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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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Exploiting the potential of the ubiquitin-proteasome system in overcoming tyrosine kinase inhibitor resistance in chronic myeloid leukemia

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Genes & Diseases 2024年第5期11卷 140-162页

作者： Xudong Li Wei Li Yanli Zhang Linping Xu Yongping Song Department of Hematology Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer HospitalZhengzhouHenan 450008China Academy of Medical Sciences Zhengzhou UniversityZhengzhouHenan 450052China Department of Hematology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan 450052China

The advent of tyrosine kinase inhibitors(TKI)targeting BCR-ABL has drastically changed the treatment approach of chronic myeloid leukemia(CML),greatly prolonged the life of CML patients,and improved their ***,TKI resistance is still a major problem with CML patients,reducing the efficacy of treatment and their quality of *** resistance is mainly divided into BCR-ABL-dependent and BCR-ABL-independent ***,the main clinical strategy addressing TKI resistance is to switch to newly developed ***,data have shown that these new drugs may cause serious adverse reactions and intolerance and cannot address all resistance ***,finding new therapeutic targets to overcome TKI resistance is crucial and the ubiquitin-proteasome system(UPS)has emerged as a *** UPS mediates the degradation of most proteins in organisms and controls a wide range of physiological *** recent years,the study of UPS in hematological malignant tumors has resulted in effective treatments,such as bortezomib in the treatment of multiple myeloma and mantle cell *** CML,the components of UPS cooperate or antagonize the efficacy of TKI by directly or indirectly affecting the ubiquitination of BCR-ABL,interfering with CML-related signaling pathways,and negatively or positively affecting leukemia stem *** of these molecules may help overcome TKI resistance and treat *** this review,the mechanism of TKI resistance is briefly described,the components of UPS are introduced,existing studies on UPS participating in TKI resistance are listed,and UPS as the therapeutic target and strategies are discussed.

关键词： chronic myeloid leukemia Deubiquitinases E3 ligase PROTAC TKI resistance Ubiquitin-proteasome system

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Network pharmacology to decipher the mechanism of Danggui Longhui Wan against chronic myeloid leukemia

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Asian Journal of Traditional Medicines 2024年第4期19卷 177-191页

作者： Xuehan Ma Qiulin Yan Shaojiang Song Guodong Yao Key Laboratory of Computational Chemistry Based Natural Antitumor Drug Research&Development Liaoning ProvinceSchool of Traditional Chinese Materia MedicaShenyang Pharmaceutical UniversityShenyang 110016China

chronic myeloid leukemia(CML)is a hematopoietic myeloproliferative *** Chinese prescription Danggui Longhui Wan(DGLHW)has been utilized in CML treatment,but its underlying mechanisms remain *** this study,we gathered 794 constituents,1249 drug targets,1654 disease genes and 129 intersection *** and KEGG were used to analyze the function of these *** of prescription study showed that monarch drug,minister drug,assistant and guide drug played a synergistic role in the treatment of *** addition,we obtained 20 hub genes and 12 key *** docking indicated that the main compounds and core proteins had good binding *** results of this study also showed that DGLHW might play a role in the treatment of CML by affecting MAPK,PI3K/AKT,FoxO and p53 signaling pathways.

关键词： chronic myeloid leukemia Danggui Longhui Wan network pharmacology compatibility analysis

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A novel coumarin derivative DBH2 inhibits proliferation and induces apoptosis of chronic myeloid leukemia cells

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Genes & Diseases 2023年第2期10卷 596-607页

作者： Jiajia Xin Huijie Zhang Dandan Yin Ning An Yaozhen Chen Jinmei Xu Jing Zhang Zhixin Liu Yongsheng Liu Wen Yin Mingkai Li Xingbin Hu Department of Blood Transfusion Xijing HospitalAir Force Medical UniversityXi’anShaanxi 710032China Key Laboratory of Biochemistry and Molecular Pharmacology of Chongqing Chongqing Medical UniversityChongqing 400016China Department of Hematology Tangdu HospitalAir Force Medical UniversityXi’anShaanxi 710038China Department of Pharmacology School of PharmacyAir Force Medical UniversityXi’anShaanxi 710032China

