Circ_0007386 Promotes the Progression of Hepatocellular Carcinoma Through the miR-507/ CCNT2 Axis.

Background: Circular RNAs (circRNAs) have been shown to play a crucial role in the initiation and development of Hepatocellular carcinoma (HCC). However, the mechanism and function of circ_0007386 in HCC are still unknown. Methods: Circ_0007386 expression level in HCC tissues, and HCC cell lines was further analyzed by qRT-PCR. Agarose gel electrophoresis and Sanger sequencing were used to figure out the structure of circ_0007386. The involvement of circ_0007386 in HCC development was evaluated by experimental investigations conducted in both laboratory settings (in vitro) and living organisms (in vivo). RNA immunoprecipitation, Western blotting, luciferase reporter assay and fluorescence in situ hybridization (FISH) were applied for finding out the interaction among circ_0007386, miR-507 and CCNT2. To assess the connection between circ_0007386 and lenvatinib resistance, lenvatinib-resistant HCC cell lines were employed. Results: The expression of circ_0007386 was found to increase in HCC tissues, and it was observed to be associated with a worse prognosis. Overexpression of circ_0007386 stimulated HCC cells proliferation, invasion, migration and the epithelial-mesenchymal transition (EMT) while silencing of circ_0007386 resulted in the opposite effect. Mechanistic investigations revealed that circ_0007386 acted as a competing endogenous RNA of miR-507 to prevent CCNT2 downregulation. Downregulating miR-507 or overexpressing CCNT2 could reverse phenotypic alterations that originated from inhibiting of circ_0007386. Importantly, circ_0007386 determines the resistance of hepatoma cells to lenvatinib treatment. Conclusion: Circ_0007386 advanced HCC progression and lenvatinib resistance through the miR-507/ CCNT2 axis. Meanwhile, circ_0007386 served as a potential biomarker and therapeutic target in HCC patients.

Effect of Cobalt on Lifetime of Sb4O5Cl2-Graphene Anode in Chloride-Ion Batteries.

Anode materials based on metal oxychlorides hold promise in addressing electrode dissolution challenges in aqueous-based chloride ion batteries (CIBs). However, their structural instability following chloride ion deintercalation can lead to rapid degradation and capacity fading. This paper investigates a cobalt-doped Sb4O5Cl2-graphene (Co-Sb4O5Cl2@GO) composite anode for aqueous-based CIBs. It exhibits significantly enhanced discharge capacity of 82.3 mAh g-1 after 200 cycles at 0.3 A g-1; while, the undoped comparison is only 23.5 mAh g-1 in the same condition. It also demonstrated with a long-term capacity retention of 72.8 % after 1000 cycles (65.5 mAh g-1) and a favorable rate performance of 25 mAh g-1 at a high current density of 2 A g-1. Undertaken comprehensive studies via in-situ experiments and DFT calculations, the cobalt (Co) dopant is demonstrated as the crucial role to enhance the lifetime of Sb4O5Cl2-based anodes. It is found that, the Co dopant improves electronic conductivity and the diffusion of chloride ions beside increases the structural stability of Sb4O5Cl2 crystal. Thus, this element doping strategy holds promise for advancing the field of Sb4O5Cl2-based anodes for aqueous-based CIBs, and insights gain from this study also offer valuable knowledge to develop high-performance electrode materials for electrochemical deionization.

Suppression of deep-level traps via semicarbazide hydrochloride additives for high-performance tin-based perovskite solar cells.

Tin perovskites with exemplary optoelectronic properties offer potential application in lead-free perovskite solar cells. However, Sn vacancies and undercoordinated Sn ions on the tin perovskite surfaces can create deep-level traps, leading to non-radiative recombination and absorption of nucleophilic O2 molecules, impeding further device efficiency and stability. Here, in this study, a new additive of semicarbazide hydrochloride (SEM-HCl) with a N-C=O functional group was introduced into the perovskite precursor to fabricate high-quality films with a low concentration of deep-level trap densities. This, in turn, serves to prevent undesirable interaction between photogenerated carriers and adsorbed oxygen molecules in the device's operational environment, ultimately reducing the proliferation of superoxide entities. As the result, the SEM-HCl-derived devices show a peak efficiency of 10.9% with improved device stability. These unencapsulated devices maintain almost 100% of their initial efficiencies after working for 100 h under continuous AM1.5 illumination conditions.

