scholarly journals Identification of the miRNA-mRNA regulatory network of small cell osteosarcoma based on RNA-seq

Oncotarget ◽  
2017 ◽  
Vol 8 (26) ◽  
pp. 42525-42536 ◽  
Author(s):  
Lin Xie ◽  
Yedan Liao ◽  
Lida Shen ◽  
Fengdi Hu ◽  
Sunlin Yu ◽  
...  
Keyword(s):  
Regulatory Network ◽  
Small Cell ◽  
Rna Seq ◽  
Small Cell Osteosarcoma

scholarly journals NKL Homeobox Gene VENTX Is Part of a Regulatory Network in Human Conventional Dendritic Cells

2021 ◽  
Vol 22 (11) ◽  
pp. 5902
Author(s):  
Stefan Nagel ◽  
Claudia Pommerenke ◽  
Corinna Meyer ◽  
Hans G. Drexler
Keyword(s):  
Dendritic Cells ◽  
Transcription Factors ◽  
Cell Lines ◽  
Expression Profiling ◽  
Regulatory Network ◽  
Homeobox Gene ◽  
Leukemia Cell Line ◽  
Specific Gene ◽  
Rna Seq ◽  
And Function

Recently, we documented a hematopoietic NKL-code mapping physiological expression patterns of NKL homeobox genes in human myelopoiesis including monocytes and their derived dendritic cells (DCs). Here, we enlarge this map to include normal NKL homeobox gene expressions in progenitor-derived DCs. Analysis of public gene expression profiling and RNA-seq datasets containing plasmacytoid and conventional dendritic cells (pDC and cDC) demonstrated HHEX activity in both entities while cDCs additionally expressed VENTX. The consequent aim of our study was to examine regulation and function of VENTX in DCs. We compared profiling data of VENTX-positive cDC and monocytes with VENTX-negative pDC and common myeloid progenitor entities and revealed several differentially expressed genes encoding transcription factors and pathway components, representing potential VENTX regulators. Screening of RNA-seq data for 100 leukemia/lymphoma cell lines identified prominent VENTX expression in an acute myelomonocytic leukemia cell line, MUTZ-3 containing inv(3)(q21q26) and t(12;22)(p13;q11) and representing a model for DC differentiation studies. Furthermore, extended gene analyses indicated that MUTZ-3 is associated with the subtype cDC2. In addition to analysis of public chromatin immune-precipitation data, subsequent knockdown experiments and modulations of signaling pathways in MUTZ-3 and control cell lines confirmed identified candidate transcription factors CEBPB, ETV6, EVI1, GATA2, IRF2, MN1, SPIB, and SPI1 and the CSF-, NOTCH-, and TNFa-pathways as VENTX regulators. Live-cell imaging analyses of MUTZ-3 cells treated for VENTX knockdown excluded impacts on apoptosis or induced alteration of differentiation-associated cell morphology. In contrast, target gene analysis performed by expression profiling of knockdown-treated MUTZ-3 cells revealed VENTX-mediated activation of several cDC-specific genes including CSFR1, EGR2, and MIR10A and inhibition of pDC-specific genes like RUNX2. Taken together, we added NKL homeobox gene activities for progenitor-derived DCs to the NKL-code, showing that VENTX is expressed in cDCs but not in pDCs and forms part of a cDC-specific gene regulatory network operating in DC differentiation and function.

Construction of an lncRNA–mRNA Co-Expression Regulatory Network Mediating Inflammation and Regeneration Following Acute Pancreatitis Injury

2021 ◽  
Author(s):  
Jing Wang ◽  
Tianjie Chen ◽  
Xiaohua Zhang ◽  
Shulei Zhao
Keyword(s):  
Acute Pancreatitis ◽  
Mrna Expression ◽  
Regulatory Network ◽  
Noncoding Rnas ◽  
Pancreatic Injury ◽  
Control Group ◽  
Rna Seq ◽  
Damage Repair ◽  
Injury And Repair ◽  
And Function

