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Your search keyword '"Chen, Chen"' showing total 5 results
5 results on '"Chen, Chen"'

1. Mechanisms of miR-128-3p in inhibiting osteoblast differentiation from bone marrow-derived mesenchymal stromal cells

Author

Chen Yao, Yu Zhu, Jiaxing Wang, Wen Zhang, Junsheng Chen, and Chen Chen

Subjects
0301 basic medicine, Cancer Research, Gene Expression, NTRK2, Biochemistry, miR-128-3p, 0302 clinical medicine, Bone Marrow, Osteogenesis, Databases, Genetic, Gene Regulatory Networks, Protein Interaction Maps, YWHAB, Regulation of gene expression, Osteoblast, Cell Differentiation, Transfection, Articles, Cell biology, Gene Expression Regulation, Neoplastic, medicine.anatomical_structure, Oncology, 030220 oncology & carcinogenesis, Molecular Medicine, RUNX1, osteogenic differentiation, Bone Marrow Cells, Biology, 03 medical and health sciences, Downregulation and upregulation, microRNA, Genetics, medicine, Animals, Humans, RNA, Messenger, Rats, Wistar, Molecular Biology, Gene, Osteoblasts, Oncogene, Gene Expression Profiling, Computational Biology, Mesenchymal Stem Cells, Fold change, Rats, MicroRNAs, 030104 developmental biology, Gene Ontology, bone marrow-derived mesenchymal stem cells
Abstract

The authors' previous study demonstrated that miR‑128 may exert an inhibitory effect on the osteogenic differentiation of bone marrow‑derived mesenchymal stem cells (BM‑MSCs), but its downstream mechanisms remain to be elucidated. The aim of the present study was to investigate the microRNA (miRNA/miR) and mRNA profiles of differentiated and undifferentiated BM‑MSCs and explore new downstream targets for miR‑128. The sequencing datasets of GSE107279 (miRNA) and GSE112318 (mRNA) were downloaded from the Gene Expression Omnibus database. The differentially expressed miRNAs (DEMs) and genes (DEGs) were identified using the DESeq2 method. The target genes of DEMs were predicted by the miRwalk 2.0 database. The hub target genes of miR‑128 were screened by constructing the protein‑protein interaction (PPI) network and module analysis. The expression levels of miR‑128 and crucial target genes were validated by reverse transcription‑quantitative (RT‑q) PCR before or after transfection of miR‑128 mimics to BM‑MSCs. The miRNA expression profile analysis identified miR‑128 as one of the significantly downregulated DEMs (total 338) in differentiated BM‑MSCs compared with the undifferentiated control. A total of 103 predicted target genes of miR‑128‑3p were overlapped with upregulated DEGs. By calculating the topological properties of each protein in the PPI network, 6 upregulated genes (KIT, NTRK2, YWHAB, GAB1, AXIN1 and RUNX1; fold change was the highest for NTRK2) were considered to be hub genes. Of these, 4 were enriched in module 4 (RUNX1, KIT, GAB1 and AXIN1; RUNX1 was particularly crucial as it can interact with the others), while one was enriched in module 7 (YWHAB). The expression levels of miR‑128 and these 6 target genes during the osteogenic differentiation were experimentally confirmed by RT‑qPCR. In addition, the expression levels of these 6 genes were significantly reversed after transfection of miR‑128‑3p mimics into rat BM‑MSCs compared with the miR‑control group. These findings indicated that miR‑128‑3p may inhibit the osteoblast differentiation of BM‑MSCs by downregulation of these 6 genes, particularly RUNX1, YWHAB and NTRK2.

Published
2020

2. Genome-wide, integrative analysis of circular RNA dysregulation and the corresponding circular RNA-microRNA-mRNA regulatory axes in autism

Author

Te-Lun Mai, Yen-Ju Chen, Chia-Ying Chen, Trees-Juen Chuang, Sachin Kumar Gupta, Yi-Da Wang, Chih-Fan Chuang, Yu-Chen Chen, and Laising Yen