Mitochondrial transfer in hematological malignancies.

Mitochondria are energy-generated organelles and take an important part in biological metabolism. Mitochondria could be transferred between cells, which serves as a new intercellular communication. Mitochondrial transfer improves mitochondrial defects, restores the biological functions of recipient cells, and maintains the high metabolic requirements of tumor cells as well as drug resistance. In recent years, it has been reported mitochondrial transfer between cells of bone marrow microenvironment and hematological malignant cells play a critical role in the disease progression and resistance during chemotherapy. In this review, we discuss the patterns and mechanisms on mitochondrial transfer and their engagement in different pathophysiological contexts and outline the latest knowledge on intercellular transport of mitochondria in hematological malignancies. Besides, we briefly outline the drug resistance mechanisms caused by mitochondrial transfer in cells during chemotherapy. Our review demonstrates a theoretical basis for mitochondrial transfer as a prospective therapeutic target to increase the treatment efficiency in hematological malignancies and improve the prognosis of patients.

Hematopoietic stem cells suppress proliferation and enhance differentiation of leukemia cells through regulating apoptotic and inflammatory genes.

PURPOSE: Stem cells are known to play an important role in tumor treatment and many of them have shown tumor-suppressing ability in different cancers; however, whether hematopoietic stem cells (HSCs) have growth-inhibiting effects on leukemia cells has not been fully evaluated. Herein, we aimed to demonstrate the growth-restraining function of HSCs in acute leukemia treatment. METHODS: Cell fusion experiment was conducted by PEG-1500. The viability, proliferation, apoptosis and differentiation of leukemia cells were evaluated by cell counting, CCK-8 and flow cytometry analysis. The morphological changes were imaged using a fluorescence microscope. The expression of genes was detected by quantitative reverse transcription PCR (qRT-PCR). RESULTS: We observed that HSCs and their lytic extracts had the capability to suppress leukemia cells proliferation, promote apoptosis and especially induce acute myelogenous leukemia (AML) cells differentiation, which might have an effect on differentiation therapy to leukemia especially AML treatment. The expression levels of Bcl-2, Survivin decreased and Bax increased following HSCs extracts treatment. Furthermore, the expression of inflammatory cytokines also changed in AML cells which might have to do with the mechanism of HSCs/extracts suppressing effect. CONCLUSION: HSCs and their extracts can suppress the proliferation of leukemia cells and enhance the differentiation of AML cells and using the extracts of HSCs might be a probable therapeutic option for acute leukemia.

Exosome-transported circHDAC1_004 Promotes Proliferation, Migration, and Angiogenesis of Hepatocellular Carcinoma by the miR-361-3p/NACC1 Axis.

Background and Aims: Hepatocellular carcinoma (HCC) is among the most common malignant tumors globally. Circular RNAs (circRNAs), as a type of noncoding RNAs, reportedly participate in various tumor biological processes. However, the role of circHDAC1_004 in HCC remains unclear. Thus, we aimed to explore the role and the underlying mechanisms of circHDAC1_004 in the development and progression of HCC. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect circHDAC1_004 expression (circ_0005339) in HCC. Sanger sequencing and agarose gel electrophoresis were used to determine the structure of circHDAC1_004. In vitro and in vivo experiments were used to determine the biological function of circHDAC1_004 in HCC. Herein, qRT-PCR, RNA immunoprecipitation, western blotting, and a luciferase reporter assay were used to explore the relationships among circHDAC1_004, miR-361-3p, and NACC1. Results: circHDAC1_004 was upregulated in HCC and significantly associated with poor overall survival. circHDAC1_004 promoted HCC cell proliferation, stemness, migration, and invasion. In addition, circHDAC1_004 upregulated human umbilical vein endothelial cells (HUVECs) and promoted angiogenesis through exosomes. circHDAC1_004 promoted NACC1 expression and stimulated the epithelial-mesenchymal transition pathway by sponging miR-361-3p. Conclusions: We found that circHDAC1_004 overexpression enhanced the proliferation, stemness, and metastasis of HCC via the miR-361-3p/NACC1 axis and promoted HCC angiogenesis through exosomes. Our findings may help develop a possible therapeutic strategy for HCC.

The genetic polymorphisms of immune-related genes contribute to the susceptibility and survival of lymphoma.

