A5059574727- Ferroptosis and cancer prognosis
- MicroRNA in disease regulation
- RNA modifications and cancer
- Extracellular vesicles in disease
- Autophagy in Disease and Therapy
- Epigenetics and DNA Methylation
- Caveolin-1 and cellular processes
- Glioma Diagnosis and Treatment
- Chromatin Remodeling and Cancer
- Cancer Mechanisms and Therapy
- Cancer, Lipids, and Metabolism
- Circular RNAs in diseases
- Tissue Engineering and Regenerative Medicine
- Cancer Research and Treatments
- Mechanisms of cancer metastasis
- Meningioma and schwannoma management
- RNA regulation and disease
- Cancer, Hypoxia, and Metabolism
- Neuroinflammation and Neurodegeneration Mechanisms
- Cancer Genomics and Diagnostics
- Regulation of Appetite and Obesity
- DNA Repair Mechanisms
- Spinal Cord Injury Research
- Tumors and Oncological Cases
- Neurofibromatosis and Schwannoma Cases
Southern Medical University
2019-2023
Nanfang Hospital
2019-2023
Glioblastoma, a common malignant intracranial tumor, has the most dismal prognosis. Autophagy was reported to act as survival-promoting mechanism in gliomas by inducing epithelial-to-mesenchymal transition (EMT). Here, we determined critical molecules involved autophagy-induced EMT and elucidated possible of chemoradiotherapy resistance tumor recurrence.We used isobaric tags for relative absolute quantitation identify proteins pathway mediating via autophagy inducer treatment, tested...
Temozolomide resistance remains a major obstacle in the treatment of glioblastoma (GBM). The combination temozolomide with another agent could offer an improved option if it overcome chemoresistance and prevent side effects. Here, we determined critical drug that cause ferroptosis GBM cells elucidated possible mechanism by which overcomes chemoresistance.Haloperidol/temozolomide synergism was assessed cell lines different dopamine D2 receptor (DRD2) expression vitro vivo. Inhibitors...
Rationale: Glioblastoma (GBM) is the most common and aggressive brain tumor, characterized by its propensity to invade surrounding parenchyma. The effect of extracellular high-mobility group box 1 (HMGB1) protein on glioblastoma progression still controversial. p62 overexpressed in glioma cells, has been associated with malignant features poor prognosis GBM patients. Hence, this study aimed clarify role HMGB1-induced epithelial-mesenchymal transition (EMT) both vitro vivo. Methods:...
Spinal schwannoma is a common benign tumor. However, the high recurrence rate and incidence of surgical complications are unsolved problems.To propose morphological classification spinal based on tumor-membrane relationships to increase gross total resection (GTR) decrease complications.Histological techniques were used study 7 adult cadavers. Following picrosirius staining, membranes around nerve root observed under microscope. Data from 101 patients with also collected for clinical...
Abstract Switch/sucrose-nonfermenting (SWI/SNF) complexes play a key role in chromatin remodeling. Recent studies have found that SMARCC2, as the core subunit of fundamental module complex, plays its early assembly. In this study, we unique function SMARCC2 inhibiting progression glioblastoma by targeting DKK1 signaling axis. Low expression is malignant (GBM) compared with low-grade gliomas. knockout promoted proliferation cells, while overexpression showed opposite effect. Mechanistically,...
Glioma is the most common type of central nervous system tumor. SWItch/sucrose non‑fermentable (SWI/SNF) a tumor suppressor that serves an important role in epithelial‑mesenchymal transition (EMT). The present study aimed to identify key molecules involved EMT process. SWI/SNF related, matrix associated, actin dependent regulator chromatin subfamily c member 2 (SMARCC2) mutated and its expression low multiple types cancer. SMARCC2 core subunit chromatin‑remodeling complex, SWI/SNF. Relative...
Necroptosis-related genes are essential for the advancement of IDH-wild-type GBM. However, putative effects necroptosis-related lncRNAs (nrlncRNAs) in GBM remain unknown.By using TCGA and GTEx databases, a nrlncRNA prognostic signature was created LASSO Cox regression. The median risk score used to categorize patients into low high-risk groups. To confirm validity, univariate, multivariate regression ROC curves were used. Furthermore, by enrichment analysis, immune correlation drug...
<p>Fig. S3. HP radiosensitive GBM cells.</p>
<p>Fig. S1. HP does not trigger apoptosis in GBM cells.</p>
<p>Fig. S4. Autophagy, endoplasmic reticulum stress and cAMP pathway are involved in TMZ+HP-induced ferroptosis GBM cells.</p>
<p>Fig. S2. TMZ+HP Hp induces ferroptosis in GBM cells.</p>
<p>Fig. S3. HP radiosensitive GBM cells.</p>
<p>Fig. S2. TMZ+HP Hp induces ferroptosis in GBM cells.</p>
<div>Abstract<p>Purpose:Temozolomide (TMZ) resistance remains a major obstacle in the treatment of glioblastoma (GBM). The combination TMZ with another agent could offer an improved option if it overcome chemoresistance and prevent side effects. Here, we determined critical drug that cause ferroptosis GBM cells elucidated possible mechanism by which overcomes chemoresistance. Experimental Design:Haloperidol/TMZ synergism was assessed cell lines different DRD2 expression...
<div>Abstract<p>Purpose:Temozolomide (TMZ) resistance remains a major obstacle in the treatment of glioblastoma (GBM). The combination TMZ with another agent could offer an improved option if it overcome chemoresistance and prevent side effects. Here, we determined critical drug that cause ferroptosis GBM cells elucidated possible mechanism by which overcomes chemoresistance. Experimental Design:Haloperidol/TMZ synergism was assessed cell lines different DRD2 expression...
<p>Fig. S2. TMZ+HP Hp induces ferroptosis in GBM cells.</p>
<p>Fig. S3. HP radiosensitive GBM cells.</p>
<p>Fig. S4. Autophagy, endoplasmic reticulum stress and cAMP pathway are involved in TMZ+HP-induced ferroptosis GBM cells.</p>
<p>Fig. S1. HP does not trigger apoptosis in GBM cells.</p>
<p>Fig. S4. Autophagy, endoplasmic reticulum stress and cAMP pathway are involved in TMZ+HP-induced ferroptosis GBM cells.</p>
<p>Fig. S1. HP does not trigger apoptosis in GBM cells.</p>