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The m^(6)A regulator KIAA1429 stabilizes RAB27B mRNA and promotes the progression of chronic myeloid leukemia and resistance to targeted therapy

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Genes & Diseases 2024年第2期11卷 993-1008页

作者： Fangyi Yao Fangmin Zhong Junyao Jiang Ying Cheng Shuai Xu Jing Liu Jin Lin Jing Zhang Shuqi Li Meiyong Li Yanmei Xu Bo Huang Xiaozhong Wang Jiangxi Province Key laboratory of laboratory medicine Jiangxi Provincial Clinical Research Center for Laboratory MedicineDepartment of Clinical LaboratoryThe Second Affiliated Hospital of Nanchang UniversityNanchangJiangxi 330006China

Chronic myeloid leukemia(CML)is a common adult *** the acute phase of the disease and the adverse effects of anti-cancer treatments can lead to a poor *** N6-methyladenine(m^(6)A)modification plays an important regulatory role in various physiological and pathological ***1429 is a known m^(6)A regulator,but the biological role of KIAA1429 in CML is *** this study,we observed that the m^(6)A levels and KIAA1429 expression were significantly up-regulated in patients with blast phase ***,KIAA1429 regulated the total level of RNA m^(6)A modification in the CML cells and promoted the malignant biological behaviors of CML cells,including proliferation,migration,and imatinib *** KIAA1429 in CML cells reduced the stability of RAB27B mRNA through the m^(6)A/YTHDF1 axis,consequently inhibiting CML proliferation and drug efflux,ultimately increasing the sensitivity of CML cells to ***,the knockdown of RAB27B also inhibited the proliferation and drug resistance of CML cells and promoted their ***,a recently developed anti-cancer agent,suppressed the expression of KIAA1429 and CML cell proliferation and promoted cell *** also inhibited the tumorigenesis of CML cells in *** combined use of rucaparib and imatinib enhanced the sensitivity of CML cells to *** study provides evidence that elevated KIAA1429 expression in the blast phase of CML enhances the stability of RAB27B mRNA through the m^(6)A/YTHDF1 axis to up-regulate RAB27B expression,thereby promoting CML *** exerts inhibitory effects on KIAA1429 expression and thus reduces CML progression.

关键词： Chronic myeloid leukemia KIAA1429 N6-methyladenine RAB27B Rucaparib YTHDF1

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A prognostic model of patients with pancreatic cancer based on four N^(6)-methyladenosine-related IncRNAs and analysis of related immune infiltration

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Genes & Diseases 2024年第4期11卷 109-112页

作者： Kaili Liao Yuhan Xu Bingying Lin Yuxuan Xie Qijun Yang Wenyige Zhang Beining Zhang Jiarong Wen Jingyi Wang Zimeng Li Yunqi Cheng Xiaozhong Wang Jiangxi Province Key laboratory of laboratory medicine Jiangxi Provincial Clinical Research Center for Laboratory MedicineDepartment of Clinical LaboratoryThe Second Affiliated Hospital of Nanchang UniversityNanchangJiangxi 330006China Queen Mary college of Nanchang University NanchangJiangxi 330001China School of Public Health Nanchang UniversityNanchangJiangxi 330006China The Second clinical Medical college Nanchang UniversityNanchangJiangxi 330006China The First clinical Medical college of Nanchang University NanchangJiangxi 330006China

Pancreatic cancer is one of the most lethal malignant tumors in the *** advances in diagnosis and treatment,the five-year survival rate for pancreatic cancer patients remains only 9%.1 Pancreatic adenocarcinoma(PAAD)belongs to pancreatic cancer,which occupies 85%of the whole pancreatic cancer.2 Reversible modification of Ne-methyladenosine(m^(6)A)has been shown to be involved in cancer progression,resulting in up-regulation of oncogene expression or down-regulation of tumor-suppressing genes and may affect the prognosis of patients with pancreatic cancer.