BACKGROUND: Though immunological abnormalities have been proven involved in the pathogenesis of lymphoma, the underlying mechanism remains unclear. METHODS: We investigated 25 single nucleotide polymorphisms (SNPs) of 21 immune-related genes and explored their roles in lymphoma. The genotyping assay of the selected SNPs was used by the Massarray platform. Logistic regression and Cox proportional hazards models were used to analyze the associations of SNPs and the susceptibility of lymphoma or clinical characteristics of lymphoma patients. In addition, Least Absolute Shrinkage and Selection Operator regression was used to further analyze the relationships with the survival of lymphoma patients and candidate SNPs, and the significant difference between genotypes was verified by the expression of RNA. RESULTS: By comparing 245 lymphoma patients with 213 healthy controls, we found eight important SNPs related to the susceptibility of lymphoma, which were involved in JAK-STAT, NF-κB and other functional pathways. We further analyzed the relationships between SNPs and clinical characteristics. Our results showed that both IL6R (rs2228145) and STAT5B (rs6503691) significantly contributed to the Ann Arbor stages of lymphoma. And the STAT3 (rs744166), IL2 (rs2069762), IL10 (rs1800871), and PARP1 (rs907187) manifested a significant relationship with the peripheral blood counts in lymphoma patients. More importantly, the IFNG (rs2069718) and IL12A (rs6887695) were associated with the overall survival (OS) of lymphoma patients remarkably, and the adverse effects of GC genotypes could not be offset by Bonferroni correction for multiple comparison in rs6887695 especially. Moreover, we determined that the mRNA expression levels of IFNG and IL12A were significantly decreased in patients with shorter-OS genotypes. CONCLUSIONS: We used multiple methods of analysis to predict the correlations between lymphoma susceptibility, clinical characteristics or OS with SNPs. Our findings reveal that immune-related genetic polymorphisms contribute to the prognosis and treatment of lymphoma, which may serve as promising predictive targets.

EIF4A3-induced Circ_0001187 facilitates AML suppression through promoting ubiquitin-proteasomal degradation of METTL3 and decreasing m6A modification level mediated by miR-499a-5p/RNF113A pathway.

Aberrant expression of circRNAs has been proven to play a crucial role in the progression of acute myeloid leukemia (AML); however, its regulatory mechanism remains unclear. Herein, we identified a novel circRNA, Circ_0001187, which is downregulated in AML patients, and its low level contributes to a poor prognosis. We further validated their expression in large-scale samples and found that only the expression of Circ_0001187 was significantly decreased in newly diagnosed (ND) AML patients and increased in patients with hematological complete remission (HCR) compared with controls. Knockdown of Circ_0001187 significantly promoted proliferation and inhibited apoptosis of AML cells in vitro and in vivo, whereas overexpression of Circ _0001187 exerted the opposite effects. Interestingly, we found that Circ_0001187 decreases mRNA m6A modification in AML cells by enhancing METTL3 protein degradation. Mechanistically, Circ_0001187 sponges miR-499a-5p to enhance the expression of E3 ubiquitin ligase RNF113A, which mediates METTL3 ubiquitin/proteasome-dependent degradation via K48-linked polyubiquitin chains. Moreover, we found that the low expression of Circ _0001187 is regulated by promoter DNA methylation and histone acetylation. Collectively, our findings highlight the potential clinical implications of Circ _0001187 as a key tumor suppressor in AML via the miR-499a-5p/RNF113A/METTL3 pathway.

Clinical and prognostic profile of SRSF2 and related spliceosome mutations in patients with acute myeloid leukemia.

BACKGROUND: Mutations in splicing factor (SF) genes are frequently detected in myelodysplastic syndrome, but their clinical and prognostic relevance in acute myeloid leukemia (AML) have rarely been reported. METHODS: A total of 368 newly diagnosed non-M3 AML patients were included in this study. Next generation sequencing including four SF genes was performed on the genomicDNA. The clinical features and survival were analyzed using statistical analysis. RESULTS: We found that 64 of 368 patients harbored SF mutations. The SF mutations were much more frequently found in older or male patients. SRSF2 mutations were shown obviously co-existed with IDH2 mutation. The level of measurable residual disease after first chemotherapy was higher in SF-mutated patients compared to that in SF-wild patients, while the complete remission rate was significantly decreased. And the overall survival of SF-mutated patients was shorter than that of SF-wild patients. Moreover, our multivariable analysis suggests that the index of male, Kit mutation or ZRSR2 mutation was the independent risk factor for overall survival. SRSF2mut was associated with older age, higher proportion of peripheral blasts or abnormal cell proportion by flow cytometry. CONCLUSION: SF mutation is a distinct subgroup of AML frequently associated with clinic-biological features and poor outcome. SRSF2mut could be potential targets for novel treatment in AML.

