Clinical significance of LINC02532 in hepatitis B virus-associated hepatocellular carcinoma and its regulatory effect on tumor progression.

BACKGROUND AND AIM: Long non-coding RNAs (lncRNAs) play an important role in tumor progression, including in hepatocellular carcinoma (HCC) induced by hepatitis B virus (HBV). Therefore, the aim of this study was to investigate the role of LINC02532 in HCC, mainly for diagnostic prognostic value and cellular function, as well as mechanistic aspects. METHODS: Initially, GEO and VirBase databases were used to screen for aberrant lncRNAs in HBV-HCC.Then, HBV-HCC persons followed up in our center were retrospectively studied to investigate the diagnostic, prognostic value of LINC02532 in HBV-HCC. Subsequently, the role of LINC02532 in HBV-HCC was measured using cellular function assay methods and possible mechanisms were analyzed in conjunction with bioinformatic predictive science. RESULTS: LINC02532 was a lncRNA abnormally expressed in HBV-HCC. LINC02532 was significantly up-regulated in the expression level in HBV-HCC tissues compared with normal tissues from patients. Moreover, LINC02532 could distinguish HBV-HCC and predict the prognosis of HBV-HCC. In vitro experiments showed that LINC02532 could regulate miR-455-3p and promote the malignant characterization of HBV-HCC cells. CHEK2 was a target gene of miR-455-3p. CONCLUSIONS: The prognosis and diagnosis of HBV-HCC can rely on the expression of LINC02532. LINC02532 was important for further progression of HBV-HCC, by moderating miR-455-3p/CHEK2.

Oral Microbiota Linking Associations of Dietary Factors with Recurrent Oral Ulcer.

Recurrent oral ulcer (ROU) is a prevalent and painful oral disorder with implications beyond physical symptoms, impacting quality of life and necessitating comprehensive management. Understanding the interplays between dietary factors, oral microbiota, and ROU is crucial for developing targeted interventions to improve oral and systemic health. Dietary behaviors and plant-based diet indices including the healthful plant-based diet index (hPDI) were measured based on a validated food frequency questionnaire. Saliva microbial features were profiled using 16S rRNA gene amplicon sequencing. In this cross-sectional study of 579 community-based participants (aged 22-74 years, 66.5% females), 337 participants had ROU. Participants in the highest tertile of hPDI exhibited a 43% lower prevalence of ROU (odds ratio [OR] = 0.57, 95%CI: 0.34-0.94), compared to the lowest tertile, independent of demographics, lifestyle, and major chronic diseases. Participants with ROU tended to have lower oral bacterial richness (Observed ASVs, p < 0.05) and distinct bacterial structure compared to those without ROU (PERMANOVA, p = 0.02). The relative abundances of 16 bacterial genera were associated with ROU (p-FDR < 0.20). Of these, Olsenella, TM7x, and unclassified Muribaculaceae were identified as potential mediators in the association between hPDI and ROU (all p-mediations < 0.05). This study provides evidence of the intricate interplays among dietary factors, oral microbiota, and ROU, offering insights that may inform preventive and therapeutic strategies targeting diets and oral microbiomes.

Structures and Dynamics of ß-Rich Oligomers of ATTR (105-115) Assembly.

Transthyretin (TTR) is a tetrameric homologous protein that can dissociate into monomers. Misfolding and aggregation of TTR can lead to amyloid transthyretin amyloidosis (ATTR), which can cause many diseases (e.g., senile systemic amyloidosis, familial amyloid cardiomyopathy, and familial amyloid polyneuropathy). Despite growing evidence indicating that small oligomers play a critical role in regulating cytotoxicity, the structures of these oligomeric intermediates and their conformational transformations are still unclear, impeding our understanding of neurodegenerative mechanisms and the development of therapeutics targeting early aggregation species. The TTR monomer protein consists of various fragments prone to self-aggregation, including the residue 105-115 sequence. Therefore, our study investigated the assembly progress of ATTR (105-115) peptides using all-atom molecular dynamics simulations. The findings indicate that the probability of ß-sheet content increases with increasing numbers of peptides. Additionally, interactions between hydrophobic residues L110 and L111 are crucial for the formation of a ß-rich oligomer formation. These ß-rich oligomers may adopt ß-barrel conformations, potentially toxic oligomer species. Free-energy analysis reveals that ß-barrel conformations serve as intermediates for these ß-rich oligomers. Our insights into the structural ensemble dynamics of ATTR (105-115) contribute to understanding the physical mechanisms underlying the ß-barrel oligomers of ATTR. These findings may shed light on the pathological role of ATTR in neurodegenerative diseases and offer potential therapeutic targets.