Abstract Long noncoding RNAs (lncRNAs) play important roles in the occurrence and development of many diseases and can be used as targets for diagnosis and treatment. However, the expression and function of lncRNAs in the injury and repair of acute pancreatitis (AP) are unclear. To decipher lncRNAs’ regulatory roles in AP, we reanalyzed an RNA-seq dataset of 24 pancreatic tissues, including those of normal control mice (BL), those 7 days after mild AP (D7), and those 14 days after mild AP (D14). The results showed significant differences in lncRNA and mRNA expression of D7/D14 groups compared with the control group. Co-expression analysis showed that differentially expressed (DE) lncRNAs were closely related to immunity- and inflammation-related pathways by trans-regulating mRNA expression. The lncRNA–mRNA network showed that the lncRNAs Dancer, Gmm20488, Terc, Snhg3, and Snhg20 were significantly correlated with AP pathogenesis. WGCNA and cis regulation analysis also showed that AP repair-associated lncRNAs were correlated with extracellular and inflammation-related genes, which affect the repair and regeneration of pancreatic injury after AP. In conclusion, the systemic dysregulation of lncRNAs is strongly involved in remodeling AP’s gene expression regulatory network, and the lncRNA–mRNA expression network could identify targets for AP treatment and damage repair.

Small cell osteosarcoma of bone: An immunohistochemical study with differential diagnostic considerations

1993 ◽  
Vol 24 (11) ◽  
pp. 1211-1225 ◽  
Author(s):  
Kenneth Devaney ◽  
Tuyethoa N. Vinh ◽  
Donald E. Sweet
Keyword(s):  
Immunohistochemical Study ◽  
Small Cell ◽  
Small Cell Osteosarcoma

Small cell osteosarcoma of the soft tissue

1995 ◽  
Vol 24 (6) ◽  
pp. 462-465 ◽  
Author(s):  
Leonard H. Robinson ◽  
Michael J. Pitt ◽  
Kenneth A. Jaffe ◽  
Gene P. Siegal
Keyword(s):  
Soft Tissue ◽  
Small Cell ◽  
Small Cell Osteosarcoma

scholarly journals Differential regulatory network-based quantification and prioritization of key genes underlying cancer drug resistance based on time-course RNA-seq data

2019 ◽  
Vol 15 (11) ◽  
pp. e1007435 ◽  
Author(s):  
Jiajun Zhang ◽  
Wenbo Zhu ◽  
Qianliang Wang ◽  
Jiayu Gu ◽  
L. Frank Huang ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Regulatory Network ◽  
Time Course ◽  
Cancer Drug ◽  
Rna Seq ◽  
Cancer Drug Resistance ◽  
Key Genes

scholarly journals Endobronchial metastasis as an uncommon pattern of metastatic dissemination from small cell osteosarcoma

2019 ◽  
Vol 12 (7) ◽  
pp. e229779
Author(s):  
Arun Kadamkulam Syriac ◽  
Amrit Ved Bhaskarla ◽  
Mohamed Elrifai ◽  
Abdul Hamid Alraiyes
Keyword(s):  
Small Cell ◽  
Radiographic Imaging ◽  
Rare Entity ◽  
Common Site ◽  
Primary Malignancy ◽  
Axillary Metastasis ◽  
Endobronchial Metastasis ◽  
Number Of Patients ◽  
Maxillary Region ◽  
Small Cell Osteosarcoma

Endobronchial metastasis (EBM) from extrapulmonary primary malignancy is a rare entity. Although the most common site of metastasis of osteosarcoma is the lungs, EBM remains a rare occurrence. Cough and dyspnea are the most common symptoms. A significant number of patients are asymptomatic, making the diagnosis without any radiographic imaging challenging. CT scan of the lung, along with bronchoscopy and biopsy, is the mainstay of diagnosis and staging. A 36-year-old man presented with small cell osteosarcoma of the left maxillary region and was treated with surgery and adjuvant chemotherapy. The patient presented 8 years later with axillary metastasis and was found to have lung metastasis on further workup. Bronchoscopy and biopsy proved an EBM that was debulked by hot snare technique. The patient was then started on chemotherapy for recurrent small cell osteosarcoma.

scholarly journals Circ_MDM2_000139, Circ_ATF2_001418, Circ_CDC25C_002079, and Circ_BIRC6_001271 Are Involved in the Functions of XAV939 in Non-Small Cell Lung Cancer

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Haixiang Yu ◽  
Lei Xu ◽  
Zhengjia Liu ◽  
Bo Guo ◽  
Zhifeng Han ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Regulatory Network ◽  
Family Members ◽  
Enrichment Analysis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Expression Levels ◽  
Relative Expression