Untargeted metabolomic analysis reveals the mechanism of Enterococcus faecium agent induced CaCO3 scale inhibition.

In this study, a lactic acid bacterium, Enterococcus faecium, was found to prevent CaCO3 precipitation through its metabolism. On analysis of all stages of E. faecium growth, static jar tests demonstrated that stationary phase E. faecium broth possessed the highest inhibition efficiency of 97.3% at a 0.4% inoculation dosage, followed by the decline and log phases with efficiencies of 90.03% and 76.07%, respectively. Biomineralization experiments indicated that E. faecium fermented the substrate to produce organic acid, which resulted in modulation of the pH and alkalinity of the environment and thus inhibited CaCO3 precipitation. Surface characterization techniques indicated that the CaCO3 crystals precipitated by the E. faecium broth tended to be significantly distorted and formed other organogenic calcite crystals. The scale inhibition mechanisms were revealed by untargeted metabolomic analysis on log and stationary phase E. faecium broth. In total, 264 metabolites were detected, 28 of which were differential metabolites (VIP ≥ 1 and p < 0.05). Of these, 15 metabolites were upregulated in stationary phase broth, and 13 metabolites were downregulated in log phase broth. Metabolic pathway analysis suggested that improved glycolysis and the TCA cycle were the main reasons for enhancement of the antiscaling performance of E. faecium broth. These findings have significant implications for microbial metabolism-induced CaCO3 scale inhibition.

Long noncoding RNA 02027 inhibits proliferation, migration and invasion of hepatocellular carcinoma via miR-625-3p/PDLIM5 pathway.

BACKGROUND: Long non-coding RNAs have been established to promote or inhibit the oncogenic and tumorigenic potential of various cancers, acting as competing endogenous RNAs (ceRNAs) for specific microRNAs. The primary objective of the study was to investigate the underlying mechanism by which the LINC02027/miR-625-3p/PDLIM5 axis affects proliferation, migration and invasion in hepatocellular carcinoma (HCC). METHODS: The differentially expressed gene was selected based on gene sequencing and bioinformation database analysis of HCC and adjacent non-tumor tissues. The expression of LINC02027 in HCC tissues and cells and its regulatory effect on the development of HCC were detected by colony formation, cell counting kit-8 assays, wound healing assays, Transwell assays and subcutaneous tumorigenesis assays in nude mice. According to the results of database prediction, quantitative real-time polymerase chain reaction and dual-luciferase reporter assay, the downstream microRNA and target gene were searched. Finally, HCC cells were transfected with lentivirus and used for cell function assays in vitro and in vivo. RESULTS: Downregulation of LINC02027 was detected in HCC tissues and cell lines and was associated with poor prognosis. The overexpression of LINC02027 suppressed the proliferation, migration and invasion of HCC cells. Mechanistically, LINC02027 inhibited epithelial-to-mesenchymal transition. As a ceRNA, LINC02027 inhibited the malignant ability of HCC by competitively binding to miR-625-3p to regulate the expression of PDLIM5. CONCLUSIONS: The LINC02027/miR-625-3p/PDLIM5 axis inhibits the development of HCC.

Biofilm-induced corrosion inhibition of Q235 carbon steel by anaerobic Bacillus cereus inoculum in simulated cooling water.

In this study, the corrosion behavior of Q235 carbon steel (CS) under a Bacillus cereus (B. cereus) inoculum in simulated cooling water was evaluated. The weight loss study proved B. cereus inoculum possessed anticorrosion efficiencies of 92.84% and 73.88% for 3-day and 14-day rotation tests, respectively. The electrochemical measurements indicated that the added B. cereus inoculum increased the charge transfer resistance and reduced corrosion current density. B. cereus cells with strong biofilm-forming capacity were able to adhere onto the Q235 CS surface to form compact biofilms and cause biomineralization. Surface characterization analysis demonstrated that the presence of the B. cereus inoculum reduced the amount of Fe2O3 and simultaneously increased the amount of CaCO3 in corrosion products. The corrosion inhibition mechanisms of the B. cereus inoculum involve forming biofilm, generating a biomineralized layer, and consuming dissolved oxygen. Thus, B. cereus inoculum provides a biological strategy for industrial cooling water anticorrosion application.