Chrysophanol induces apoptosis and ferroptosis of gastric cancer cells by targeted regulation of mTOR.

Programmed cell death (PCD) induction is a promising strategy for killing gastric cancer cells. In this study, we investigated the effects of chrysophanol on apoptosis and ferroptosis in gastric cancer cells. Chrysophanol in concentrations ranging from 0 to 100 µM were used to treat GES-1, HGC-27 and AGS cells. Cell counting kit-8 assay, colony formation assay, 5-ethynyl-2'-deoxyuridine staining, flow cytometry, JC-1 probe insertion, dihydroethidium staining and western blotting were performed. The effects of chrysophanol on gastric cancer cells were evaluated in vivo using a xenograft mouse model. Chrysophanol had no cytotoxic effects on GES-1 cells. Chrysophanol with concentrations higher than 25 µM inhibited gastric cancer cell colony formation and proliferation. Chrysophanol induces gastric cancer cell apoptosis in a dose-dependent manner, accompanied by mitochondrial membrane potential dysfunction and cytochrome c release. Additionally, chrysophanol increased the levels of reactive oxygen species, total iron, and Fe2+ in HGC-27 and AGS cells, in a dose-dependent manner. Treatment of cells with the ferroptosis inhibitor ferrostatin-1 attenuated the effects of chrysophanol on cell survival and the expression of ferroptosis markers SLC7A11 and GPX4. Screening by GEO software indicated that the mTOR signalling pathway is possibly regulated by chrysophanol. Furthermore, mTOR overexpression significantly reversed the inhibitory effects of chrysophanol on gastric cancer cells. In gastric cancer xenograft mouse models, chrysophanol treatment inhibited tumour growth and downregulated SLC7A11 and GPX4. Chrysophanol induces apoptosis and ferroptosis, making it a potential candidate for killing gastric cancer cells. The beneficial effects of chrysophanol may be attribute to the targeted regulation of mTOR.

The role of meteorological factors on influenza incidence among children in Guangzhou China, 2019-2022.

Objective: Analyzing the epidemiological characteristics of influenza cases among children aged 0-17 years in Guangzhou from 2019 to 2022. Assessing the relationships between multiple meteorological factors and influenza, improving the early warning systems for influenza, and providing a scientific basis for influenza prevention and control measures. Methods: The influenza data were obtained from the Chinese Center for Disease Control and Prevention. Meteorological data were provided by Guangdong Meteorological Service. Spearman correlation analysis was conducted to examine the relevance between meteorological factors and the number of influenza cases. Distributed lag non-linear models (DLNM) were used to explore the effects of meteorological factors on influenza incidence. Results: The relationship between mean temperature, rainfall, sunshine hours, and influenza cases presented a wavy pattern. The correlation between relative humidity and influenza cases was illustrated by a U-shaped curve. When the temperature dropped below 13°C, Relative risk (RR) increased sharply with decreasing temperature, peaking at 5.7°C with an RR of 83.78 (95% CI: 25.52, 275.09). The RR was increased when the relative humidity was below 66% or above 79%, and the highest RR was 7.50 (95% CI: 22.92, 19.25) at 99%. The RR was increased exponentially when the rainfall exceeded 1,625 mm, reaching a maximum value of 2566.29 (95% CI: 21.85, 3558574.07) at the highest rainfall levels. Both low and high sunshine hours were associated with reduced incidence of influenza, and the lowest RR was 0.20 (95% CI: 20.08, 0.49) at 9.4 h. No significant difference of the meteorological factors on influenza was observed between males and females. The impacts of cumulative extreme low temperature and low relative humidity on influenza among children aged 0-3 presented protective effects and the 0-3 years group had the lowest RRs of cumulative extreme high relative humidity and rainfall. The highest RRs of cumulative extreme effect of all meteorological factors (expect sunshine hours) were observed in the 7-12 years group. Conclusion: Temperature, relative humidity, rainfall, and sunshine hours can be used as important predictors of influenza in children to improve the early warning system of influenza. Extreme weather reduces the risk of influenza in the age group of 0-3 years, but significantly increases the risk for those aged 7-12 years.