关键词： patients cancer diagnosis

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A novel mechanism of PHB2-mediated mitophagy participating in the development of Parkinson's disease

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Neural Regeneration Research 2024年第8期19卷 1828-1834页

作者： Yongjiang Zhang Shiyi Yin Run Song Xiaoyi Lai Mengmeng Shen Jiannan Wu Junqiang Yan Key laboratory of Neuromolecular Biology The First Affiliated HospitalCollege of Clinical Medicine of Henan University of Science and TechnologyLuoyangHenan ProvinceChina Department of Neurology The First Affiliated HospitalCollege of Clinical Medicine of Henan University of Science and TechnologyLuoyangHenan ProvinceChina

Endoplasmic reticulum stress and mitochondrial dysfunction play important roles in Parkinson s disease,but the regulato ry mechanism remains ***-2(PHB2)is a newly discove red autophagy receptor in the mitochondrial inner membrane,and its role in Parkinson’s disease remains *** kinase R(PKR)-like endoplasmic reticulum kinase(PERK)is a factor that regulates cell fate during endoplasmic reticulum *** is regulated by PERK and is a target of the unfolded protein *** is unclear whether PERK regulates PHB2-mediated mitophagy thro ugh *** this study,we established a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced mouse model of Parkinson’s *** used adeno-associated virus to knockdown PHB2 *** res ults showed that loss of dopaminergic neurons and motor deficits were aggravated in the MPTP-induced mouse model of Parkinson’s *** rexpression of PHB2 inhibited these *** also established a 1-methyl-4-phenylpyridine(MPP+)-induced SH-SY5Y cell model of Parkinson’s *** found that ove rexpression of Parkin increased co-localization of PHB2 and microtubule-associated protein 1 light chain 3,and promoted *** addition,MPP+regulated Parkin involvement in PHB2-mediated mitophagy through phosphorylation of *** findings suggest that PHB2 participates in the development of Parkinson’s disease by intera cting with endoplasmic reticulum stress and Parkin.

关键词： endoplasmic reticulum dopaminergic neuron microtubule-associated protein 1 light chain 3 mitophagy oxidative stress Parkin Parkinson’s disease PKR-like endoplasmic reticulum kinase reactive oxygen species prohibitin-2

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MiR-4465-modified mesenchymal stem cell-derived small extracellular vesicles inhibit liver fibrosis development via targeting LOXL2 expression

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2024年第7期25卷 594-604页

作者： Yanjin WANG Yifei CHEN Fuji YANG Xiaolong YU Ying CHU Jing ZHOU Yongmin YAN Jianbo XI Department of laboratory medicine Wujin Hospital Affiliated with Jiangsu UniversityJiangsu UniversityChangzhou 213017China Department of laboratory medicine School of MedicineJiangsu UniversityZhenjiang 212013China Changzhou Key laboratory of Molecular Diagnostics and Precision Cancer medicine Wujin Clinical College of Xuzhou Medical UniversityChangzhou 213017China

Liver fibrosis is a significant health burden,marked by the consistent deposition of ***,the currently available treatment approaches for this condition are far from *** oxidase-like protein 2(LOXL2)secreted by hepatic stellate cells(HSCs)is a crucial player in the cross-linking of matrix collagen and is a significant target for treating liver *** stem cell-derived small extracellular vesicles(MSC-sEVs)have been proposed as a potential treatment option for chronic liver *** studies have found that MSC-sEV can be used for microRNA delivery into target cells or *** is currently unclear whether microRNA-4465(miR-4465)can target LOXL2 and inhibit HSC ***,it is uncertain whether MSC-sEV can be utilized as a gene therapy vector to carry miR-4465 and effectively inhibit the progression of liver *** study explored the effect of miR-4465-modified MSC-sEV(MSC-sEVmiR-4465)on LOXL2 expression and liver fibrosis *** results showed that miR-4465 can bind specifically to the promoter of the LOXL2 gene in ***,MSC-sEVmiR-4465 inhibited HSC activation and collagen expression by downregulating LOXL2 expression in ***-sEVmiR-4465 injection could reduce HSC activation and collagen deposition in the CCl4-induced mouse ***-sEVmiR-4465 mediating via LOXL2 also hindered the migration and invasion of HepG2 *** conclusion,we found that MSC-sEV can deliver miR-4465 into HSC to alleviate liver fibrosis via altering LOXL2,which might provide a promising therapeutic strategy for liver diseases.

