scholarly journals MPC-8 Serum anti-zinc finger FYVE domain-containing protein 21 (ZFYVE21) autoantibody as a novel biomarker for oligodendroglioma IDH-mutant and 1p/19q co-deletion

2021 ◽  
Vol 3 (Supplement_6) ◽  
pp. vi17-vi17
Author(s):  
Tomoo Matsutani ◽  
Zhang Boshi ◽  
Seiichiro Hirono ◽  
Motoo Nagane ◽  
Atsuo Yoshino ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Cns Tumors ◽  
Idh Mutation ◽  
Glutathione S Transferase ◽  
Invasion And Migration ◽  
Fyve Domain ◽  
Healthy Donors ◽  
Homogeneous Assay ◽  
And Migration ◽  
Antibody Levels

Abstract Background: Glioma is one of the most challenging diseases to cure, and it would be beneficial to discover new serum biomarkers for early diagnosis. Moreover, zinc finger FYVE domain-containing protein 21 (ZFYVE21) was a regulator of tumor invasion and migration. In this study, we examined the levels of serum anti-ZFYVE21 antibodies in patients with glioma. Methods: This is a multicenter observational prospective study to discover a novel serum autologous antibody marker. We analyzed 286 pre-surgically collected sera of CNS tumors and compared them to healthy donors(HD). Bacterially expressed glutathione-S-transferase-fused ZFYVE21 protein was purified, and its antibody levels were measured by amplified luminescent proximity homogeneous assay-linked immunosorbent assay (AlphaLISA). Results: The anti-ZFYVE21 antibody levels were significantly elevated in patients with gliomas (P<0.001) than those in HD, instead of patients with other CNS tumors. Among gliomas, the highest sensitivity was observed for oligodendroglioma containing IDH mutation and 1p/19q co-deletion to HD (sensitivity: 72.00%, specificity: 67.71%, AUC: 0.7565, P<0.0001), while there is no significance in astrocytoma containing only IDH mutation. In comparing 1p/19q co-deleted oligodendroglioma with IDH-mutated astrocytoma, the sensitivity and specificity were 50% and 100%, respectively. Conclusion: Serum anti-ZFYVE21 antibodies might be a novel diagnostic marker distinguishing 1p/19q co-deleted oligodendroglioma from IDH-mutant astrocytoma.

miR-216a-5p Suppresses the Proliferation, Invasion and Migration of Fibroblast-Like Synoviocyte in Rheumatoid Arthritis by Targeting Zinc Finger and BTB Domain-Containing Protein 2 (ZBTB2)

2021 ◽  
Vol 11 (5) ◽  
pp. 896-902
Author(s):  
Jinwei Zhao ◽  
Ling Li
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Proliferation ◽  
Zinc Finger ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Healthy Controls ◽  
Invasion And Migration ◽  
Btb Domain ◽  
And Migration

MicroRNAs have been reported to be associated with the initiation and progression of rheumatoid arthritis (RA). miR-216a-5p, one of the miRNAs, is involved in cancer cell proliferation, invasion and migration. However, the role of miR-216a-5p in RA remains to be explored. The expressions of miR-216a-5p and zinc finger and BTB domain-containing protein 2 (ZBTB2) in fibroblast-like synoviocytes (FLS) of RA or healthy controls were detected by qRT-PCR and western blot analysis. Transfection of overexpressed and silenced miR-216a-5p were performed to explore the functional role of miR-216a-5p in RA-FLS. Cell Counting Kit-8 (CCK-8) assay and transwell assay were employed to assess cell proliferation and cell invasion, respectively. Moreover, luciferase reporter assay was executed to verify the combination of miR-216a-5p and ZBTB2. The results showed that miR-216a-5p expression in RA-FLS was downregulated than healthy controls. Overexpres-sion of miR-216a-5p inhibited RA-FLS cell proliferation, invasion and migration, while miR-216a-5p silencing revealed the opposite results. In addition, ZBTB2 was identified to be a direct target of miR-216a-5p in RA-FLS and its expression was higher than that in healthy controls. Rescue experiments revealed that ZBTB2 overexpression reversed the effects of miR-216a-5p on the proliferation, invasion and migration of RA-FLS. These data indicated the suppressive role of miR-216a-5p in RA-FLS via the regulation of ZBTB2, suggesting that miR-216a-5p and ZBTB2 may be the new targets for the treatment of RA.