Exploring the misfolding and self-assembly mechanism of TTR (105-115) peptides by all-atom molecular dynamics simulation.

Pathological aggregation of essentially dissociative Transthyretin (TTR) monomers protein, driven by misfolded and self-interaction, is connected with Amyloid Transthyretin amyloidosis (ATTR) disease. The TTR monomers protein contains several fragments that tend to self-aggregate, such as residue 105-115 sequence [TTR (105-115)]. However, the misfolding and aggregation mechanisms of TTR are still unknown. In this study, we explored the misfolding and self-assembly of TTR (105-115) peptides by all-atom molecular dynamics simulation. Our results indicated that the conformation of the two-peptides appears unstable. In the tetramerization and hexamerization simulations, the results are reversed. When the number of peptides increases, the probability and the length of ß-Sheet contents increase. Our results show that that the four- and six-peptides both can form ß-Barrel intermediates and then aggregate into fibers. The critical nucleation for the formation of fibril should be larger than four-peptides. The interactions between hydrophobic residues I107-L111 play an important role in the formation of stable fibrils at an early stage. Our results on the structural ensembles and early aggregation dynamics of TTR (105-115) will be useful to comprehend the nucleation and fibrillization of TTR (105-115).

Identifying the anti-metastasis effect of Anhydroicaritin on breast cancer: Coupling network pharmacology with experimental validation.

ETHNOPHARMACOLOGICAL RELEVANCE: Epimedium brevicornu Maxim. and Cullen corylifolium (L.) Medik. are part of a traditional Chinese medicine (TCM) drug pair (ECDP) widely used in the clinical treatment of breast cancer (BC). Both drugs have been proven to have anti-tumor effect. However, the active ingredients and molecular mechanism of ECDP remain to be explored. AIM OF THE STUDY: To explore the efficacy and potential mechanisms of actions of herb pair through network pharmacology and in vitro and in vivo experiments. MATERIALS AND METHODS: The active ingredients of ECDP were identified using high-performance liquid chromatography. The corresponding potential target genes for ECDP components and BC were extracted from established databases, and the protein-protein interaction network of shared genes was constructed using STRING database. The effective ingredients and targets of ECDP for BC were obtained through the TCMSP database and GeneCards database. The potential targets and pathways were selected through the protein interaction network and enrichment analysis. Proliferation and migration experiments in vitro and tumor growth in vivo were performed to evaluate the effects of Anhydroicaritin (AHI) on BC. RESULTS: AHI is the potential candidate active ingredient of ECDP through TCMSP. Molecular docking revealed that AHI has excellent binding ability with TP53, VEGFA, MMP2, and Met. In vitro experiment results showed that AHI inhibits the growth of MDA-MB-231, 4T1, MCF-7, and SK-BR-3 BC cells. The inhibitory effect of AHI on triple-negative BC cells is more obvious. With the increase of AHI concentration, the colony-forming, migration, and metastasis abilities of the MDA-MB-231 and 4T1 cells gradually decreases. In addition, Western blot and reverse transcription polymerase chain reaction analyses results indicated that AHI downregulates HIF-1α/VEGFA signaling in triple-negative BC cells. AHI inhibits tumor growth and lung metastasis while downregulating the expression of HIF-1α and VEGFA. CONCLUSION: AHI may play an anti-BC effect by inhibiting cancer cell proliferation, invasion, and metastasis. The results of this study may provide a theoretical basis for AHI research and the clinical application of ECDP in BC.

COVID-19 and the digestive system: A comprehensive review.