关键词： Mesenchymal stem cell(MSC) Small extracellular vesicle(sEV) MicroRNA-4465(miR-4465) Hepatic stellate cell(HSC) Liver fibrosis

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Comparison of clinical features and outcomes of proliferative,fibrotic,and mixed subtypes of IgG4-related disease:A retrospective cohort study

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Chinese Medical Journal 2024年第3期137卷 303-311页

作者： Linyi Peng Xinlu Zhang Jiaxin Zhou Jieqiong Li Zheng Liu Hui Lu Yu Peng Yunyun Fei Yan Zhao Xiaofeng Zeng Wen Zhang Department of Rheumatology and clinical Immunology Peking Union Medical College HospitalNational Clinical Research Center for Dermatologic and Immunologic DiseasesState Key Laboratory of Complex Severe and Rare DiseasesThe Ministry of Education Key LaboratoryBeijing 100730China Institute of clinical medicine Peking Union Medical College Hospital(PUMCH)Chinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing 100730China

Background:Immunoglobulin G4-related disease(IgG4-RD)is a recently recognized immune-mediated disorder that can affect almost any organ in the human ***4-RD can be categorized into proliferative and fibrotic subtypes based on patients’clinicopathological *** study aimed to compare the clinical manifestations,laboratory findings,and treatment outcomes of IgG4-RD among different ***:We prospectively enrolled 622 patients with newly diagnosed IgG4-RD at Peking Union Medical college Hospital from March 2011 to August *** patients were divided into three groups according to their clinicopathological characteristics:proliferative,fibrotic,and mixed *** compared demographic features,clinical manifestations,organ involvement,laboratory tests,and treatment agents across three *** then assessed the differences in treatment outcomes among 448 patients receiving glucocorticoids alone or in combination with ***,risk factors of relapse were revealed by applying the univariate and multivariate Cox regression ***:We classified the 622 patients into three groups consisting of 470 proliferative patients,55 fibrotic patients,and 97 mixed patients,*** found that gender distribution,age,disease duration,and frequency of allergy history were significantly different among *** terms of organ involvement,submandibular and lacrimal glands were frequently involved in the proliferative subtype,while retroperitoneum was the most commonly involved site in both fibrotic subtype and mixed *** comparison of laboratory tests revealed that eosinophils(P=0.010),total IgE(P=0.006),high-sensitivity C-reactive protein(P<0.001),erythrocyte sedimentation rate(P<0.001),complement C4(P<0.001),IgG(P=0.001),IgG1(P<0.001),IgG4(P<0.001),and IgA(P<0.001),at baseline were significantly different among three *** with proliferative and mixed subtypes,the fibrotic subtype showed the

关键词： IgG4-related disease Proliferative subtype Fibrotic subtype clinical features Treatment outcome

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Enterogenic Stenotrophomonas maltophilia migrates to the mammary gland to induce mastitis by activating the calcium-ROS-AMPK-mTOR-autophagy pathway

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Journal of Animal Science and Biotechnology 2024年第1期15卷 236-252页

作者： Zhaoqi He Caijun Zhao Yuhong He Zhuoyu Liu Guyue Fan Kun Zhu Yiqi Wang Naisheng Zhang Yunhe Fu Xiaoyu Hu Department of clinical Veterinary medicine College of Veterinary MedicineJilin UniversityChangchun 130062Jilin ProvinceChina

Background Mastitis is an inflammatory disease of the mammary gland that has serious economic impacts on the dairy industry and endangers food *** previous study found that the body has a gut/rumen-mammary gland axis and that disturbance of the gut/rumen microbiota could result in‘gastroenterogenic mastitis'.However,the mechanism has not been fully ***,we found that long-term feeding of a high-concentrate diet induced mastitis in dairy cows,and the abundance of Stenotrophomonas maltophilia(***)was significantly increased in both the rumen and milk ***,we hypothesized that‘gastroenterogenic mastitis'can be induced by the migration of endogenous gut bacteria to the mammary ***,this study investigated the mechanism by which enterogenic *** induces *** First,*** was labelled with superfolder GFP and administered to mice via *** results showed that treatment with *** promoted the occurrence of mastitis and increased the permeability of the blood-milk barrier,leading to intestinal inflammation and intestinal ***,tracking of ingested *** revealed that *** could migrate from the gut to the mammary gland and induce ***,mammary gland transcriptome analysis showed that the calcium and AMPK signalling pathways were significantly upregulated in mice treated with ***,using mouse mammary epithelial cells(MMECs),we verified that *** induces mastitis through activation of the calcium-ROS-AMPK-mTOR-autophagy *** In conclusion,the results showed that enterogenic *** could migrate from the gut to the mammary gland via the gut-mammary axis and activate the calcium-ROS-AMPK-mTOR-autophagy pathway to induce *** the gut-mammary gland axis may also be an effective method to treat mastitis.