With the development of tyrosine kinase inhibitor(TKI)resistance,finding the novel effective chemotherapeutic agent is of seminal importance for chronic myelogenous leukemia(CML)*** study aims to find the effective anti-leukemic candidates and investigate the possible underlying *** synthesized the novel coumarin derivatives and evaluated their anti-leukemic *** viability assay revealed that compound DBH2 exhibited the potent inhibitory activity on the proliferation of CML K562 cells and TKI resistant K562 *** observation and flow cytometry confirmed that DBH2 could selectively induce cell apoptosis and cell cycle arrest at G2/M phase of the K562 cells,which was further confirmed on the bone marrow cells from CML transgenic model mice and CD34+bone marrow leukemic cells from CML *** of DBH2 in combination with imatinib could prolong the survival rate of SCL-tTA-BCR/ABL transgenic model mice *** RT-PCR revealed that DBH2 inhibited the expression of STAT3 and STAT5 in K562 cells,and caspase-3 knockout alleviated the DBH2 induced ***,DBH2 could induce the expression of PARP1 and ROCK1 in K562 cells,which may play the important role in caspase-dependent *** results concluded that coumarin derivative DBH2 serves as a promising candidate for the CML treatment,especially in the combination with imatinib for the TKI resistant CML,and STAT/caspase-3 pathway was involved in the molecular mechanism of anti-leukemic activity of DBH2.

关键词： Apoptosis Caspase chronic myeloid leukemia Coumarin STAT

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Molecular mechanisms for survival regulation of chronic myeloid leukemia stem cells

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Protein & Cell 2013年第3期4卷 186-196页

作者： Haojian Zhang Shaoguang Li Division of Hematology/Oncology Department of MedicineUniversity of Massachusetts Medical SchoolWorcesterMA 01605USA

Studies on chronic myeloid leukemia(CML)have served as a paradigm for cancer research and *** studies involve the identifi cation of the fi rst cancer-associated chromosomal abnormality and the subsequent development of tyrosine kinase inhibitors(TKIs)that inhibit BCR-ABL kinase activity in *** becomes clear that leukemia stem cells(LSCs)in CML which are resistant to TKIs,and eradication of LSCs appears to be extremely ***,one of the major issues in current CML biology is to understand the biology of LSCs and to investigate why LSCs are insensitive to TKI monotherapy for developing curative therapeutic *** from our group and others have revealed that CML LSCs form a hierarchy similar to that seen in normal hematopoiesis,in which a rare stem cell population with limitless self-renewal potential gives rise to progenies that lack such *** also possess biological features that are different from those of normal hematopoietic stem cells(HSCs)and are critical for their malignant *** this review,we summarize the latest progress in CML field,and attempt to understand the molecular mechanisms of survival regulation of LSCs.

关键词： molecular mechanisms chronic myeloid leukemia leukemia stem cell

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Tetrandrine citrate eliminates imatinib-resistant chronic myeloid leukemia cells in vitro and in vivo by inhibiting Bcr-Abl/β-catenin axis

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2012年第11期13卷 867-874页

作者： Xiao-hua XU Yi-chao GAN Gen-bo XU Ting CHEN Hong ZHOU Jin-fen TANG Ying GU Fei XU Ying-ying XIE Xiao-ying ZHAO Rong-zhen XU Department of Hematology the Second Affiliated Hospital School of Medicine Zhejiang University Hangzhou 310009 China Department of Cancer Institute the Second Affiliated Hospital School of Medicine Zhejiang University Hangzhou 310009 China

Objective:To evaluate the effects of tetrandrine citrate, a novel tetrandrine salt with high water solubility, on the growth of imatinib (IM)-resistant chronic myeloid leukemia (CML) in vitro and in vivo, and reveal action molecular mechanisms. Methods:Cell viability in vitro was measured using methyl thiazolyl tetrazolium (MTT) assay. CML cell growth in vivo was assessed using a xenograft model in nude mice. Bcr-Abl and β-catenin protein levels were determined using Western blotting. Bcr-Abl messenger RNA (mRNA) was measured by reverse transcription polymerase chain reaction (RT-PCR). Flow cytometry (FCM) was used to determine cell cycle status. Results:Tetrandrine citrate inhibited the growth of IM-resistant K562 cells, primary leukemia cells, and primitive CD34 + leukemia cells, and their inhibition concentration that inhibited 50% of target cells (IC 50 ) ranged from 1.20 to 2.97 μg/ml. In contrast, tetrandrine citrate did not affect normal blood cells under the same conditions, and IC 50 values were about 10.12-13.11 μg/ml. Oral administration of tetrandrine citrate caused complete regression of IM-resistant K562 xeno-grafts in nude mice without overt toxicity. Western blot results revealed that treatment of IM-resistant K562 cells with tetrandrine citrate resulted in a significant decrease of both p210 Bcr-Abl and β-catenin proteins, but IM did not affect the Bcr-Abl protein levels. Proteasome inhibitor, MG132, did not prevent tetrandrine-mediated decrease of the p210 Bcr-Abl protein. RT-PCR results showed that tetrandrine treatment caused a decrease of Bcr-Abl mRNA. FCM analysis indicated that tetrandrine induced gap 1 (G 1 ) arrest in CML cells. Conclusions:Tetrandrine citrate is a novel orally active tetrandrine salt with potent anti-tumor activity against IM-resistant K562 cells and CML cells. Tetrandrine citrate-induced growth inhibition of leukemia cells may be involved in the depletion of p210 Bcr-Abl mRNA and β-catenin protein.