The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is spreading at an alarming rate, and it has created an unprecedented health emergency threatening tens of millions of people worldwide. Previous studies have indicated that SARS-CoV-2 ribonucleic acid could be detected in the feces of patients even after smear-negative respiratory samples. However, demonstration of confirmed fecal-oral transmission has been difficult. Clinical studies have shown an incidence rate of gastrointestinal (GI) symptoms ranging from 2% to 79.1% in patients with COVID-19. They may precede or accompany respiratory symptoms. The most common GI symptoms included nausea, diarrhea, and abdominal pain. In addition, some patients also had liver injury, pancreatic damage, and even acute mesenteric ischemia/thrombosis. Although the incidence rates reported in different centers were quite different, the digestive system was the clinical component of the COVID-19 section. Studies have shown that angiotensin-converting enzyme 2, the receptor of SARS-CoV-2, was not only expressed in the lungs, but also in the upper esophagus, small intestine, liver, and colon. The possible mechanism of GI symptoms in COVID-19 patients may include direct viral invasion into target cells, dysregulation of angiotensin-converting enzyme 2, immune-mediated tissue injury, and gut dysbiosis caused by microbiota. Additionally, numerous experiences, guidelines, recommendations, and position statements were published or released by different organizations and societies worldwide to optimize the management practice of outpatients, inpatients, and endoscopy in the era of COVID-19. In this review, based on our previous work and relevant literature, we mainly discuss potential fecal-oral transmission, GI manifestations, abdominal imaging findings, relevant pathophysiological mechanisms, and infection control and prevention measures in the time of COVID-19.

Therapeutic potential of targeting HSPA5 through dual regulation of two candidate prognostic biomarkers ANXA1 and PSAT1 in osteosarcoma.

Osteosarcoma is the most common primary malignant bone tumor that mostly affects young people's health. The prognosis of patients with unresectable or recurrent osteosarcoma still remains dismal. Based on gene integration analysis from GEO and TARGET databases by R language, the differentially expressed genes of osteosarcoma patients were identified. Biological molecular function analysis indicated that these genes were importantly enriched in the process of cell adhesion molecule binding. Gene significance highly-related to clinical traits of osteosarcoma was found by weighted gene co-expression network analysis. Additionally, receiver operating characteristic curve analysis was conducted to find prognostic markers in LASSO Cox regression model. Two candidate biomarkers, ANXA1 and PSAT1, for the prognosis of osteosarcoma were detected separately on the basis of WGCNA and LASSO model. Of note, their expression profiles were interrelated with an important therapeutic target HSPA5. In vitro pharmaceutical experiments were performed to explore the biological role and prognostic benefit of candidates. Suppression of HSPA5 effectively upregulated ANXA1 and inhibited PSAT1, resulting in osteosarcoma cell proliferation arrest and apoptosis. These findings suggest that HSPA5 serves as a core molecule for osteosarcoma therapy due to its bidirectional regulation of candidate prognostic biomarkers ANXA1 and PSAT1.

Immunological role and underlying mechanisms of B7-H6 in tumorigenesis.

B7 homolog 6 (B7-H6) has been identified as involved in tumorigenesis. Elucidating its role and potential mechanism of action is essential for understanding tumorigenesis and the potential development of an effective clinical strategy. Abnormal overexpression of B7-H6 in various types of tumors was reported to be linked with poor prognosis. B7-H6 suppresses the initiation of the "caspase cascade" and induces anti-apoptosis by STAT3 pathway activation to provoke tumorigenesis. B7-H6 facilitates tumor proliferation and cell cycle progression by regulating apoptosis suppressors. B7-H6 induces cellular cytotoxicity, secretion of TNF-α and IFN-γ and B7-H6-specific BiTE triggers T cells to accelerate tumorigenesis. B7-H6 induces abnormal immunological progression by HER2-scFv mediated ADCC and NKp30 immune escape to promote tumorigenesis. B7-H6 promotes tumorigenesis via apoptosis inhibition, proliferation and immunological progression. B7-H6 may a valuable potential biomarker and therapeutic strategy for diagnostics, prognostics and treatment in cancer.