Dopamine Hydrochloride-Assisted Synergistic Modulation of Perovskite Crystallization and Sn2+ Oxidation for Efficient and Stable Lead-free Solar Cells.

Tin perovskites have received great concern in solar cell research owing to their favorable optoelectronic performance and environmental friendliness. However, due to their poor crystallization and easy oxidation, the performance improvement for tin-based perovskite solar cells (TPSCs) is rather challenging. Herein, reductive 3-hydroxytyramine hydrochloride (DACl) with NH2·HCl and phenol groups as co-additives with SnF2 is added into the precursor to modulate perovskite crystallization and inhibit Sn2+ oxidation for high-performance TPSCs. The Lewis base group of NH2 HCl in DACl could bind to perovskite lattices to modulate the crystallization with suppressed defects in the bulk and grain boundary, whereas reductive phenol groups effectively constrain the Sn2+ oxidation. Moreover, the undissociated DACl decreases the supersaturated concentration of tin perovskite solution and creates a pre-nucleation site for rapid nucleation to further regulate crystallization. Consequently, the DACl-derived TPSCs achieve a high power-conversion efficiency (PCE) that reaches up to 11%. More impressively, the device remains at 84% of the initial PCE after full-sun illumination in N2 over 600 h without being encapsulated. This DACl-based synergistic modulation of a lead-free perovskite demonstrates a feasible approach using one molecule with different functional groups to manipulate crystallization, Sn2+ oxidation, and defect reparation of tin perovskite films, providing a critical guideline for constructing high-quality perovskites by multifunctional additives with high photovoltaic performance.

Chenodeoxycholic acid suppresses AML progression through promoting lipid peroxidation via ROS/p38 MAPK/DGAT1 pathway and inhibiting M2 macrophage polarization.

PURPOSE: Bile acids are steroid synthesized in liver, which are essential for fat emulsification, cholesterol excretion and gut microbial homeostasis. However, the role of bile acids in leukemia progression remains unclear. We aim at exploring the effects and mechanisms of chenodeoxycholic acid (CDCA), a type of bile acids, on acute myeloid leukemia (AML) progression. RESULTS: Here, we found that CDCA was decreased in feces and plasma of AML patients, positively correlated with the diversity of gut microbiota, and negatively associated with AML prognosis. We further demonstrated that CDCA suppressed AML progression both in vivo and in vitro. Mechanistically, CDCA bound to mitochondria to cause mitochondrial morphology damage containing swelling and reduction of cristae, decreased mitochondrial membrane potential and elevated mitochondrial calcium level, which resulted in the production of excessive reactive oxygen species (ROS). Elevated ROS further activated p38 MAPK signaling pathway, which collaboratively promoted the accumulation of lipid droplets (LDs) through upregulating the expression of the diacylglycerol O-acyltransferase 1 (DGAT1). As the consequence of the abundance of ROS and LDs, lipid peroxidation was enhanced in AML cells. Moreover, we uncovered that CDCA inhibited M2 macrophage polarization and suppressed the proliferation-promoting effects of M2 macrophages on AML cells in co-cultured experiments. CONCLUSION: Our findings demonstrate that CDCA suppresses AML progression through synergistically promoting LDs accumulation and lipid peroxidation via ROS/p38 MAPK/DGAT1 pathway caused by mitochondrial dysfunction in leukemia cells and inhibiting M2 macrophage polarization.

Retrospective analysis of hepatic perivascular epithelioid cell tumour (PEComa) in a single centre for clinical diagnosis and treatment clinical diagnosis and treatment of hepatic PEComa.