Background. The small molecule inhibitor XAV939 could inhibit the proliferation and promote the apoptosis of non-small cell lung cancer (NSCLC) cells. This study was conducted to identify the key circular RNAs (circRNAs) and microRNAs (miRNAs) in XAV939-treated NSCLC cells. Methods. After grouping, the NCL-H1299 cells in the treatment group were treated by 10 μM XAV939 for 12 h. RNA-sequencing was performed, and then the differentially expressed circRNAs (DE-circRNAs) were analyzed by the edgeR package. Using the clusterprofiler package, enrichment analysis for the hosting genes of the DE-circRNAs was performed. Using Cytoscape software, the miRNA-circRNA regulatory network was built for the disease-associated miRNAs and the DE-circRNAs. The DE-circRNAs that could translate into proteins were predicted using circBank database and IRESfinder tool. Finally, the transcription factor (TF)-circRNA regulatory network was built by Cytoscape software. In addition, A549 and HCC-827 cell treatment with XAV939 were used to verify the relative expression levels of key DE-circRNAs. Results. There were 106 DE-circRNAs (including 61 upregulated circRNAs and 45 downregulated circRNAs) between treatment and control groups. Enrichment analysis for the hosting genes of the DE-circRNAs showed that ATF2 was enriched in the TNF signaling pathway. Disease association analysis indicated that 8 circRNAs (including circ_MDM2_000139, circ_ATF2_001418, circ_CDC25C_002079, and circ_BIRC6_001271) were correlated with NSCLC. In the miRNA-circRNA regulatory network, let-7 family members⟶circ_MDM2_000139, miR-16-5p/miR-134-5p⟶circ_ATF2_001418, miR-133b⟶circ_BIRC6_001271, and miR-221-3p/miR-222-3p⟶circ_CDC25C_002079 regulatory pairs were involved. A total of 47 DE-circRNAs could translate into proteins. Additionally, circ_MDM2_000139 was targeted by the TF POLR2A. The verification test showed that the relative expression levels of circ_MDM2_000139, circ_CDC25C_002079, circ_ATF2_001418, and circ_DICER1_000834 in A549 and HCC-827 cell treatment with XAV939 were downregulated comparing with the control. Conclusions. Let-7 family members and POLR2A targeting circ_MDM2_000139, miR-16-5p/miR-134-5p targeting circ_ATF2_001418, miR-133b targeting circ_BIRC6_001271, and miR-221-3p/miR-222-3p targeting circ_CDC25C_002079 might be related to the mechanism in the treatment of NSCLC by XAV939.

scholarly journals Differential Expression Profiles of the Transcriptome and miRNA Interactome in Synovial Fibroblasts of Rheumatoid Arthritis Revealed by Next Generation Sequencing

Diagnostics ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 98
Author(s):  
Chia-Chun Tseng ◽  
Ling-Yu Wu ◽  
Wen-Chan Tsai ◽  
Tsan-Teng Ou ◽  
Cheng-Chin Wu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Differential Expression ◽  
Regulatory Network ◽  
Functional Annotation ◽  
Interaction Analysis ◽  
Expression Profiles ◽  
Synovial Fibroblasts ◽  
Rna Seq ◽  
Network Mapping ◽  
Generation Sequencing

Using next-generation sequencing to decipher the molecular mechanisms underlying aberrant rheumatoid arthritis synovial fibroblasts (RASF) activation, we performed transcriptome-wide RNA-seq and small RNA-seq on synovial fibroblasts from rheumatoid arthritis (RA) subject and normal donor. Differential expression of mRNA and miRNA was integrated with interaction analysis, functional annotation, regulatory network mapping and experimentally verified miRNA–target interaction data, further validated with microarray expression profiles. In this study, 3049 upregulated mRNA and 3552 downregulated mRNA, together with 50 upregulated miRNA and 35 downregulated miRNA in RASF were identified. Interaction analysis highlighted contribution of miRNA to altered transcriptome. Functional annotation revealed metabolic deregulation and oncogenic signatures of RASF. Regulatory network mapping identified downregulated FOXO1 as master transcription factor resulting in altered transcriptome of RASF. Differential expression in three miRNA and corresponding targets (hsa-miR-31-5p:WASF3, hsa-miR-132-3p:RB1, hsa-miR-29c-3p:COL1A1) were also validated. The interactions of these three miRNA–target genes were experimentally validated with past literature. Our transcriptomic and miRNA interactomic investigation identified gene signatures associated with RASF and revealed the involvement of transcription factors and miRNA in an altered transcriptome. These findings help facilitate our understanding of RA with the hope of serving as a springboard for further discoveries relating to the disease.

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