LncRNA HRCEG, regulated by HDAC1, inhibits cells proliferation and epithelial-mesenchymal-transition in gastric cancer.

Recently, a number of long noncoding RNAs (lncRNAs) have been reported to play significant roles in human tumorigenesis. However, only few gastric cancer related lncRNAs have been well characterized. Here, we identified one lncRNA HRCEG, whose expression was decreased in the gastric cancer tissues compared with adjacent normal tissues. Overexpression of HRCEG significantly promoted cell apoptosis and inhibited cell proliferation. Importantly, we demonstrated that HRCEG levels inversely correlated with EMT process and HRCEG was regulated by the histone deacetylase 1 (HDAC1) in gastric cancer. These findings suggest that HRCEG might be regulated by HDAC1 to inhibit gastric cancer progress and metastatic capability via EMT pathway.

FOXD3 may be a new cellular target biomarker as a hypermethylation gene in human ovarian cancer.

BACKGROUND: FOXD3 is aberrantly regulated in several tumors, but its underlying mechanisms in ovarian cancer (OC) remains largely unknown. The present study aimed to explore the role and associated mechanisms of FOXD3 in OC. METHODS: Microarray data from GEO was used to analyze differential CpG sites and differentially methylated regions (DMR) in tumor tissues and Illumina 450 genome-wide methylation data was employed. The FOXD3 expression level was determined through qRT-PCR and western blot analysis. Wound healing test, colony formation and flow cytometry assay were utilized to analyze cell migration, proliferation abilities, cell cycle and cell apoptosis, respectively. Finally, the effect of FOXD3 on tumor growth was investigated through in vivo xenograft experiments. RESULTS: GEO data analysis showed that FOXD3 was hypermethylated in OC tissues. Also, qRT-PCR revealed that FOXD3 was low expressed and methylation-specific PCR (MSP) confirmed that the methylation level of FOXD3 was hypermethylated. Combined treatment of 5-aza-2'-deoxycytidine (5-Aza-dC) could synergistically restored FOXD3 expression. Finally, in vitro and in vivo experiments showed that demethylated FOXD3 decreased cell proliferation and migration abilities, and increased the cell apoptosis. In vivo experiment detected that demethylated FOXD3 restrained tumor growth. CONCLUSIONS: FOXD3 could act as a tumor suppressor to inhibit cell proliferation, migration and promote cell apoptosis in OC cells.

Association of serum ferritin with non-alcoholic fatty liver disease: a meta-analysis.

BACKGROUND: A growing number of studies reported the connection between the level of serum ferritin (SFL) and non-alcoholic fatty liver disease (NAFLD). However, such connection was still disputable. The aim of our meta-analysis was to estimate SFL between the groups as below: patients with NAFLD against control group; non-alcoholic steatohepatitis (NASH) patients against control group; non-alcoholic fatty liver (NAFL) patients against a control group and NASH patients vs NAFL patients. METHODS: We screened the studies in PubMed, EMBASE, the Cochrane Database and the Cochrane Central register controlled trials from the beginning to July 10, 2016 to find the studies indicated the connection between SFL and NAFLD (NAFL and/or NASH). Fourteen published studies which evaluate the SFL in NAFLD patients were selected. RESULTS: Higher SFL was noticed in NAFLD patients against control group (standardized mean difference [SMD] 1.01; 95% CI 0.89, 1.13), NASH patients against control group (SMD 1.21; 95% CI 1.00, 1.42), NAFL patients against control group (SMD 0.51; 95% CI 0.24, 0.79) and NASH patients against NAFL patients (SMD 0.63; 95% CI 0.52, 0.75). These results remained unaltered actually after the elimination of studies which were focused on paediatric or adolescent populations. Higher SFL was presented in NAFLD patients against the control group (SMD 1.08; 95% CI 0.95, 1.20) in adults and NASH patients against NAFL patients in adults (SMD 0.74; 95% CI 0.62, 0.87). The connection between SFL and NASH against NAFL group in paediatric or adolescent populations was observed inconsistently (SMD 0.10; 95% CI -0.18, 0.38). CONCLUSIONS: The level of SFL was elevated in patients with NAFLD (NAFL and/or NASH) compared with the controls. Compared with NAFL, The level of SFL was increased in NASH. The result remained unaltered actually after the elimination of studies focused on paediatric or adolescent populations.