Cross Correlation Statistical Study of Biomarker for Cerebral Infarction

2019 ◽  
Vol 9 (6) ◽  
pp. 1272-1277
Author(s):  
Hao Lu ◽  
Mingjie Mai ◽  
Min Guan ◽  
Kazuo Sugimoto ◽  
Shikai Wu ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Statistical Study ◽  
Smoking Habit ◽  
Serum Antibody ◽  
Human Aortic Endothelial Cell ◽  
Cerebrovascular Disorder ◽  
Healthy Donors ◽  
Homogeneous Assay ◽  
Ischemic Attack ◽  
Antibody Levels

Cerebral infarction (CI) is the most common cerebrovascular disorder with high fatality and disability rates worldwide, and transient ischemic attack (TIA) is a warning of CI, and early diagnosis and intervention of TIA are very important for the prevention of CI. We screened a human aortic endothelial cell cDNA library using serum from TIA patients to obtain lysosomal-associated membrane protein 1 (LAMP1) antigen. Amplified luminescent proximity homogeneous assay-linked immunosorbentassay (AlphaLISA) revealed that the antibody levels against LAMP1 were significantly higher in patients with TIA or acute-phase CI (aCI) compared with healthy donors (HDs) (P < 0.01) by examined in three independent cohorts (77 and 158 in the TIA and acute aCI patient cohorts, respectively, and 122 in HD cohort used as normal control). Spearman correlation analysis demonstrated that LAMP1-Abs levels were positively correlated with cigarette smoking habit. The serum antibody levels against LAMP1 could potentially serve as a useful biomarker for early detection of TIA or predicting of the onset of CI.

Glioblastoma invasion and NMDA receptors: A novel prospect

2019 ◽  
Vol 106 (3) ◽  
pp. 250-260 ◽  
Author(s):  
DN Nandakumar ◽  
P Ramaswamy ◽  
C Prasad ◽  
D Srinivas ◽  
K Goswami
Keyword(s):  
Glutamate Receptors ◽  
Cell Lines ◽  
Intracellular Signaling ◽  
Transcript Level ◽  
Glioblastoma Cells ◽  
Invasion And Migration ◽  
Matrigel Invasion ◽  
Nmdar Activation ◽  
And Migration

Purpose Glioblastoma cells create glutamate-rich tumor microenvironment, which initiates activation of ion channels and modulates downstream intracellular signaling. N-methyl-D-aspartate receptors (NMDARs; a type of glutamate receptors) have a high affinity for glutamate. The role of NMDAR activation on invasion of glioblastoma cells and the crosstalk with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) is yet to be explored. Main methods LN18, U251MG, and patient-derived glioblastoma cells were stimulated with NMDA to activate NMDAR glutamate receptors. The role of NMDAR activation on invasion and migration and its crosstalk with AMPAR were evaluated. Invasion and migration of glioblastoma cells were investigated by in vitro trans-well Matrigel invasion and trans-well migration assays, respectively. Expression of NMDARs and AMPARs at transcript level was evaluated by quantitative real-time polymerase chain reaction. Results We determined that NMDA stimulation leads to enhanced invasion in LN18, U251MG, and patient-derived glioblastoma cells, whereas inhibition of NMDAR using MK-801, a non-competitive antagonist of the NMDAR, significantly decreased the invasive capacity. Concordant with these findings, migration was significantly augmented by NMDAR in both cell lines. Furthermore, NMDA stimulation upregulated the expression of GluN2 and GluA1 subunits at the transcript level. Conclusions This study demonstrated the previously unexplored role of NMDAR in invasion of glioblastoma cells. Furthermore, the expression of the GluN2 subunit of NMDAR and the differential overexpression of the GluA1 subunit of AMPAR in both cell lines provide a plausible rationale of crosstalk between these calcium-permeable subunits in the glutamate-rich microenvironment of glioblastoma.

STUDY OF CXCL12, CCR4, EGFR GENE EXPRESSION IN MIGRATING MYELOMONOBLASTIC LEUKEMIA CELLS BEFORE AND AFTER CHEMOTHERAPY

2019 ◽  
Vol 1 (1) ◽  
pp. 100-104
Author(s):  
A. B. Filina ◽  
O. A. Svitich ◽  
Yu. I. Ammur ◽  
A. K. Golenkov ◽  
E. F. Klinushkina ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Mononuclear Cells ◽  
Boyden Chamber ◽  
External Stimulation ◽  
Healthy Donors ◽  
Genes Expression ◽  
Before And After ◽  
Chemokine Cxcl12 ◽  
And Migration ◽  
Cell Chemotaxis

Аim. A study of CXCL12 effect on the migration of mononuclear cells isolated from healthy patients, from patients with myelomonoblastic leukemia before and after chemotherapy and the study of CCR4, EGFR and CXCL12 genes expression after exposure to CXCL12. Materials and methods. The chemotaxis of mononuclear cells (MNCs) of healthy donors and patients with myelomonoblastic leukemia was studied in a Boyden chamber, followed by isolation of RNA, reverse transcription and PCR-RV. Results. A significant increase in myelomonoblasic cell chemotaxis towards CXCL12 after chemotherapy was demonstrated, as well as a decrease in the expression of this chemokine in tumor cells before chemotherapy after exposure to CXCL12. Сonclusion. Presumably, the tumor cells themselves produce CXCL12 in large amounts, which is necessary for the disturbance of intercellular interactions and further intravasation, whose production may decrease with external stimulation by the same chemokine. CXCL12 also helps to increase the expression level of EGFR and CCR4, which leads to increased tumor proliferation and migration of tumor cells.

