Jianmin Wang

ORCID: 0000-0003-2238-4132
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About
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Research Areas
  • Cancer-related molecular mechanisms research
  • Circular RNAs in diseases
  • MicroRNA in disease regulation
  • RNA modifications and cancer
  • Cancer Genomics and Diagnostics
  • Peroxisome Proliferator-Activated Receptors
  • Cancer, Lipids, and Metabolism
  • Autophagy in Disease and Therapy
  • Cancer, Hypoxia, and Metabolism
  • Acute Myeloid Leukemia Research
  • interferon and immune responses
  • Sarcoma Diagnosis and Treatment
  • Cancer Cells and Metastasis

Shangqiu First People's Hospital
2018-2020

Shangqiu Institute of Technology
2019

Second Military Medical University
2016

Changhai Hospital
2016

St. Jude Children's Research Hospital
2014

Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To define the landscape of mutations in pediatric osteosarcoma, we performed whole-genome sequencing DNA from 20 tumor samples matched normal tissue a discovery cohort, as well 14 validation cohort. Single-nucleotide (SNVs) exhibited pattern localized hypermutation called kataegis 50% tumors. We identified p53 pathway lesions all tumors...

10.1016/j.celrep.2014.03.003 article EN cc-by-nc-nd Cell Reports 2014-04-01

Increasing evidence has suggested the involvement of long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in chemoresistance cancer treatment. However, its function and molecular mechanisms acute myeloid leukemia (AML) are still not well elucidated. In present study, we investigate functional role TUG1 Adriamycin (ADR) resistance AML discover underlying mechanism. Our study revealed that was up-regulated ADR-resistant tissues cells. High expression correlated with poor prognosis...

10.1016/j.biopha.2018.11.003 article EN Biomedicine & Pharmacotherapy 2018-11-26

Renal cell carcinoma (RCC), including pediatric RCC, is one of the high cancer-associated death cause in adults and children. The mechanism by which long non-coding RNA SCAMP1 regulates RCC not fully understood.mRNA protein levels were detected RT-qPCR westernblot. MTT assay was used to examine viability TUNEL utilized measure apoptosis ACHN Caki-1 cells.in vivo tumor growth determined xenograft assay.H2O2 treatment remarkably inhibited induced apoptosis. elevated cells tumors. depletion...

10.1016/j.biopha.2019.109460 article EN Biomedicine & Pharmacotherapy 2019-09-21

// Yinghan Su 1, 2, * , Bin Sun Xuejing Lin Xinying Zhao 3 Weidan Ji 2 Miaoxia He Haihua Qian Xianmin Song Jianmin Yang Wang Jie Chen 1 School of Life Science, University Liverpool, L3 4PH, UK Department Molecular Oncology, Eastern Hepatobiliary Surgical Hospital & National Center Liver Cancer, Second Military Medical University, Shanghai 200438, China Hematology Pathology, Changhai Hospital, 200168, These authors have contributed equally to this work Correspondence to: Chen, email:...

10.18632/oncotarget.9237 article EN Oncotarget 2016-05-09

Acute myeloid leukemia (AML) is a serious threat to human health. Long non-coding RNA (lncRNA) Taurine-Upregulated Gene1 (TUG1) has been reported participate in the development and progression of several cancers, including AML. Herein, we aimed investigate pathognomonic role TUG1 AML cells its potential mechanistic pathway. Quantitative real-time PCR (qRT-PCR) assay was applied detect expression levels lncRNA TUG1, miR-193a-5p Rab10 bone marrow cell lines. The CCK-8 conducted assess...

10.2147/ott.s234935 article EN OncoTargets and Therapy 2020-02-01

Background: Development of chemoresistance remains a major obstacle for pediatric acute myeloid leukemia (AML) management. Zinc finger antisense 1 (ZFAS1) is novel tumor-related lncRNA that has been reported as an oncogene involved in the development AML. The purpose present study was to investigate role and underlying mechanism ZFAS1 AML chemoresistance. Methods: expression levels miR-195 were assessed by qRT-PCR Myb detected using western blotting. CCK-8 assay used determine IC50 value...

10.1039/c9ra04843j article EN cc-by-nc RSC Advances 2019-01-01

<p>Supplementary Figures - Figure S1 shows CC expression in AA and CA PCa cells. S2 cell death DEVDase activity cells response to docetaxel treatment. S3 effect of knockdown on docetaxel-induced apoptotic death, caspase-3 PARP cleavage cells; mtDNA content S4 levels Nrf1, c-Myc, NF-κB, PGC-1α activity, treatment the presence c-Myc NF-κB inhibitors S5 Nrf1 or AKT activator S6 genetic inhibition PTEN after S7 p-Drp1S616 p-Drp1S637 primary prostate tumor (PT) matching non-tumor (MN)...

10.1158/0008-5472.22423932.v1 preprint EN cc-by 2023-03-31
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