关键词： Calcium-ROS-AMPK-mTOR-autophagy pathway Gut-mammary axis Mastitis S.maltophilia

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Meiotic nuclear divisions 1 suppresses the proliferation and invasion of pancreatic cancer cells via regulating H2A.X variant histone

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BIOCELL 2024年第1期48卷 111-122页

作者： DONGQIN WANG YAN SHI ZHIQIANG WANG JING ZHANG LUYAO WANG HONGYU MA SHUHUA SHI XIAOFU LIAN HUA HUANG XIAOJING WANG CHAOQUN LIAN Anhui Province Key laboratory of clinical and Preclinical Research in Respiratory Disease Molecular Diagnosis CenterThe Department of Pulmonary Critical Care MedicineFirst Affiliated Hospital of Bengbu Medical CollegeBengbu233030China Department of Genetics School of Life SciencesBengbu Medical CollegeBengbu233000China Department of clinical medicine Bengbu Medical CollegeBengbu233030China Research Center of clinical laboratory Science Bengbu Medical CollegeBengbu233030China

Introduction:Among all malignant tumors of the digestive system,pancreatic carcinoma exhibits the highest mortality ***,prevention and effective treatment are urgent issues that need to be ***:The study focused on meiotic nuclear divisions 1(MND1),integrating data from the Gene Expression Profiling Interactive Analysis(GEPIA)database with prognostic survival ***,experiments at cellular level were employed to demonstrate the effect of MND1 on the proliferation and migration of *** small-molecule inhibitor of MND1 was used to suppress the migration of PC cells by knocking down MND1 using small interfering RNA(siRNA)in Patu-8988 and Panc1 cell ***:The results of Cell Counting Kit-8 indicated that the suppression of MND1 resulted in a decrease in cell *** healing and Transwell assays revealed that MND1 knockdown reduced cell migration and *** cytometry revealed that inhibiting MND1 hindered the cell ***,MND1 could stimulate the proliferation,migration,and invasion of Patu-8988 and Panc1 cells by increasing the expression of ***,MND1 had a positive effect on H2AFX expression in PC *** MND1 expression suggests the low overall survival rate of individuals diagnosed with ***:These findings suggest that MND1 has the potential to be a gene with the ability to accurately diagnose and treat PC.

关键词： Pancreatic carcinoma MND1 H2AFX Cell cycle

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PDK1 promotes breast cancer progression by enhancing the stability and transcriptional activity of HIF-1α

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Genes & Diseases 2024年第4期11卷 353-367页

作者： Yu Wei Dian Zhang He Shi Husun Qian Hongling Chen Qian Zeng Fangfang Jin Yan Ye Zuli Ou Minkang Guo Bianqin Guo Tingmei Chen Key laboratory of clinical laboratory Diagnostics(Ministry of Education) College of Laboratory MedicineChongqing Medical UniversityChongqing 400016China Chongqing Key laboratory of Translational Research for Cancer Metastasis and Individualized Treatment Chongqing University Cancer HospitalChongqing 400030China

Pyruvate dehydrogenase kinase 1(PDK1)phosphorylates the pyruvate dehydroge-nase complex,which inhibits its *** pyruvate dehydrogenase complex inhibits the tricarboxylic acid cycle and the reprogramming of tumor cell metabolism to glycolysis,which plays an important role in tumor *** study aims to elucidate how PDK1 pro-motes breast cancer *** found that PDK1 was highly expressed in breast cancer tissues,and PDK1 knockdown reduced the proliferation,migration,and tumorigenicity of breast cancer cells and inhibited the HIF-1α(hypoxia-inducible factor 1α)*** investigation showed that PDK1 promoted the protein stability of HIF-1αby reducing the level of ubiquitination of HIF-1α.The HIF-1αprotein levels were dependent on PDK1 kinase ***,HIF-1αphosphorylation at serine 451 was detected in wild-type breast cancer cells but not in PDK1 knockout breast cancer *** phosphorylation of HIF-1αat Ser 451 stabilized its protein levels by inhibiting the interaction of HIF-1αwith von Hippel-Lindau and prolyl hydroxylase *** also found that PDK1 enhanced HIF-1αtranscriptional *** summary,PDK1 enhances HIF-1αprotein stability by phosphorylating HIF-1αat Ser451 and promotes HIF-1αtranscriptional activity by enhancing the binding of HIF-1αto ***1 and HIF-1αform a positive feedback loop to promote breast cancer progression.