关键词： chronic myeloid leukemia Imatinib-resistance Tetrandrine citrate Bcr-Abl protein β-catenin protein

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Characteristics of the TCR Vβ repertoire in imatinib-resistant chronic myeloid leukemia patients with ABL mutations

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Science China(Life Sciences) 2015年第12期58卷 1276-1281页

作者： XU Ling LU Yu Hong LAI Jing YU Wei ZHANG Yi Kai JIN Zhen Yi XU Yan CHEN Jie ZHA Xian Feng CHEN Shao Hua YANG Li Jian LI Yang Qiu Institute of Hematology Jinan University Department of Hematology First Affiliated Hospital Jinan University Department of Hematology Guangzhou No.12 People's Hospital Key Laboratory for Regenerative Medicine of Ministry of Education Jinan University Department of clinical laboratory First Affiliated Hospital Jinan University

Diversity in the T cell receptor(TCR) repertoire provides a miniature defense ability for the T cell immune system that may be related to tumor initiation and progression. Understanding the T cell immune status of leukemia patients is critical for establishing specific immunotherapies. Previous studies have reported abnormal TCR repertoires and clonally expanded TCR V? T cells in chronic myeloid leukemia in chronic phase(CP-CML). In this study, we investigated the distribution and clonality of the TCR V? repertoire in 4 cases with imatinib-resistant CML in blast crisis(BC-CML) with abelson murine leukemia viral oncogene homolog 1(ABL1) kinase domain mutations(KDMs). Examination of TCR V? expression and clonality was performed by reverse transcription-polymerase chain reaction(RT-PCR) and Gene Scan analysis. Significantly skewed TCR V? repertoires were observed in BC-CML patients with different KDMs, and 4 to 8 oligoclonally expanded TCR V? subfamilies could be identified in each sample. Intriguingly, a relatively highly expanded V?9 clone with the same length as complementarity-determining region 3(CDR3)(139 bp) was found in all three CML patients in lymphoid blast crisis(LBC-CML) who had different KDMs, but the clone was not detected in the only CML patient in myeloid blast crisis(MBC-CML). In conclusion, restricted TCR V? repertoire expression and decreased clone complexity was a general phenomenon observed in the BC-CML patients with different KDMs, indicating the T-cell immunodeficiency of these patients. In addition, clonally expanded V?9 T cell clones may indicate a specific immune response to leukemia-associated antigens in LBC-CML patients.

关键词： T cell repertoire chronic myeloid leukemia blast crisis imatinib resistance BCR-ABL mutation

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Loss of the vitamin D receptor triggers senescence in chronic myeloid leukemia via DDIT4-mediated DNA damage

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Journal of Molecular Cell Biology 2023年第10期15卷 65-76页

作者： Yan Xu Wentao Qi Chengzu Zheng Yuan Li Zhiyuan Lu Jianmin Guan Chunhua Lu Baobing Zhao Key Lab of Chemical Biology(MOE) School of Pharmaceutical SciencesCheeloo College of MedicineShandong UniversityJinan 250012China NMPA Key Laboratory for Technology Research and Evaluation of Drug Products School of Pharmaceutical SciencesCheeloo College of MedicineShandong UniversityJinan 250012China Department of Pharmacology School of Pharmaceutical SciencesCheeloo College of MedicineShandong UniversityJinan 250012China School of Pharmaceutical Sciences&Institute of Materia Medica Shandong First Medical University&Shandong Academy of Medical SciencesJinan 250012China Department of Hematology Heze Municipal HospitalHeze 274031China