ABSTRACT: Our primary objective was to investigate the clinical features, diagnosis, treatment and prognosis of hepatic perivascular epithelioid cell tumour (PEComa).Thirty-five cases of pathologically proven hepatic PEComa that were treated in the Department of Hepatobiliary Centre of the First Affiliated Hospital of Nanjing Medical University from January 2008 to February 2019 were retrospectively analysed, and the literature was also reviewed.Twenty-nine females and 6 males were included in this study. The mean age of these patients was 48.0 years (range, 21-75 years). Thirteen patients complained of upper abdominal pain or discomfort, while others were accidentally discovered by imaging examination. Hepatic PEComas tended to occur in the right lobe of the liver (20 cases in the right lobe, 13 in the left lobe and 2 in the caudate lobe). Two cases were characterized by multiple tumours, and the remaining cases were single lesions (range, 1.2-12 cm). Only 8 cases were correctly diagnosed by the preoperative imaging examination, and the correct diagnosis rate was only 22.9%. The postoperative immunohistochemistry analysis showed that hepatic PEComas are positive for human melanoma black 45, Melan-A and smooth muscle actin, with the exception of 1 case that was negative for Melan-A. All patients undergoing an operation accepted regular follow-up, and the average time was 66.5 months (range, 3-132 months). Two patients who experienced tumour recurrence and 1 patient who died of cardiovascular disease, but the remaining patients showed no evidence of tumour recurrence or metastasis during the follow-up period.Hepatic PEComas are a rare type of tumours that mainly occur in young and middle-aged women. The lack of clinical manifestations and imaging findings increases the difficulty of determining a preoperative diagnosis, which mainly depends on the results of pathological examinations. Surgery is currently the only effective treatment, and long-term clinical follow-up is necessary due to the aggressive behaviour and relapse of hepatic PEComa in some patients.

LINC01291 promotes hepatocellular carcinoma development by targeting the miR-186-5p/OXSR1 axis.

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. Recent studies have demonstrated that lncRNAs play an important role in tumorigenesis. LINC01291 has been confirmed to be involved in the proliferation and migration of different cancers, although the function of LINC01291 in HCC is still unknown. METHODS: First, the expression of LINC01291 in 50 paired HCC tissues, adjacent normal tissues and HCC cell lines was measured by a quantitative real-time polymerase chain reaction. Then, the function of LINC01291 in HCC cell proliferation, migration and invasion was measured by colony formation, Cell Counting Kit-8 assays, wound healing assays and transwell assays. In addition, E-cadherin, N-cadherin, vimentin and oxidative stress-responsive 1 (OXSR1) protein expression levels were assessed via western blotting. Luciferase reporter assays were used to confirm the relationship between LINC01291 and miR-186-5p, as well as miR-186-5p and OXSR1 mRNA. Rescue assays and in vivo experiments further confirmed the LINC01291/miR-186-5p/OXSR1 axis in the progression of HCC. RESULTS: LINC01291 was upregulated in both HCC tissues and cell lines. Knockdown of LINC01291 inhibited the proliferation, migration, invasion and epithelial-mesenchymal progression (EMT) of HCC cells. In addition, LINC01291 could overexpress OXSR1 by sponging miR-186-5p, and OXSR1 overexpression or miR-186-5p inhibition could rescue the effect of LINC01291 knockdown in YY-8103 cell lines. In addition, lentiviral sh-LINC01291 could effectively inhibit the growth of subcutaneous YY-8103 xenograft tumors, whereas the anticancer effect could be reversed by cotransfection with in-miR-186-5p or ov-OXSR1. CONCLUSIONS: LINC01291 can promote the proliferation, migration, invasion and EMT of HCC cells via the miR-186-5p/OXSR1 axis, and sh-LINC01291 can inhibit tumor growth in a xenograft mouse model.

FER Regulated by miR-206 Promotes Hepatocellular Carcinoma Progression via NF-κB Signaling.

OBJECTIVES: Feline sarcoma-related protein (FER) is known to play a critical regulatory role in several carcinomas. However, the exact biological function of FER in hepatocellular carcinoma (HCC) still needs to be investigated. The primary objective of this research was to investigate the unknown function and molecular mechanisms of FER in HCC. MATERIALS AND METHODS: The expression level of FER in HCC tissue samples and cells was examined by RT-qPCR, immunohistochemistry and western blot. Cellular and animal experiments were used to explore the effect of FER on the proliferative and metastatic capacities of HCC cells. The crosstalk between FER and NF-κB signaling was explored by western blot. The upstream factors that regulate FER were evaluated through dual-luciferase experiments and western blot assays. RESULTS: FER was overexpressed in HCC specimens and HCC cell lines. FER expression levels were positively associated with unfavorable clinicopathological characteristics. The higher the expression of FER was, the worse the overall survival of HCC patients was. The results of loss-of-function and gain-of-function experiments indicated that knockdown of FER decreased, while overexpression of FER increased, the proliferation, invasion and metastasis of HCC cells in vitro and in vivo. Mechanistically, we found that FER activated the NF-κB signaling pathway and stimulated epithelial-to-mesenchymal transition (EMT). We also found that FER was directly regulated by miR-206, and the downregulation of miR-206 was associated with proliferation and metastatic progression in HCC. CONCLUSIONS: The present research was the first to reveal that a decrease in miR-206 levels results in an increase in FER expression in HCC, leading to enhanced cell growth and metastatic abilities via activation of the NF-κB signaling pathway.

