Er Nie

ORCID: 0000-0001-9889-0723
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About
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Research Areas
  • MicroRNA in disease regulation
  • Glioma Diagnosis and Treatment
  • Cancer-related molecular mechanisms research
  • RNA modifications and cancer
  • RNA Research and Splicing
  • Epigenetics and DNA Methylation
  • Circular RNAs in diseases
  • FOXO transcription factor regulation
  • DNA Repair Mechanisms
  • Genetic factors in colorectal cancer
  • Extracellular vesicles in disease
  • Histone Deacetylase Inhibitors Research
  • Cancer-related Molecular Pathways
  • interferon and immune responses
  • Cell Adhesion Molecules Research
  • Genetic Syndromes and Imprinting
  • Kruppel-like factors research
  • RNA Interference and Gene Delivery
  • Chromatin Remodeling and Cancer
  • Cancer, Hypoxia, and Metabolism
  • Neurofibromatosis and Schwannoma Cases
  • Ubiquitin and proteasome pathways
  • NF-κB Signaling Pathways
  • TGF-β signaling in diseases
  • Nanoplatforms for cancer theranostics

Xuzhou Medical College
2014-2024

Baylor Scott & White Medical Center - Temple
2023

Baylor Scott & White Health
2023

Nanjing Medical University
2016-2018

Jiangsu Province Hospital
2016-2018

Affiliated Hospital of Xuzhou Medical College
2018

Second Hospital of Shanxi Medical University
2017

Shanxi Medical University
2017

MIR155 host gene (MIR155HG) is a long noncoding RNA that has been considered as the primary micro (mi)RNA of miR-155. MIR155HG plays an essential role in hematopoiesis, inflammation, and tumorigenesis. Our study investigated clinical significance, biological function, mechanisms, small-molecule inhibitors MIR155HG/miR-155 axis glioma. We analyzed expression correlation with glioma grade patient survival using 2 different datasets. Biological significance was elucidated through series vitro...

10.1093/neuonc/nox017 article EN Neuro-Oncology 2017-03-06

Abstract H19 expression is elevated in many human tumors including glioblastomas, suggesting an oncogenic role for the long noncoding RNA; yet upregulation of glioblastomas remains unclear. Here we report that hypoxia significantly stimulated glioblastoma cell lines, which was related to hypoxia-inducible factors 1α (Hif-1α). Hif-1α promoted U87 and U251 cells. Meanwhile PTEN advantageous factor affect expression, through attenuating stability. also positively correlates with samples...

10.1038/srep45029 article EN cc-by Scientific Reports 2017-03-22

Exosomes are carriers of pro-tumorigenic factors that participate in glioblastoma (GBM) progression, and many fusion genes strong driver mutations neoplasia involved tumorigenesis. However, the ability to be transduced by exosomes is unknown. We characterized from GBM cells harbouring not PTPRZ1–MET (ZM fusion). also determined effect ZM exosomes) on pro-oncogenic secretions showed internalized recipient cells. In addition, we studied exosome-mediated intercellular communication...

10.1038/onc.2017.134 article EN cc-by-nc-sa Oncogene 2017-05-15

Abstract Background Our previous studies have indicated that miR-198 reduces cellular methylguanine DNA methyltransferase (MGMT) levels to enhance temozolomide sensitivity. Transforming growth factor beta 1 (TGF-β1) switches off expression by repressing K-homology splicing regulatory protein (KSRP) in epidermal keratinocytes. However, the underlying role of TGF-β1 resistance has remained unknown. Methods The distribution KSRP was detected western blotting and immunofluorescence. Microarray...

10.1093/neuonc/noaa198 article EN cc-by-nc Neuro-Oncology 2020-08-11

Glioblastoma multiforme is the most common primary malignancy in brain and confers a uniformly poor prognosis. MicroRNAs have been shown to activate or inhibit tumorigenesis. Abnormalities p53 signaling pathway are found various cancers correlate with tumor formation. We examined expression of microRNA-141-3p (miR-141-3p) glioma different grades by analysis profiling databases clinical specimens. Cell proliferation flow cytometry assays were performed evaluate promotion miR-141-3p...

10.18632/oncotarget.20528 article EN Oncotarget 2017-08-24

Temozolomide was recognized as the first-line therapy for glioblastoma to prolong survival of patients noticeably, while recent clinical studies found that some were not sensitive temozolomide treatment. The possible mechanisms seemed be methylguanine-DNA-methyltransferase (MGMT), mismatch repair, PARP, etc. And abnormal expression MGMT might most direct factor. In this study, we provide evidence Fstl1 plays a vital role in resistance by sequentially regulating DIP2A protein distribution,...

10.1038/s41388-018-0596-2 article EN cc-by Oncogene 2018-12-12

Abstract The acquisition of drug resistance is a persistent clinical problem limiting the successful treatment glioblastoma (GBM). However, molecular mechanisms by which initially chemoresponsive tumors develop therapeutic remain poorly understood. In this study, we report that BACH1, heme-binding protein participates in transcriptional repression or activation, was significantly upregulated tissues. Overexpression BACH1 GBM cells conferred to temozolomide, whereas its inhibition markedly...

