance of chemokine-like factor-like MARVEL transmembrane domain-containing family member 2 (CMTM2) in hepatocellular carcinoma (HCC) tissues. Bioinformatics analysis showed that CMTM2 was downregulated in HCC tissues and correlated with vascular invasion of HCC patients. The immunohistochemistry (IHC) method found that CMTM2 expression was negative in 29/75 (38.67%) cases of HCC tissues and 13/75 (17.33%) cases of paracancerous tissues, also showed a significantly lower expression of CMTM2 in HCC tissues than the paired paracancerous tissues (

The defects of DNA repair genes may lead to genomic instability and cancer. As an important DNA mismatch repair gene that maintains genomic stability from DNA replication errors, genetic variants of mutS homolog 2 (MSH2) are associated with some cancers. In this study, 1021 hepatocellular carcinoma (HCC) cases and 1021 non-HCC controls from Guangxi were included to explore the association between MSH2 single-nucleotide polymorphisms (SNPs) and HCC. Among the eight MSH2 SNPs, only genotype distribution of rs2303428 was significantly different from HCC and non-HCC patients (p 0.05). Moreover, CT, TT, and CT/TT genotype of rs2303428 could increase HCC risk [OR (95% CI) = 1.758 (1.195-2.657), 1.846 (1.213-2.896), and 1.823 (1.219-2.763), respectively] and decrease the survival time of HCC patients [codominant, HR (95% CI) = 1.267 (1.046-1.535); dominant, HR (95% CI) = 1.675 (1.162-2.414)]. In addition, rs2303428 was found to interact with HBV infection and family history to increase HCC risk by gene-environment analysis (p 0.05). Finally, multivariate COX regression analysis showed that rs2303428, tumor number, tumor staging, and metastasis had a significant influence on HCC prognosis. Our results provide MSH2 SNP, rs2303428, as a new prognostic biomarker for HCC patients.

Hepatocellular carcinoma (HCC) is a malignant cancer causing deleterious health effect worldwide, especially in China. So far clinical cure rate and long-term survival rate of HCC remains low. Most HCC patients after cancer resection have recurrence or metastasis within 5 years. This study aims to explore the genetic association of mutL homolog 1 (MLH1) polymorphisms with HCC risk and prognosis. Four candidate MLH1 polymorphisms, rs1800734, rs10849, rs3774343 and rs1540354 were studied from a hospital-based case-control study including 1,036 cases (HCC patients) and 1,036 controls (non-HCC patients) in Guangxi, China. All these SNPs interacted with environmental risk factors, such as HBV infection, alcohol intake and smoking in the pathogenesis of HCC. However, only rs1800734 had significant difference between cases and controls. Compared to the AA genotype, patients with AG, GG and AG/GG genotype of rs1800734 had an increased risk of HCC [ORs (95% CI) = 1.217 (1.074∼1.536), 1.745 (1.301∼2.591) and 1.291 (1.126∼1.687)] and a decreased survival time [co-dominant, HR (95% CI) = 1.553 (1.257∼1.920); dominant, HR (95% CI) = 2.207 (1.572∼3.100)]. Furthermore, we found that tumor number, tumor staging, metastasis and rs1800734 were associated with the overall survival of HCC patients by multivariate COX regression analysis. No significant difference was found between the other three MLH1 polymorphisms with HCC risk and prognosis. Our study suggests MLH1 SNP, rs1800734 as a new predictor for poor prognosis of HCC patients.

Xiaonian Zhu,1,* Wei Luo,2,* Wenjin Liang,2 Fen Tang,3 Chunhua Bei,1 Yuan Ren,1 Linyuan Qin,1 Chao Tan,1 Ying Zhang,1 Shengkui Tan1 1School of Public Health, Guilin Medical University, Guilin, People’s Republic of China; 2Department of Hepatobiliary Surgery, The Affiliated Hospital of Guilin Medical University, Guilin, People’s Republic of China; 3Department of Hepatology, Nanxishan Hospital of Guangxi Zhuang Autonomous Region, Guilin, People’s Republic of China *These authors contributed equally to this work Abstract: This study aimed to investigate the expression and clinical significance of MYC-associated zinc finger protein (MAZ) in pancreatic carcinoma (PC), and the biological functions of MAZ in PC cells. MAZ expression was detected in 57 PC tissues and 41 paired adjacent nontumor tissues by immunohistochemistry. Compared to the expression in adjacent nontumor tissues, MAZ was significantly higher expressed in PC tissues (P