Dynamic Changes of Collagen Ⅳ During Cancer Invasion and Migration: Pulse Mode

2013 ◽  
Vol 40 (10) ◽  
pp. 1056
Author(s):  
Min FANG ◽  
Jing-Ping YUAN ◽  
Chun-Wei PENG ◽  
Shao-Ping LIU ◽  
Yan LI
Keyword(s):  
Cancer Invasion ◽  
Pulse Mode ◽  
Dynamic Changes ◽  
Invasion And Migration ◽  
And Migration

Wnt/beta-catenin and PI3K/Akt/mTOR Signaling Pathways in Glioblastoma: Two Main Targets for Drug Design: A Review

2020 ◽  
Vol 26 (15) ◽  
pp. 1729-1741 ◽  
Author(s):  
Seyed H. Shahcheraghi ◽  
Venant Tchokonte-Nana ◽  
Marzieh Lotfi ◽  
Malihe Lotfi ◽  
Ahmad Ghorbani ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Cellular Proliferation ◽  
Chemotherapy Resistance ◽  
Wnt Signaling Pathway ◽  
Therapeutic Interventions ◽  
Beta Catenin ◽  
Clinical Prognosis ◽  
Invasion And Migration ◽  
And Migration

: Glioblastoma (GBM) is the most common and malignant astrocytic glioma, accounting for about 90% of all brain tumors with poor prognosis. Despite recent advances in understanding molecular mechanisms of oncogenesis and the improved neuroimaging technologies, surgery, and adjuvant treatments, the clinical prognosis of patients with GBM remains persistently unfavorable. The signaling pathways and the regulation of growth factors of glioblastoma cells are very abnormal. The various signaling pathways have been suggested to be involved in cellular proliferation, invasion, and glioma metastasis. The Wnt signaling pathway with its pleiotropic functions in neurogenesis and stem cell proliferation is implicated in various human cancers, including glioma. In addition, the PI3K/Akt/mTOR pathway is closely related to growth, metabolism, survival, angiogenesis, autophagy, and chemotherapy resistance of GBM. Understanding the mechanisms of GBM’s invasion, represented by invasion and migration, is an important tool in designing effective therapeutic interventions. This review will investigate two main signaling pathways in GBM: PI3K/Akt/mTOR and Wnt/beta-catenin signaling pathways.

Effects and Mechanisms of Anlotinib and Dihydroartemisinin Combination Therapy in Ameliorating Malignant Biological Behavior of Gastric Cancer Cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Qiong Luo ◽  
Suyun Zhang ◽  
Donghuan Zhang ◽  
Rui Feng ◽  
Nan Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Chorioallantoic Membrane ◽  
Cell Counting ◽  
Biological Behavior ◽  
Gastric Cancer Cells ◽  
Invasion And Migration ◽  
Apoptosis Related Protein ◽  
And Migration

Background: Gastric cancer(GC) is currently one of the major malignancies that threatens human lives and health. Anlotinib is a novel small-molecule that inhibits angiogenesis to exert anti-tumor effects. However, the function in gastric cancer is incompletely understood. Objective: The aim of the present study was to investigate the anti-tumor effects and molecular mechanisms of anlotinib combined with dihydroartemisinin (DHA) in SGC7901 gastric cancer cells. Method: Different concentrations of anlotinib and DHA were used to treat SGC7901 gastric cancer cells, after which cell proliferation was measured. Drug interactions of anlotinib and DHA were analyzed by the Chou-Talalay method with CompuSyn software. proliferation, apoptosis, invasion, migration, and angiogenesis were measured using the cell counting kit-8 (CCK8) assay, flow cytometry, Transwell invasion assays, scratch assays, and chicken chorioallantoic membrane (CAM) assays. proliferation-associated protein (Ki67), apoptosis-related protein (Bcl-2), and vascular endothelial growth factor A (VEGF-A) were quantified by Western bloting. Results: The combination of 2.5 μmol/L of anlotinib and 5 of μmol/L DHA was highly synergistic in inhibiting cell growth, significantly increased the apoptosis rate and suppressed obviously the invasion and migration capability and angiogenesis of gastric cancer cells. In addition, the expression levels of Ki67, Bcl-2, and VEGF-A, as well as angiogenesis, were significantly decreased in the Combination of drugs compared with in control and either drug alone. Conclusion: The combination of anlotinib and DHA showed synergistic antitumor activity, suggesting their potential in treating patients with gastric cancer.

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