10.1038/srep39743 article EN cc-by Scientific Reports 2016-12-21

MutS protein homolog 2 (MSH2) is a key element involved in the DNA mismatch repair (MMR) system, which responsible for recognizing and repairing mispaired bases. Simultaneously, MSH2 identifies adducts induced by temozolomide (TMZ) triggers apoptosis autophagy tumor cells. Previous work has revealed that reduced expression often observed patients with glioblastoma (GBM) who relapse after chemotherapy. Elucidation of mechanism behind TMZ-mediated reduction could help improve GBM treatment....

10.1158/0008-5472.can-22-2036 article EN Cancer Research 2022-09-15

Background: Gliomas result in the highest morbidity and mortality rates of intracranial primary central nervous system tumors because their aggressive growth characteristics high postoperative recurrence. They are characterized by genetic instability, intratumoral histopathological variability unpredictable clinical behavior patients. Proliferation is a key aspect progression malignant gliomas, complicating complete surgical resection enabling tumor regrowth further proliferation surviving...

10.1159/000485759 article EN cc-by-nc-nd Cellular Physiology and Biochemistry 2017-01-01

Chromobox homolog 7 (CBX7) cooperates with other polycomb group (PcG) proteins to maintain target genes in a silenced state. However, the precise role of CBX7 tumor progression is still controversial. We found that expression four public databases was significantly lower high grade glioma (HGG). The reduced correlated poor outcome HGG patients. Both KEGG and GO analyses indicated were negatively strongly associated cell cycle pathway. observed decreased protein levels enhanced cells...

10.18632/oncotarget.15789 article EN Oncotarget 2017-03-01

Abstract Patients with malignant glioma often suffered from depression, which leads to an increased risk of detrimental outcomes. Imipramine, FDA‐approved tricyclic antidepressant, has been commonly used relieve depressive symptoms in the clinic. Recently, imipramine reported participate suppression tumour progression several human cancers, including prostate cancer, colon cancer and lymphomas. However, effect on is largely unclear. Here, we show that significantly retarded proliferation...

10.1111/jcmm.16874 article EN Journal of Cellular and Molecular Medicine 2021-09-01

Recent data have been shown that EZH2 is a critical oncogene via the repression of tumor suppressor genes in human cancers. In our study, we performed genome-wide miRNA screen with bioinformatics analysis to identify specific miRNAs. Of these miRNAs, miR-524-5p and miR-324-5p were decreased glioma tissues, confered poor prognosis for patients. Upregulation reduced cell proliferation increased temozolomide (TMZ) chemosensitivity by targeting EZH2. Importantly, effection on TMZ reversed...

10.18632/oncotarget.21996 article EN Oncotarget 2017-10-24

ABSTRACT Low expression of certain ribosomal proteins leads to the inactivation p53, which is mediated mainly by RPL5 or RPL11 (ribosomal protein L11). It also unknown what mechanisms drive aberrant in tumor. SRBD1 (S1 RNA‐binding domain 1), as a highly conserved protein, lowly expressed glioma tissues and correlated with prognosis. In this study, we observed that was closely related p53 signaling. The upregulation elevated levels, thereby activating signaling pathway. As an RNA bind could...

10.1002/tox.24396 article EN Environmental Toxicology 2024-09-11

Background: CAPON has two isoforms in human brain: long form of (CAPON-L) and short (CAPON-S). Recent studies have indicated the involvement tumor cell growth. We aimed to reveal role proliferation glioma cells this study. Materials Methods: Lentivirus-mediated stable lines with CAPON-L or CAPON-S overexpression were established U87 U251 cells. Cell counting kit-8 colony formation assays used evaluate proliferation. Western blot analysis cycle-related proteins flow cytometry performed...

10.7150/ijms.31579 article EN cc-by-nc International Journal of Medical Sciences 2019-01-01

Polycomb group (PcG) proteins form at least two key complexes, namely polycomb repressive complex 1 and 2. These complexes are involved in the progression of various cancers. Systematic research has not been conducted on aberrant expression PcG members gliomas. Using Chinese Glioma Genome Atlas data set, patterns between normal brain tissues glioma samples were analyzed, a PcG-based classifier was then developed using BRB Cox regression risk-score model. results validated an independent...

10.3892/ol.2017.5753 article EN Oncology Letters 2017-02-20

<div>Abstract<p>MutS protein homolog 2 (MSH2) is a key element involved in the DNA mismatch repair (MMR) system, which responsible for recognizing and repairing mispaired bases. Simultaneously, MSH2 identifies adducts induced by temozolomide (TMZ) triggers apoptosis autophagy tumor cells. Previous work has revealed that reduced expression often observed patients with glioblastoma (GBM) who relapse after chemotherapy. Elucidation of mechanism behind TMZ-mediated reduction could...

10.1158/0008-5472.c.6514197.v1 preprint EN 2023-03-31

<div>Abstract<p>MutS protein homolog 2 (MSH2) is a key element involved in the DNA mismatch repair (MMR) system, which responsible for recognizing and repairing mispaired bases. Simultaneously, MSH2 identifies adducts induced by temozolomide (TMZ) triggers apoptosis autophagy tumor cells. Previous work has revealed that reduced expression often observed patients with glioblastoma (GBM) who relapse after chemotherapy. Elucidation of mechanism behind TMZ-mediated reduction could...

10.1158/0008-5472.c.6514197 preprint EN 2023-03-31
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