Background: As an essential member of the Polycomb group (PcG) proteins, chromobox homolog 7 (CBX7) is found deregulated in some human cancers, and is thought to be a contributing factor in carcinogenesis. However, the expression and role of CBX7 in hepatocellular carcinoma (HCC) is still not well characterized. Materials and Methods: The levels of the CBX7 protein were quantified in 75 paired HCC and adjacent nontumor tissues by immunohistochemistry; comparisons were made using McNemar's chi-square test. The Kaplan-Meier estimate was used for survival analysis. Results: We found that the expression of CBX7 in HCC tissues was significantly lower than that of adjacent nontumor tissues. In addition, decreased CBX7 expression levels were correlated with liver cirrhosis in HCC patients. Furthermore, the survival times of HCC patients who were CBX7-expression-negative were shorter than HCC patients who were CBX7-expression-positive. Conclusion: Our results show that downregulation of CBX7 is related to HCC progression and a poor prognosis in HCC patients.

Additional file 1: Table S1. Correlation between CBX8 expression and clinic-pathological characteristics of HCC patients.

This study aimed to examine the expression level and clinical significance of chemokine-like factor-like MARVEL transmembrane domain-containing family member 6 (CMTM6) in paired hepatocellular carcinoma (HCC) and adjacent nontumor tissues. The expression of CMTM6 was detected in 75 paired HCC and adjacent nontumor tissues by immunohistochemistry. Chi-square test was used to compare the difference of CMTM6 expression between HCC tissues and adjacent nontumor tissues. The clinic-pathological features and prognosis of HCC patients were collected to analyze the relationship with CMTM6 expression. The positive expression of CMTM6 in HCC tissues was significantly lower than that of adjacent nontumor tissues. The difference of CMTM6 expression between HCC tissues and paired adjacent nontumor tissues was statistically significant (p 0.05). Furthermore, CMTM6 expression was correlated with HCC metastasis and alpha-fetoprotein (AFP) (p 0.05). Multivariate logistic regression analysis showed tumor staging, metastasis, and AFP had a significant relationship with CMTM6 expression. In addition, the survival time of HCC patients was different between CMTM6 positive group and CMTM6 negative group by Kaplan-Meier survival analysis (p 0.05). Downregulation of CMTM6 is related to HCC metastasis and the prognosis of HCC patients.

Background The chromobox (CBX) proteins CBX2, CBX4, CBX6, CBX7, and CBX8, also known as Polycomb (Pc) proteins, are canonical components of the Polycomb repressive complex 1 (PRC1). Abundant evidence indicates that abnormal expression of Pc proteins is associated with a variety of tumors, but their role in the pathogenesis of hepatocellular carcinoma (HCC) has not been fully elucidated. In the present study, we performed a case-control study to investigate the relationship between single nucleotide polymorphisms (SNPs) of CBX genes and HCC. Methods Nine SNPs on CBX genes (rs7217395, rs2036316 of CBX2; rs3764374, rs1285251, rs2289728 of CBX4; rs7292074 of CBX6; and rs710190, rs139394, rs5750753 of CBX7) were screened and genotyped using MassARRAY technology in 334 HCC cases and 321 controls. The association between SNPs and their corresponding gene expressions was analyzed through bioinformatics methods using the Ensembl database and Blood eQTL browser online tools. Results The results indicated that rs2289728 (G>A) of CBX4 (P = 0.03, OR = 0.56, 95% CI: 0.33-0.94) and rs139394 (C>A) of CBX7 (P = 0.02, OR = 0.55, 95% CI: 0.33-0.90) decreased the risk of HCC. Interaction between rs2036316 and HBsAg increased the risk of HCC (P = 0.02, OR = 6.88, 95% CI: 5.20-9.11), whereas SNP-SNP interaction between rs710190 and rs139394 reduced the risk of HCC (P = 0.03, OR = 0.33, 95% CI: 0.12-0.91). Gene expression analyses showed that the rs2289728 A allele and the rs139394 A allele significantly reduced CBX4 and CBX7 expression, respectively. Conclusion Our findings suggest that CBX4 rs2289728 and CBX7 rs139394 are protective SNPs against HCC. The two SNPs may reduce the risk of HCC while suppressing the expression of CBX4 and CBX7.

