A meta-analysis of caspase-8-652 6N del polymorphism and digestive tract cancer risk

Caspase-8(CASP8) is one key regulator of apoptosis of T lymphocytes and is encoded by the CASP8 gene. It has been reported that the six-nucleotide deletion polymorphism(-652 6 N del) of the CASP8 gene had effect on some cancer risk. Few studies explored the association between CASP8 gene polymorphism and digestive tract cancer risk.To evaluate the association between the CASP8-652 6 N del polymorphism and the risk of digestive tract cancer, we conducted this meta-analysis. We found that CASP8-652 6 N del polymorphism was associated with a significantly reduced risk of digestive tract cancer in the co-dominant model(del/del vs. ins/ins: OR= 0.82, 95%CI= 0.72-0.95;del/ins vs. ins/ins: OR = 0.92,95%CI = 0.87-0.97;dominant model(del/ins + del/del vs. ins/ins: OR = 0.91,95%CI =0.87-0.96, recessive model: del/del vs. del/ins + ins/ins: OR = 0.85, 95%CI = 0.75-0.97). In the stratified analysis by cancer types, we found that all genetic models had protective effect on gastric cancer. Similar results were observed for colorectal cancer under heterozygote comparison and dominant model, but not under homozygote comparison or recessive model. In addition, a significantly decreased risk was found on esophageal cancer for most genetic models,except heterozygote comparison. When stratified by ethnicity and source of control, an evidently decreased risk was identified in the Asian populations and population-based studies. In conclusion, there exists an association between the CASP8-652 6 N del polymorphism and reduced digestive cancer risk, especially among Asians and populationbased studies.

Polyphenol-mediated interfacial deposition strategy for supported manganese oxide catalysts with excellent pollutant degradation performance

In persulfate-based advanced oxidation process(PS-AOPs),fixing nanosized metal oxide on processable substrates is highly desirable to avoid the aggregation and loss of nanocatalysts during the practical application.However,it is still challenging to develop a versatile strategy for the deposition of metal oxide nanocatalysts on various substrates with different physicochemical properties.Herein,polyphenols are utilized as a“molecular glue”and reductant to mediate the interfacial deposition of MnO_(2) nanocatalysts on different substrates.MnO_(2) nanocatalysts were in-situ grown on macroscope mineral substrates(e.g.,airstone)via an interfacial redox strategy between tannic acid(TA)and oxidized KMnO4,and then employed as a fixed catalyst of peroxymonosulfate(PMS)activation for treating pharmaceutical and personal care products(PPCPs)in water.The fixed MnO_(2) exhibited superior catalytic performance toward different PPCPS via a singlet oxygen(^(1)O_(2))-dominated nonradical oxidation pathway.PPCPs in the secondary effluent of wastewater treatment plants could be effectively removed by a fixed-bed column of the fixed MnO_(2) with long term stability.Redox cycle of Mn^(4+)/Mn^(3+)and surface hydroxyl group of the fixed MnO_(2) was proved to be responsible for the activation of PMS.This work provides a new avenue for developing fixed metal oxides for sustainable water treatment.

H19 recruited N^(6)-methyladenosine(m^(6)A)reader YTHDF1 to promote SCARB1 translation and facilitate angiogenesis in gastric cancer

Background:Angiogenesis is described as a complex process in which new microvessels sprout from endothelial cells of existing vasculature.This study aimed to determine whether long non-coding RNA(lncRNA)H19 induced the angiogenesis of gastric cancer(GC)and its possible mechanism.Methods:Gene expression level was determined by quantitative real-time polymerase chain reaction and western blotting.Cell counting kit-8,transwell,5-Ethynyl-2′-deoxyuridine(EdU),colony formation assay,and human umbilical vein endothelial cells(HUVECs)angiogenesis assay as well as Matrigel plug assay were conducted to study the proliferation,migration,and angiogenesis of GC in vitro and in vivo.The binding protein of H19 was found by RNA pull-down and RNA Immunoprecipitation(RIP).High-throughput sequencing was performed and next Gene Ontology(GO)as well as Kyoto Encyclopedia of Genes and Genomes(KEGG)analysis was conducted to analyze the genes that are under H19 regulation.Methylated RIP(me-RIP)assay was used to investigate the sites and abundance among target mRNA.The transcription factor acted as upstream of H19 was determined through chromatin immunoprecipitation(ChIP)and luciferase assay.Results:In this study,we found that hypoxia-induced factor(HIF)-1a could bind to the promoter region of H19,leading to H19 overexpression.High expression of H19 was correlated with angiogenesis in GC,and H19 knocking down could inhibit cell proliferation,migration and angiogenesis.Mechanistically,the oncogenic role of H19 was achieved by binding with the N^(6)-methyladenosine(m^(6)A)reader YTH domain-containing family protein 1(YTHDF1),which could recognize the m^(6)A site on the 3′-untransated regions(3′-UTR)of scavenger receptor class B member 1(SCARB1)mRNA,resulting in over-translation of SCARB1 and thus promoting the proliferation,migration,and angiogenesis of GC cells.Conclusion:HIF-1a induced overexpression of H19 via binding with the promoter of H19,and H19 promoted GC cells proliferation,migration and angiogenesis through YTHDF1/SCARB1,which might be a beneficial target for antiangiogenic therapy for GC.

miR-338-3p acts as a tumor suppressor in lung squamous cell carcinoma by targeting FGFR2/FRS2

Background:Lung cancer refers to the occurrence of malignant tumors in the lung,and squamous cell carcinoma is one of the most common pathological types of non-small cell lung cancer.Studies have shown that microRNAs(miRNAs)play an important role in the occurrence,development,early diagnosis,and treatment of lung cancer.This study aimed to explore the role and possible mechanism of MicroRNA-338-3p(miR-338-3p)in lung squamous cell carcinoma(LUSC).

Verification of SARS-CoV-2-encoded small RNAs and contribution to infection-associated lung inflammation

To the Editor:Severe_acute_respiratory,syndrome coronavirus 2(SARS-CoV-2)is the virus causing coronavirus disease2019(COVID-19).[1]As anewevolutionary branch within coronaviruses,SARS-CoV-2 contains around 29.8 kilobase and shows 79.2%identity with SARS-CoV-1.