关键词： Breast cancer HIF-1α PDK1 Protein phosphorylation Transcriptional activity

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Investigation of the feasibility of NRAV as a biomarker for hepatocellular carcinoma

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Oncology Research 2024年第4期32卷 717-726页

作者： JUN LIU WENLI LI RUYUE LU JIAQING XU CHUNHUI JIANG JUNLIN DUAN LINGZHI ZHANG GUANFU WANG JIAXI CHEN Department of clinical laboratory Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical UniversityLinhaiChina Key laboratory of System medicine and Precision Diagnosis and Treatment of Taizhou TaizhouChina Department of clinical laboratory Dongguan Hospital of Traditional Chinese MedicineDongguanChina School of Basic Medical Sciences Forensic medicine Hangzhou Medical CollegeHangzhouChina

The long non-coding RNA,Negative Regulator of Antiviral Response(NRAV)has been identified as a participant in both respiratory virus replication and immune checkpoints,however,its involvement in pan-cancer immune regulation and prognosis,particularly those of hepatocellular carcinoma(HCC),remains *** address this knowledge gap,we analyzed expression profiles obtained from The Cancer Genome Atlas(TCGA)database,comparing normal and malignant tumor *** found that NRAV expression is significantly upregulated in tumor tissues compared to adjacent nontumor ***-Meier(K-M)analysis revealed the prognostic power of NRAV,wherein overexpression was significantly linked to reduced overall survival in a diverse range of tumor ***,noteworthy associations were observed between NRAV,immune checkpoints,immune cell infiltration,genes related to autophagy,epithelial-mesenchymal transition(EMT),pyroptosis,tumor mutational burden(TMB),and microsatellite instability(MSI)across different cancer types,including ***,NRAV upregulation expression was associated with multiple pathological stages by clinical ***,our investigation revealed a substantial elevation in the expression of NRAV in both HCC tumor tissues and cells compared to normal tissues and *** inhibition of NRAV resulted in the inhibition of cell proliferation,migration,and invasion in HCC cells,while also influencing the expression of CD274(PD-L1)and CD44,along with various biomarkers associated with EMT,autophagy,and *** aforementioned results propose NRAV as a promising prognostic biomarker for HCC.

关键词： NRAV Hepatocellular carcinoma Prognosis Biomarker Pan-cancer

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Mechanism Exploration of Euphorbia fischeriana Steud. for Liver Cancer Based on Aspartic Acid Identification in Metabolomics

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Chinese Journal of Integrative medicine 2024年第6期30卷 507-514页

作者： ZHAO Jing TIAN Xin-chen ZHANG Jia-qi HUANG Chen SUN Yan QIAO Sen JIANG Shu-long clinical Medical laboratory Center Jining First People’s HospitalJiningShandong Province272000China Cheeloo college of medicine Shandong UniversityJinan250000China

Objective:To investigate the anti-liver cancer effects and aspartic acid(Asp)-related action mechanism of Euphorbia fischeriana Steud.(LD).Methods:The mice model of liver cancer was established by injection of H22 *** 5 days,mice were randomly divided into model group,sorafenib group(20 mg/kg),LD high-dose(LDH,1.36 g/kg) group,LD medium-dose(LDM,0.68 g/kg) group,and LD low-dose(LDL,0.34 g/kg)group,10 mice each *** were intragastrically administered to the mice once daily for 10 days,*** weight,tumor size and tumor weight were *** index was *** changes of liver cancer tissues were evaluated by hematoxylin and eosin staining and TUNEL *** chromatography-mass spectrometer was used to analyze different metabolites between the model and LDH ***:After LD treatment,tumor weight,tumor size and hepatic index were reduced compared with the model *** and karyorrhexis of tumor cells were ***,61 differential metabolites(18 up-regulated,43 down-regulated) were affirmed and 20 pathways of KEGG(P<0.05) were *** addition,Bel-7402,HepG2 and H22 cell viabilities were significantly increased after adding Asp into the *** then,the cell proliferation effect induced by Asp was ameliorated by ***:The anti-liver cancer efficacy of LD extract was validated in H22 mice model,and inhibition of Asp level might be the underlying mechanism.

关键词： liver cancer Euphorbia fischeriana Steud. aspartic acid metabolomics

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