Comparison between smaller ruptured intracranial aneurysm and larger un-ruptured intracranial aneurysm: gene expression profile analysis.

As it grows in size, an intracranial aneurysm (IA) is prone to rupture. In this study, we compared two extreme groups of IAs, ruptured IAs (RIAs) smaller than 10 mm and un-ruptured IAs (UIAs) larger than 10 mm, to investigate the genes involved in the facilitation and prevention of IA rupture. The aneurismal walls of 6 smaller saccular RIAs (size smaller than 10 mm), 6 larger saccular UIAs (size larger than 10 mm) and 12 paired control arteries were obtained during surgery. The transcription profiles of these samples were studied by microarray analysis. RT-qPCR was used to confirm the expression of the genes of interest. In addition, functional group analysis of the differentially expressed genes was performed. Between smaller RIAs and larger UIAs, 101 genes and 179 genes were significantly over-expressed, respectively. In addition, functional group analysis demonstrated that the up-regulated genes in smaller RIAs mainly participated in the cellular response to metal ions and inorganic substances, while most of the up-regulated genes in larger UIAs were involved in inflammation and extracellular matrix (ECM) organization. Moreover, compared with control arteries, inflammation was up-regulated and muscle-related biological processes were down-regulated in both smaller RIAs and larger UIAs. The genes involved in the cellular response to metal ions and inorganic substances may facilitate the rupture of IAs. In addition, the healing process, involving inflammation and ECM organization, may protect IAs from rupture.

Expression profile of long noncoding RNAs in human cerebral aneurysms: a microarray analysis.

OBJECTIVE The pathogenesis of cerebral aneurysms (CAs) remains largely unknown. Long noncoding RNAs (lncRNAs) were reported recently to play crucial roles in many physiological and biological processes. Here, the authors compared the gene-expression profiles of CAs and their control arteries to investigate the potential functions of lncRNAs in the formation of CAs. METHODS A prospective case-control study was designed to identify the changes in expression of lncRNAs and mRNAs between 12 saccular CA samples (case group) and 12 paired superficial temporal artery samples (control group). Microarray analysis was performed to investigate the expression of lncRNAs and messenger RNAs (mRNAs), and reverse-transcription quantitative polymerase chain reaction was used to validate the microarray analysis findings. Then, an lncRNA target-prediction program and gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were applied to explore potential lncRNA functions. RESULTS A comparison between the case and control groups revealed that 1518 lncRNAs and 2545 mRNAs were expressed differentially. By using target-prediction program analysis, the authors constructed a complex network consisting of 2786 matched lncRNA-mRNA pairs, in which ine1 mRNA was potentially targeted by one to tens of lncRNAs, and vice versa. The results of further gene ontology and KEGG pathway analyses indicated that lncRNAs were involved mainly in regulating immune/inflammatory processes/pathways and vascular smooth muscle contraction, both of which are known to have crucial pathobiological relevance in terms of CA formation. CONCLUSIONS By comparing CAs with their control arteries, the authors created an expression profile of lncRNAs in CAs and propose here their possible roles in the pathogenesis of CAs. The results of this study provide novel insight into the mechanisms of CA pathogenesis and shed light on developing new therapeutic intervention for CAs in the future.

Differential long non­coding RNA and mRNA expression in differentiated human glioblastoma stem cells.