Background HIV prevalence has been rapidly increasing among men who have sex with men (MSM) attending university in China, but HIV testing rates remain suboptimal. The factors associated with past HIV testing in this population in Beijing, China, were investigated. Methods: This study used data from the baseline survey of an HIV intervention clinical trial among MSM who did not have a history of a positive HIV diagnosis. This analysis focused on the HIV testing experience in a subgroup of university student MSM participants. Log-binomial models were used to evaluate factors associated with past HIV testing. Results: Of 375 university student MSM, the median age was 22 years; 89.3% were Han ethnic. Approximately half (50.4%, n = 189) had ever taken an HIV test before the survey. In a multivariable log-binomial model, older age (adjusted prevalence ratio (APR), 1.04; 95% confidence interval (CI), 1.02–1.06), had first sexual intercourse at age

// Wei Luo 1, * , Xiaonian Zhu 1, * , Wei Liu 1 , Yuan Ren 1 , Chunhua Bei 1 , Linyuan Qin 1 , Xueyan Miao 1 , Fen Tang 2 , Guifang Tang 2 , Shengkui Tan 1 1 School of Public Health, Guilin Medical University, Guilin 541004, Guangxi, People’s Republic of China 2 Department of Hepatology, The Affiliated Nanxishan Hospital of Guilin Medical University, Guilin 541004, Guangxi, People’s Republic of China * These authors contributed equally to this work Correspondence to: Shengkui Tan, email: sktan2008@sina.cn Keywords: MYC associated zinc finger protein (MAZ), hepatocellular carcinoma (HCC), zinc finger E-box binding homeobox 1 (ZEB1), zinc finger E-box binding homeobox 2 (ZEB2), epithelial-mesenchymal transition (EMT) Received: July 11, 2016 Accepted: November 09, 2016 Published: November 16, 2016 ABSTRACT MYC associated zinc finger protein (MAZ) plays a key role in regulation of gene expression and tumor development. Studies have shown that deregulated expression of MAZ is closely related to the progression of tumors such as glioblastoma, breast cancer, prostate cancer and liposarcoma. However, the role of MAZ in hepatocellular carcinoma (HCC) has not been fully elucidated. Here, we found that expression of MAZ was increased in HCC and correlated to the distant metastasis of HCC. Moreover, we found that MAZ had a relationship with zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), two important mesenchymal markers in epithelial-mesenchymal transition (EMT) that were over-expressed in HCC. After knocking-down MAZ expression in HCC cell lines using RNA interruption, HCC cell proliferation, tumorigenesis, invasion and migration were significantly inhibited. In addition, we found that expression of other EMT markers was also changed besides ZEB1 and ZEB2 by decreasing MAZ expression, both detected in vivo and in vitro assays. Therefore, we conclude that MAZ can promote the invasion and metastasis of HCC by inducing EMT.

MicroRNAs (miRNAs) can regulate gene expression at post-transcriptional levels, thereby influence cancer risk. The aim of the current study is to investigate association between miR-199a rs74723057 and MET rs1621 and HCC risk in 1032 HCC patients and 1060 cancer-free controls. These two SNPs were genotyped by using the Agena MassARRAY genotyping system. Odds ratio (OR) and 95% confidence interval (95%CI) were calculated to assess the strength of the associations. We found that compared with the wild-type AA genotype of MET rs1621, the variant GG genotype was associated with a decreased risk for HCC (OR = 0.24, 95% CI = 0.06-0.96, P = 0.043). No association between miR-199a rs74723057 and HCC risk was observed. In addition, an interaction effect on HCC risk between the selected two SNPs was found. Among those who carried the CG/GG genotypes of miR-199a rs74723057, those who carried the GG genotype of MET rs1621 had a reduced risk of HCC, when compared with those who carried the AG/AA genotypes of MET rs1621 (OR = 0.15, 95% CI = 0.03~0.73, P for interaction = 0.018). Our results suggest that MET rs1621 polymorphism, alone and combined with miR-199a rs74723057, may influence susceptibility to HCC. Further large-scale association studies and functional studies are needed to validate our findings.