Subjects
Autism Spectrum Disorder, Computational biology, Biology, Genome, behavioral disciplines and activities, Cell Line, 03 medical and health sciences, 0302 clinical medicine, Neural Stem Cells, Circular RNA, microRNA, Gene expression, mental disorders, Genetics, Humans, RNA, Messenger, Gene, Genetics (clinical), 030304 developmental biology, Regulation of gene expression, Neurons, 0303 health sciences, Genome, Human, Research, RNA, Brain, RNA, Circular, Gene expression profiling, MicroRNAs, Gene Expression Regulation, Astrocytes, 030217 neurology & neurosurgery
Abstract

Circular RNAs (circRNAs), a class of long noncoding RNAs, are known to be enriched in mammalian neural tissues. Although a wide range of dysregulation of gene expression in autism spectrum disorder (ASD) have been reported, the role of circRNAs in ASD remains largely unknown. Here, we performed genome-wide circRNA expression profiling in postmortem brains from individuals with ASD and controls and identified 60 circRNAs and three coregulated modules that were perturbed in ASD. By integrating circRNA, microRNA, and mRNA dysregulation data derived from the same cortex samples, we identified 8170 ASD-associated circRNA-microRNA-mRNA interactions. Putative targets of the axes were enriched for ASD risk genes and genes encoding inhibitory postsynaptic density (PSD) proteins, but not for genes implicated in monogenetic forms of other brain disorders or genes encoding excitatory PSD proteins. This reflects the previous observation that ASD-derived organoids show overproduction of inhibitory neurons. We further confirmed that some ASD risk genes (NLGN1, STAG1, HSD11B1, VIP, and UBA6) were regulated by an up-regulated circRNA (circARID1A) via sponging a down-regulated microRNA (miR-204-3p) in human neuronal cells. Particularly, alteration of NLGN1 expression is known to affect the dynamic processes of memory consolidation and strengthening. To the best of our knowledge, this is the first systems-level view of circRNA regulatory networks in ASD cortex samples. We provided a rich set of ASD-associated circRNA candidates and the corresponding circRNA-microRNA-mRNA axes, particularly those involving ASD risk genes. Our findings thus support a role for circRNA dysregulation and the corresponding circRNA-microRNA-mRNA axes in ASD pathophysiology.

Published
2020

3. Construction of a circular RNA–microRNA–messenger RNA regulatory network of hsa_circ_0043256 in lung cancer by integrated analysis.

Author

Li, Yongwen, Shi, Ruifeng, Zhu, Guangsheng, Chen, Chen, Huang, Hua, Gao, Min, Xu, Songlin, Cao, Peijun, Zhang, Zihe, Wu, Di, Li, Xuanguang, Liu, Hongyu, and Chen, Jun

Subjects
LUNG cancer & genetics, LUNG cancer prognosis, LUNG cancer treatment, LUNG cancer diagnosis, PROTEIN metabolism, CIRCULAR RNA, FLOW cytometry, GENETICS, INTEGRATIVE medicine, IMMUNOHISTOCHEMISTRY, MICRORNA, QUANTITATIVE research, CELL cycle, CELLULAR signal transduction, GENE expression, BIOINFORMATICS, MESSENGER RNA, GENE expression profiling, SURVIVAL analysis (Biometry), KAPLAN-Meier estimator, CELL proliferation, MOLECULAR structure, TUMOR markers, POLYMERASE chain reaction
Abstract

Background: Patients with non‐small cell lung cancer (NSCLC) are diagnosed in advanced stages and with a poor 5‐year survival rate. There is a critical need to identify novel biomarkers to improve the therapy and overall prognosis of this disease. Methods: Differentially expressed genes (DEGs) were identified from three profiles of GSE101586, GSE101684 and GSE112214 using Venn diagrams. hsa_circ_0043256 were validated using quantitative real‐time polymerase chain reaction (RT‐qPCR). The circular RNA–microRNA–messenger RNA (circRNA–miRNA–mRNA) regulatory network was constructed with Cytoscape 3.7.0. Hub genes were identified with protein interaction (PPI) and validated with the Gene Expression Profiling Interactive Analysis (GEPIA), Human Protein Atlas (HPA) databases, and immunohistochemistry. Survival analyses were also performed using a Kaplan–Meier (KM) plotter. The effects of hsa_circ_0043256 on cell proliferation and cell cycles were evaluated by EdU staining and flow cytometry, respectively. Results: hsa_circ_0043256, hsa_circ_0029426 and hsa_circ_0049271 were obtained. Following RT‐qPCR validation, hsa_circ_0043256 was selected for further analysis. In addition, functional experiment results indicated that hsa_circ_0043256 could inhibit cell proliferation and cell‐cycle progression of NSCLC cells in vitro. Prediction by three online databases and combining with DEGs identified from The Cancer Genome Atlas (TCGA), a network containing one circRNAs, three miRNAs, and 209 mRNAs was developed. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated DEGs might be associated with lung cancer onset and progression. A PPI network based on the 209 genes was established, and five hub genes (BIRC5, SHCBP1, CCNA2, SKA3, and GINS1) were determined. Following verification of five hub genes using GEPIA database, HPA database, and immunohistochemistry. High expression of all five hub genes led to poor overall survival. Conclusion: Our study constructed a circRNA–miRNA–mRNA network of hsa_circ_0043256. hsa_circ_0043256 may be a potential therapeutic target for lung cancer. [ABSTRACT FROM AUTHOR]