chronic myeloid leukemia(CML)is a hematopoietic malignancy driven by the fusion gene BCR::*** resistance to tyrosine kinase inhibitors(TKIs),due to BCR::ABL1 mutations and residual leukemia stem cells(LSCs),remains a major challenge in CML ***,we revealed the requirement of the vitamin D receptor(VDR)in the progression of *** was upregulated by BCR::ABL1 and highly expressed in CML ***,VDR knockdown inhibited the proliferation of CML cells driven by both BCR::ABL1 and TKI-resistant BCR::ABL1 ***,VDR transcriptionally regulated DDIT4 expression;reduced DDIT4 levels upon VDR knockdown triggered DNA damage and senescence via p53 signaling activation in CML ***,VDR deficiency not only suppressed tumor burden and progression in primary CML mice but also reduced the self-renewal capacity of ***,our study demonstrated that targeting VDR is a promising strategy to overcome TKI resistance and eradicate LSCs in CML.

关键词： vitamin D receptor senescence chronic myeloid leukemia DDIT4

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Effects of Quercetin on Hedgehog Signaling in chronic myeloid leukemia KBM7 Cells

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Chinese Journal of Integrative Medicine 2014年第10期20卷 776-781页

作者：李蔚赵瑛陶波张颖 Department of Pharmacy Harbin Commercial University

Objective：To investigate the effects of quercetin on Hedgehog（Hh） signaling in chronic myeloid leukemia KBM7 ***：The KBM7 cells were treated with 50,100 and 200 μmol/L quercetin for48 h *** then the trypan blue assay was used to examine the proliferative inhibition of *** cells and cell cycle were measured by flow *** mRNA and protein expression were detected by quantitative real-time polymerase chain reaction（PCR） and Western blot,***：Quercetin significantly inhibited KBM7 cell proliferation,induced cell apoptosis,and blocked cell cycle at G1 phase,which were in dose-dependent *** mRNA and protein expression of Smoothened and Gliomal（Gli1）,the members of Hh pathway decreased after treatment with *** Bcl-2 and Cyclin D1,targets of Hh signaling,also decreased after treatment with quercetin,*** also could increase p53 and Caspase-3 ***-abl mRNA copies decreased,but no changes of phosphorylated Bcr-abl and Bcr-abl proteins were observed,after treatment with ***：Quercetin could inhibit Hh signaling and its downstream targets in the KBM7 *** it might be one of mechanisms of inducing apoptosis and inhibiting cell cycle by quercetin.

关键词： quercetin hedgehog signaling chronic myeloid leukemia apoptosis cell cycle Bcr-abl

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Development of plasma cell dyscrasias in a patient with chronic myeloid leukemia:A case report

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World Journal of Clinical Cases 2022年第14期10卷 4698-4703页

作者： Na Zhang Ting-De Jiang Shu-Hua Yi Department of Hematology People’s Hospital of DeyangDeyang 618000Sichuan ProvinceChina Hematology Hospital of the Institute of Hematology Chinese Academy of Medical SciencesTianjin 300020China

BACKGROUND chronic myeloid leukemia(CML)is a clonal hematopoietic stem cell *** cell dyscrasias are a rare heterogeneous group of hematological *** co-occurrence of CML and plasma cell dyscrasias in the same patient is an extremely rare incident and has been reported in several cases in the *** SUMMARY In the present report,we described a rare case of the co-occurrence of CML and plasma cell dyscrasias in a 48-year-old man,and we discussed the reason why monoclonal gammopathy of undetermined significance progressed to smoldering multiple myeloma and eventually to multiple myeloma while being treated with dasatinib for *** tyrosine kinase inhibitor treatment and cytogenetic change may contribute to this phenomenon,and clonal hematopoiesis of indeterminate potential may lead to both CML and multiple myeloma cells in a *** studies are warranted to further explain the hidden *** This case highlights that gene translocation may contribute to initiation and sustainability of clonal ***,the treatment with tyrosine kinase inhibitor and cytogenetic change may contribute to progression from monoclonal gammopathy of undetermined significance to smoldering multiple myeloma and eventually to multiple myeloma.

关键词： chronic myeloid leukemia Plasma cell dyscrasias Multiple myeloma Tyrosine kinase inhibitor Translocation Case report

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