Ring1 and YY1 binding protein (RYBP), a member of the polycomb group proteins, has been implicated in transcription repression and tumor cell-specific apoptosis. Previously, RYBP has been reported as a putative tumor suppressor in cancer tissues by regulating mouse double minute 2 homolog-p53 signaling. However, the exact role and underlying mechanisms of RYBP in cancer remain to be fully elucidated. The present study investigated the expression profile of RYBP in hepatocellular carcinoma (HCC) and examined the association between the expression of RYBP and metastasis of HCC. It was found that RYBP was downregulated in HCC tissues, compared with matched adjacent non-tumor tissues, as detected by reverse transcription-quantitative polymerase chain reaction and immunohistochemistry. In addition, Kaplan-Meier survival analysis showed that the negative expression of RYBP was associated with decreased overall survival rates in patients with HCC. It was also found that RYBP was associated with zinc finger E-box binding homeobox 1 and zinc finger E-box binding homeobox 2, which were overexpressed in HCC and correlated with epithelial-mesenchymal transition. The results of the present study suggested the importance of RYBP in HCC and its possible mechanism in the metastasis of HCC.

Polymorphisms in genes may affect its expression and alter individual susceptibility to cancer. In this study, we investigate associations between CMTM family gene polymorphisms and hepatocellular carcinoma (HCC) in a southern Chinese population. Ten selected single-nucleotide polymorphisms (SNPs) in CMTM family genes were genotyped in 315 HCC patients and 315 cancer-free controls using Sequenom MassARRAY platform and the associations of the selected SNPs with HCC risk were evaluated. We found individuals with the rs164207 AA genotypes had a significantly increased risk of HCC than those with CC genotypes (adjusted OR = 2.794, 95% CI = 1.143-6.828). Also, individuals with the rs3811178 GG genotypes showed a significant association with increased risk of HCC when compared with the AA genotypes (adjusted OR = 2.578, 95% CI = 1.114-5.969). Furthermore, there was also a significantly increased risk of HCC when combined risk genotypes of these loci, i.e., rs164207 AA, CA and rs3811178 GG, GA. Compared with the low-risk group (0 risk genotypes), the high-risk group (2 risk genotypes) was at significantly increased risk of HCC (adjusted OR = 3.339, 95% CI = 1.119-9.964, p = 0.031). Our results suggest that polymorphisms of rs3811178 in CMTM5 and rs164207 in CMTM6 might contribute to the genetic susceptibility of HCC in the southern Chinese population. Further well-designed studies with larger sample sizes are needed to confirm our findings.

Chunhua Bei,1,* Ying Zhang,1,* Riming Wei,1 Xiaonian Zhu,1 Zhigang Wang,1 Wen Zeng,2 Qiuyue Chen,3 Shengkui Tan1 1Department of Epidemiology and Statistics, School of Public Health, Guilin Medical University, 2Department of Hepatobiliary Surgery, The Affiliated Hospital of Guilin Medical University, 3Department of Pathology,181st Hospital of Chinese People’s Liberation Army, Guilin, People’s Republic of China *These authors contributed equally tothis work Abstract: CMTM4 is the most conserved member of chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing (CMTM) family on chromosome 16q22.1, a locus that harbors a number of tumor-suppressor genes. In previous studies, CMTM4 was reported to be downregulated and exhibited tumor-suppressor activities by regulating cell growth and cell cycle in clear cell renal cell carcinoma. However, its roles in tumorigenesis of hepatocellular carcinoma (HCC) remain poorly studied. This study first investigated the expression of CMTM4 in HCC, and then examined the association between the expression of CMTM4 with the clinicopathological features and prognosis of HCC patients. It was found that CMTM4 was downregulated in HCC tissues, compared with matched adjacent nontumor tissues, as detected by immunohistochemistry. In addition, Kaplan–Meier survival analysis showed that the negative expression of CMTM4 was associated with decreased overall survival rates in patients with HCC. The results of this study suggest CMTM4 plays a role as a tumor suppressor in HCC and CMTM4 negative expression is a risk factor for poor prognosis of HCC. Keywords: chemokine-like factor-like MARVEL transmembrane domain-containing 4, hepatocellular carcinoma, immunohistochemistry, prognosis