Differentiation of glioblastoma stem cells (GSCs) may lead to inhibition of their self­renewing ability and tumorigenic potential, as well as increasing their sensitivity to treatment. The critical role of long non­coding RNAs (lncRNAs) in numerous biological processes has been revealed. However, the involvement of lncRNAs in GSC differentiation remains to be elucidated. In the present study, GSCs were isolated from patient samples and differentiation was induced. Using a high­throughput microarray, the present study identified a profile of 1,545 lncRNAs and 2,729 mRNAs that differed between GSCs and their non­differentiated counterparts. To ascertain the association between the altered lncRNAs and mRNAs, a co­expression network was constructed in which 1,087 lncRNAs and 1,928 mRNAs altered upon GSC differentiation formed a total of 19,642 lncRNA­mRNA pairs. Based on the co­expression network, the lncRNA functions were additionally predicted by a cis­ or trans­ targeting program. Furthermore, three pairs of lncRNAs and their nearby target mRNAs were selected [ENSG00000261924.1­regulatory associated protein of MTOR complex 1, ENSG00000235427.1­caveolin 1 and Tax1 binding protein 3 (TAX1BP3)­purinergic receptor P2X 5 (P2RX5)­TAX1BP3] and their expression levels were validated by reverse transcription­quantitative polymerase chain reaction. The altered lncRNAs were also regulated by various pluripotency transcription factors (POU domain, class 3, transcription factor, sex determining region Y­box 2, spalt­like transcription factor 2 and oligodendrocyte lineage transcription factor 2). In conclusion, the results of the present study revealed that lncRNAs may function in GSC differentiation by regulating their target mRNAs, and a set of lncRNAs were identified as candidates for further study concerning the future treatment of GSCs.

LncRNA MT1JP functions as a tumor suppressor by interacting with TIAR to modulate the p53 pathway.

Accumulating evidence suggests that long noncoding RNAs (lncRNAs) play important roles in transcriptional regulation, whereas the extent to which the lncRNAs also function at the posttranscriptional level is less known. In the present study, we report a lncRNA named MT1JP which acts as a tumor suppressor through a posttranscriptional mechanism. We found that MT1JP is differentially expressed in tumor tissues by analyzing data from a customized microarray applied to 76 pairs of matched normal and cancer tissue samples. By associating with the RNA-binding protein TIAR, MT1JP enhanced the translation of the master transcription factor p53, thereby regulating a series of pathways involving p53, such as the cell cycle, apoptosis and proliferation. When MT1JP was down-regulated, the protein level of p53 declined, which in turn accelerated cell deterioration and tumor formation. Moreover, differential expression of MT1JP in cancerous and normal tissues suggests that it may be a promising prognostic marker and a therapeutic target. Taken together, we identified MT1JP as a critical factor in restraining cell transformation by modulating p53 translation through interactions with TIAR, and this finding is likely to shed new light on future investigations about posttranscriptional or translational effects of lncRNAs during cell transformation.

BioCircos.js: an interactive Circos JavaScript library for biological data visualization on web applications.

UNLABELLED: We here present BioCircos.js, an interactive and lightweight JavaScript library especially for biological data interactive visualization. BioCircos.js facilitates the development of web-based applications for circular visualization of various biological data, such as genomic features, genetic variations, gene expression and biomolecular interactions. AVAILABILITY AND IMPLEMENTATION: BioCircos.js and its manual are freely available online at http://bioinfo.ibp.ac.cn/biocircos/ CONTACT: rschen@ibp.ac.cn SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

Transcriptional profiling analysis and functional prediction of long noncoding RNAs in cancer.

Long noncoding RNAs (lncRNAs), which are noncoding RNAs (ncRNAs) with length more than 200 nucleotides (nt), have been demonstrated to be involved in various types of cancer. Consequently, it has been frequently discussed that lncRNAs with aberrant expression in cancer serve as potential diagnostic biomarkers and therapeutic targets. However, one major challenge of developing cancer biomarkers is tumor heterogeneity which means that tumor cells show different cellular morphology, metastatic potential as well as gene expression. In this study, a custom designed microarray platform covering both mRNAs and lncRNAs was applied to tumor tissues of gastric, colon, liver and lung. 316 and 157 differentially expressed (DE-) protein coding genes and lncRNAs common to these four types of cancer were identified respectively. Besides, the functional roles of common DE-lncRNAs were inferred based on their expression and genomic position correlation with mRNAs. Moreover, mRNAs and lncRNAs with tissue specificity were also identified, suggesting their particular roles with regard to specific biogenesis and functions of different organs. Based on the large-scale survey of mRNAs and lncRNAs in four types of cancer, this study may offer new biomarkers common or specific for various types of cancer.