Published
2022
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4. bmo-miR-275 down-regulates expression of Bombyx mori sericin gene 2 in vitro.

Author

Qian, Ping, Jiang, Tao, Wang, Xin, Song, Fei, Chen, Chen, and Shen, Xingjia

Subjects
MICRORNA, DOWNREGULATION, GENE expression, INSECT genetics, INSECT larvae, SILKWORMS
Abstract

We hypothesized that bmo-miR-275 has a potential regulatory function regarding the expression of sericin gene 2 (BmSer-2). First, we examined the expression of bmo-miR-275 and its target gene BmSer-2 in seven different tissues from 5th instar day-3 silkworm larvae. The results showed that they were both specifically expressed in the middle silk gland, implying that spatio-temporal conditions are required for bmo-miR-275 to regulate the expression of BmSer-2. To test this hypothesis, we constructed a pri-bmo-miR-275 expressing plasmid pcDNA3.0 [ie1-egfp-pri-bmo-miR-275-SV40] and BmSer-2-3´UTR recombinant reporter plasmids pGL3.0 [A3-luc-Ser-2-3′ UTR-SV40]. Finally, BmN cells were harvested and luciferase activity was detected. Results showed that luciferase activity was reduced significantly (P<0.05) in BmN cells co-transfected with pcDNA3.0 [ie1-egfp-pri-bmo-miR-275-SV40] and pGL3.0 [A3-luc-Ser-2-3’UTR-SV40], suggesting that bmo-miR-275 can down-regulate the expression of BmSer-2 in vitro. Our results improve the understanding of the regulatory function of Bombyx mori miRNA on the expression of genes regulating silk formation. [ABSTRACT FROM AUTHOR]

Published
2018
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5. Interleukin-23 Facilitates Thyroid Cancer Cell Migration and Invasion by Inhibiting SOCS4 Expression via MicroRNA-25.

Author

Mei, Zhidan, Chen, Shiming, Chen, Chen, Xiao, Bokui, Li, Fen, Wang, Yongping, and Tao, Zezhang

Subjects
THYROID cancer, INTERLEUKIN-23, CELL migration, CANCER invasiveness, INFLAMMATION, CYTOKINES, MICRORNA, GENE expression, GENETICS
Abstract

Interleukin–23 (IL–23) is a conventional proinflammatory cytokine that plays a role in tumor progression by inducing inflammation in the tumor microenvironment. However, the role of IL–23 in thyroid cancer migration and invasion remains unclear. In the present study, we observed that the treatment with IL–23, induced migration and invasion in human thyroid cancer cells. Additional data demonstrate that SOCS4 negatively regulates IL-23-mediated migration and invasion. On investigating the mechanisms involved in IL–23 mediated migration and invasion, we observed that miR–25 promotes the migration and invasion of thyroid cancer cells by directly binding to the 3′-UTR of SOCS4 that leads to the inhibition of SOCS4. In addition, we also demonstrated that IL–23 increases miR–25 expression levels, and overexpressed miR–25 is involved in IL-23-associated SOCS4 inhibition and cell migration and invasion. Together, our data suggest that IL–23 induces migration and invasion in thyroid cancer cells by mediating the miR–25/SOCS4 signaling pathway. [ABSTRACT FROM AUTHOR]

Published
2015
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