Down-regulated RINGl and YYl binding protein (RYBP) is reported to be an independent predictor of a poor prognosis in patients with hepatocellular carcinoma (HCC). However, the genetic association of RYBP polymorphisms with HCC risk and prognosis has not been investigated now. In this study, five RYBP SNPs, rs12956, rs2118593, rs17009699, rs4676875 and rs4532099, were studied from a hospital-based case-control study including 1100 cases (HCC patients) and 1100 controls (non-HCC patients) in Guangxi, China. All these SNPs interacted with environmental risk factors, such as HBV infection, alcohol intake and smoking in the pathogenesis of HCC. Compared to the CC genotype, patients with TT genotype of rs12956 had a decreased risk of HCC (OR = 0.587, 95% CI = 0.403~0.923) and an increased survival time (Co-dominant, HR = 0.745, 95% CI = 0.594~0.934), while those with TT genotype of rs2118593 had an increased risk of HCC (OR = 1.538, 95% CI = 1.093~2.735) and a decreased survival time (Co-dominant, HR = 1.447, 95% CI = 1.174~1.782). No significant difference was found between the other three RYBP polymorphisms with HCC risk and prognosis. Furthermore, we found that tumor number, tumor staging, metastasis and rs2118593 were associated with the overall survival of HCC patients by multivariate COX regression analysis. Our study suggests RYBP SNP, rs2118593 as a new predictor for poor prognosis of HCC patients.

Cytokine gene single nucleotide polymorphisms (SNPs) are involved in the genesis and progression of hepatocellular carcinoma (HCC). We hypothesized that combined effects of cytokine gene SNPs and SNP-SNP interactions are associated with HCC risk. Six SNPs in cytokine genes (IL-2, IFN-γ, IL-1β, IL-6, and IL-10) were genotyped in a study of 720 Chinese HCC cases and 784 cancer-free controls. Although none of these SNPs individually had a significant effect on the risk of HCC, we found that the combined effects of these six SNPs may contribute to HCC risk (OR=1.821, 95% CI=1.078-3.075). This risk was pronounced among smokers, drinkers, and hepatitis B virus carriers. A SNP-SNP interaction between IL-2-330 and IFN-γ-1615 was associated with an increased HCC risk (OR=1.078, 95% CI=1.022-1.136). In conclusion, combined effects of SNPs and SNP-SNP interactions in cytokine genes may contribute to HCC risk.

// Shengkui Tan 1 , Ruoyun Qin 2 , Xiaonian Zhu 1 , Chao Tan 3 , Jiale Song 1 , Linyuan Qin 1 , Liu Liu 2 , Xiong Huang 2 , Anhua Li 3 , Xiaoqiang Qiu 2 1 Department of Epidemiology, School of Public Health, Guilin Medical University, Guilin 541004, Guangxi, People’s Republic of China 2 Department of Epidemiology, School of Public Health, Guangxi Medical University, Nanning 530021, Guangxi, People’s Republic of China 3 Guangxi Center for Disease Prevention and Control, Nanning 530021, Guangxi, People’s Republic of China Correspondence to: Xiaoqiang Qiu, email: xqqiu9999@sina.com Keywords: hepatocellular carcinoma (HCC), human exonuclease 1 ( hEXO1 ), single-nucleotide polymorphisms (SNPs), interaction Received: May 31, 2016 Accepted: October 17, 2016 Published: November 23, 2016 ABSTRACT Human exonuclease 1 ( hEXO1 ) is an important nuclease involved in mismatch repair system that contributes to maintain genomic stability and modulate DNA recombination. This study is aimed to explore the associations between single-nucleotide polymorphisms (SNPs) of hEXO1 and the hereditary susceptibility of hepatocellular carcinoma (HCC). SNPs rs1047840, rs1776148, rs3754093, rs4149867, rs4149963, and rs1776181 of hEXO1 were examined from a hospital-based case-control study including 1,196 cases (HCC patients) and 1,199 controls (non-HCC patients) in Guangxi, China. We found the rs3754093 AG genotype decreased the risk of HCC (OR=0.714, 95% CI: 0.539~0.946). According to the results of stratification analysis, rs3754093 mutant genotype AG/GG decreased the risk of HCC with some HCC protective factors such as non-smoking, non-alcohol consumption and non-HCC family history, but also decreased the risk of HCC with HBV infection. Moreover, it was correlated to non-tumor metastasis and increased the survival of HCC patients. The results from gene-environment interaction assay indicated all hEXO1 SNPs interacted with smoking, alcohol consumption, HBV infection in pathogenesis of HCC. However, gene-gene interaction assay suggested the interaction between rs3754093 and other 5 SNPs were associated with reducing the HCC risk. These results suggest rs3754093 exhibits a protective activity to decrease the incidence risk of HCC in Guangxi, China. In addition, all SNPs in this study interacted with environment risk factors in pathogenesis of HCC.

