ABSTRACT
Optical coherence tomography (OCT) is a noninvasive high-resolution imaging technology that can accurately acquire the internal characteristics of tissues within a few millimeters. Using OCT technology, the internal fingerprint structure, which is consistent with external fingerprints and sweat glands, can be collected, leading to high anti-spoofing capabilities. In this paper, an OCT fingerprint anti-spoofing method based on a 3D convolutional neural network (CNN) is proposed, considering the spatial continuity of 3D biometrics in fingertips. Experiments were conducted on self-built and public datasets to test the feasibility of the proposed anti-spoofing method. The anti-spoofing strategy using a 3D CNN achieved the best results compared with classic networks.
ABSTRACT
In this study, the function and regulation of long non-coding RNA (lncRNA) LINC00342 in lung adenocarcinoma were investigated. From The Cancer Genome Atlas (TCGA) datasets and Gene Expression Omnibus (GEO) datasets, LINC00342 was found to be up-regulated in lung adenocarcinoma. The high expression of LINC00342 was also validated in lung cancer cell lines. LINC00342 induced invasion and epithelial-mesenchymal transition (EMT) process of A549 cells. By analyzing GEO datasets, TPBG was confirmed positively correlated to LINC00342 and highly expressed in lung adenocarcinoma. In addition, TPBG induced invasion and EMT process of A549 cells. Through bioinformatics analysis and luciferase assay, miR-15b was validated as a direct target of both LINC00342 and TPBG. Ectopic miR-15 expression repressed LINC00342 and TPBG. Interestingly, LINC00342 overexpression inhibited miR-15b and induced TPBG, whereas ectopic TPBG unchanged LINC00342 and miR-15b levels. In conclusion, LINC00342 promotes metastasis of lung adenocarcinoma through inducing TPBG targeted by miR-15b.
Subject(s)
Adenocarcinoma , Lung Neoplasms , MicroRNAs , RNA, Long Noncoding , A549 Cells , Adenocarcinoma/genetics , Cell Proliferation/genetics , Epithelial-Mesenchymal Transition/genetics , Gene Expression Regulation, Neoplastic , Humans , Lung/metabolism , Lung Neoplasms/pathology , Membrane Glycoproteins/genetics , MicroRNAs/genetics , Neoplasm Metastasis , RNA, Long Noncoding/geneticsABSTRACT
Current conventional treatment strategies for glioblastoma (GBM) have limited efficacy due to the rapid development of resistance to temozolomide (TMZ). It is particularly urgent to develop novel therapeutic strategies that can overcome TMZ resistance and provide patients with better prognoses. Here, a TMZ-resistant GBM cell strain and a mouse model of TMZ resistance are established as valuable tools to explore novel therapeutic strategies against TMZ resistance. Experimentally, p38MAPK inhibitor reduces the accumulation of F4/80+/CD11b+ macrophages/microglia in glioma and prolongs the survivals of glioma-bearing mice. Glioma-associated macrophages/microglia have a significanct expression of PD-L1. p38MAPK inhibitor in combination with PD-L1 antibody can effectively prolongs the survivals of TMZ-resistant GBM-bearing hosts, and differentially reduces the accumulation of circulating monocytes-derived tumor-associated macrophages and PD-L1 abundances of resident glioma-associated microglia. This combination therapy could be a treatment option for patients at the recurrence or chronic TMZ maintenance stages. A clinical study to confirm the safety and effectiveness of this combination therapy is warranted.
Subject(s)
Antibodies, Monoclonal/pharmacology , Antibodies, Monoclonal/therapeutic use , Antineoplastic Agents, Alkylating/pharmacology , B7-H1 Antigen/genetics , B7-H1 Antigen/metabolism , Enzyme Inhibitors/pharmacology , Enzyme Inhibitors/therapeutic use , Gene Expression Regulation, Neoplastic/drug effects , Gene Expression Regulation, Neoplastic/genetics , Glioblastoma/genetics , Glioblastoma/pathology , Microglia/metabolism , Temozolomide/pharmacology , Tumor-Associated Macrophages/pathology , p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors , Animals , Antineoplastic Agents, Alkylating/therapeutic use , B7-H1 Antigen/immunology , Cell Line, Tumor , Disease Models, Animal , Drug Resistance, Neoplasm/genetics , Drug Therapy, Combination , Glioblastoma/drug therapy , Glioblastoma/mortality , Humans , Mice , Survival RateABSTRACT
As a major contributor of chemotherapy resistance and malignant recurrence, glioma stem cells (GSCs) have been proposed as a target for the treatment of gliomas. To evaluate the therapeutic potential of quetiapine (QUE), an atypical antipsychotic, for the treatment of malignant glioma, we established mouse models with GSCs-initiated orthotopic xenograft gliomas and subcutaneous xenograft tumors, using GSCs purified from glioblastoma cell line GL261. We investigated antitumor effects of QUE on xenograft gliomas and its underlying mechanisms on GSCs. Our data demonstrated that (i) QUE monotherapy can effectively suppress GSCs-initiated tumor growth; (ii) QUE has synergistic effects with temozolomide (TMZ) on glioma suppression, and importantly, QUE can effectively suppress TMZ-resistant (or -escaped) tumors generated from GSCs; (iii) mechanistically, the anti-glioma effect of QUE was due to its actions of promoting the differentiation of GSCs into oligodendrocyte (OL)-like cells and its inhibitory effect on the Wnt/ß-catenin signaling pathway. Together, our findings suggest an effective approach for anti-gliomagenic treatment via targeting OL-oriented differentiation of GSCs. This also opens a door for repurposing QUE, an FDA approved drug, for the treatment of malignant glioma.