MiR-3174 promotes proliferation and inhibits apoptosis by targeting FOXO1 in hepatocellular carcinoma.

INTRODUCTION: MicroRNAs (miRNAs) have been confirmed to play a crucial part in oncogenesis. Several studies suggested that MiR-3174 act as a tumor promoter in various Malignant neoplasm. However, the biological function of miR-3174 in hepatocellular carcinoma (HCC) still highly unexplored. METHODS: We screened differentially over-expressed miRNAs by The Cancer Genome Atlas (TCGA) and the GEO databases. The expression of miR-3174 in HCC cells and tissues was detected by qRT-PCR. The cellular behaviors of transfected cells were respectively examined by colony formation assays, EdU Assays and flow cytometry. Forkhead box O1 transcription factor (FOXO1) was predicted and confirmed as a direct target of miR-3174 by bioinformatics analysis and dual-luciferase reporter gene assay. RESULTS: MiR-3174 was up-regulated in HCC tissues and cells, and the expression level of it was highly associated with tumor size and Edmondson grade. Our study pioneering validates that upregulated miR-3174 promote cell proliferation and inhibit cell apoptosis in vitro and in vivo. Meanwhile, our study verified that miR-3174 regulate Bim, P21, cyclin D1 and c-MYC expression by directly targeting FOXO1. CONCLUSION: The upregulated miR-3174 promote cell proliferation and inhibit cell apoptosis by downregulating FOXO1 expression in HCC. MiR-3174 may be a novel candidate for targeted delivery of miRNA therapeutics for HCC patients.

Distribution of mercury in the combustion products from coal-fired power plants in Guizhou, southwest China.

Method 30B and the Ontario Hydro Method (OHM) were used to sample the mercury in the flue gas discharged from the seven power plants in Guizhou Province, southwest China. In order to investigate the mercury migration and transformation during coal combustion and pollution control process, the contents of mercury in coal samples, bottom ash, fly ash, and gypsum were measured. The mercury in the flue gas released into the atmosphere mainly existed in the form of Hg°. The precipitator shows a superior ability to remove Hgp (particulate mercury) from flue gas. The removal efficiency of Hg2+ by wet flue gas desulfurization (WFGD) was significantly higher than that for the other two forms of mercury. The synergistic removal efficiency of mercury by the air pollution control devices (APCDs) installed in the studied power plants is 66.69-97.56%. The Hg mass balance for the tested seven coal-fired power plants varied from 72.87% to 109.67% during the sampling time. After flue gas flowing through APCDs, most of the mercury in coal was enriched in fly ash and gypsum, with only a small portion released into the atmosphere with the flue gas. The maximum discharge source of Hg for power plants was fly ash and gypsum instead of Hg emitted with flue gas through the chimney into the atmosphere. With the continuous upgrading of APCDs, more and more mercury will be enriched in fly ash and gypsum. Extra attention should be paid to the re-release of mercury from the reutilization of by-products from APCDs. Implications: Method 30B and the Ontario Hydro Method (OHM) were used to test the mercury concentration in the flue gas discharged from seven power plants in Guizhou Province, China. The concentrations of mercury in coal samples, bottom ash, fly ash, and gypsum were also measured. By comparison of the mercury content of different products, we found that the maximum discharge source of Hg for power plants was fly ash and gypsum, instead of Hg emitted with flue gas through the chimney into the atmosphere. With the continuous upgrading of APCDs, more and more mercury will be enriched in fly ash and gypsum. Extra attention should be paid to the re-release of mercury from the reutilization of by-products from APCDs.