We conducted a systematic review to evaluate the efficacy and safety of Chinese herbal medicine (CHM) for dysfunctional uterine bleeding (DUB) by performing a meta-analysis. Randomized controlled trials (RCTs) or quasi-RCTs comparing CHM vs no treatment, placebo, conventional western medicine (CWM), or general non-specific surgical treatment for DUB were identified by electronic and manual searches. Trials of CHM treatments with CWM treatments were compared with CWM treatments alone. Jadad scale and allocation concealment were used to assess the quality of included studies. Four RCTs or quasi-RCTs involving 525 patients were included. The methodological quality was poor in all trials except one trial. No serious adverse events were reported in the included studies. With the lack of trials comparing CHM with no treatment or placebo, it is impossible to accurately evaluate the efficacy of CHM. However, CHM in these studies seem to show an encouraging comparative effectiveness with CWM. More RCTs with a higher quality are required.

To use a hospital-based case-control study design to investigate the relationship between hepatocellular carcinoma (HCC) and the interaction of polymorphisms in the human mismatch repair gene,hMSH2,with environmental factors.Cases of new-onset,histopathology-diagnosed,and untreated (no chemotherapy or radiation therapy) HCC were enrolled between September 2009 and September 2012.A non-HCC healthy control group was also enrolled and was composed of individuals living in the same region as the cases for more than 10 years and age-/sex-matched with similar socioeconomic characteristics.All enrollees underwent hMSH2 genotyping by real-time PCR.T-test,chi-square test and unconditional logistic regression analysis was used to analyze the difference in allele frequencies among the case and control groups and the relationship between hMSH2 polymorphisms and environmental factors.Frequencies of hMSH2 rs2303428 CC,CT and TT genotypes in the HCC group were significantly different than in the control group (14.13% vs.8.21%,47.02% vs.49.47%,and 38.85% vs.42.32%;x 2=8.289,P =0.016).Individuals carrying the hMSH2 rs2303428 T allelic gene had a significantly increased risk compared to those with the hMSH2 rs2303428 C allelic gene (adjusted OR=1.228).Interactions were found between the hMSH2 genotype and hepatitis B surface antigen (HBsAg)-positive hepatitis infection (adjusted OR=1.865) and history of cancer (adjusted OR=5.634).There was no relation between hMSH2 gene rs4952887 and rs2059520 and liver cancer development or interaction with environmental factors.The hMSH2 rs2303428 genotype is positively related to risk of HCC in Chinese,with HBsAg-positive hepatitis infection starus and history of cancer increasing the risk.

To investigate the significance and relationship between the expression of FOXC1 and clinicopathological features, and to explore its correlation with E-cadherin.Immunohistochemical SP method was used to detected the expression of FOXC1 in nasopharyngeal carcinoma tissues and nasopharyngitis tissues.(1) Immunoreaction to FOXC1 was mainly located in nucleus of nasopharyngeal carcinoma cells. The positive expression rate of FOXC1 in nasopharyngeal carcinoma tissues was 85.3% (81/95), which was significantly higher than that in nasopharyngitis tissues (59.4%) (P0.05). (2) The expression of FOXC1 was not related to patients' age and gender, clinical stage of cancer and lymph node metastasis (P0.05). (3) There was a correlation between the expression of FOXC1 and down-regulated expression of E-cadherin in nasopharyngeal carcinoma tissues (P0.05).FOXC1 may play an important role in generation and progression of nasopharyngeal carcinoma, there may be a correlation between the expression of FOXC1 and down-regulated expression of E-cadherin, also FOXC1 may play an important role in the process of EMT in nasopharyngeal carcinoma by regulating E-cadherin.