4 results on '"Xin-Xin Zeng"'
Search Results
2. Integration of scRNA-Seq and Bulk RNA-Seq to analyze the heterogeneity of colorectal cancer immune cells and establish a molecular risk model.
- Author
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Li-Yue Sun, Jiao-Jiao Yang, Xin-Xin Zeng, Yu-Ying Jiang, Ju Shen, Fang Wang, and Xu-Hui Zhang
- Subjects
COLORECTAL cancer ,GENE expression ,CANCER cells ,RNA sequencing ,TH2 cells ,TUMOR classification ,SHOTGUN sequencing - Abstract
Background: Colorectal cancer(CRC) is a highly heterogeneous malignant tumor that significantly impacts clinical diagnosis and treatment. Single-cell RNA sequencing is an innovative method for exploring tumor heterogeneity and understanding its role at cellular and genetic levels. Method: The colorectal cancer Single-cell RNA sequencing data were analysed on the immune. RNA-seq data in bulk form was utilized to assess the major genes of the immune cell subsets linked to CRC. We conducted an analysis of the abundance of immune cells in the microenvironment of CRC, and also performed weighted gene co-expression network analysis. Gene set enrichment analysis helped perform two analytical procedures of subtype groups. Furthermore, Least absolute shrinkage and selection operator regression was employed to analyse and screen for a gene signature. Finally, quantitative PCR was performed to detect the expression levels of signature genes in CRC. Results: The Single-cell RNA sequencing (GSE146771) dataset was integrated to obtain 9 cell clusters. The Single-sample gene set enrichment analysis showed that the related gene expression of T-cell subsets of different functional statuses could vary greatly between patients with GSE146771. Immune cell analysis of TCGA-CRC indicated an improved overall survival rate for patients with elevated Th2 cell abundance. Five-gene signature (Risk Score = -0.205 × CDC25C - 0.231 × GSTCD - 0.010 × KPNA2 - 0.002 × KIF15 - 0.171 × ORC1) was developed by weighted correlation network analysis, and lasso Cox regression. Then, the risk prediction efficacy of the signature was validated in four GSE datasets. Furthermore, the expression of five genes was reduced in CRC tissue by quantitative PCR. Conclusion: Five-gene signature based on CRC heterogeneity was developed as a prognosis predictor, which can serve as a potential treatment target. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
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3. Induced in vivo transdifferentiation of vertebrate muscle into early endoderm-like cells
- Author
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Jonatan Matalonga, Chengjian Zhao, Jan Huisken, Xin-Xin Zeng, Clyde Campbell, Joseph J. Lancman, Rashmi Mishra, P. Duc Dong, Alyssa Graves, Raquel Espín-Palazón, Jun Yin, Jiaye He, and David Traver
- Subjects
medicine.anatomical_structure ,biology ,In vivo ,biology.animal ,embryonic structures ,Transdifferentiation ,medicine ,Vertebrate ,Endoderm ,Cell biology - Abstract
The extent to which differentiated cells, while remaining in their native microenvironment, can be reprogrammed to assume a different identity will reveal fundamental insight into cellular plasticity and impact regenerative medicine. To investigate in vivo cell lineage potential, we leveraged the zebrafish as a practical vertebrate platform to determine factors and mechanisms necessary to induce differentiated cells of one germ layer to adopt the lineage of another. We discovered that ectopic co-expression of Sox32 and Oct4 in several non-endoderm lineages, including skeletal muscle, can specifically trigger an early endoderm genetic program in a cell-autonomous manner. Gene expression, live imaging, and functional studies reveal that the endoderm-induced muscle cells lose muscle gene expression and morphology, while specifically gaining endoderm organogenesis lineage markers, such as the pancreatic specification genes, hhex and ptf1a, via a mechanism resembling normal development. Endoderm induction by a pluripotent defective form of Oct4, endoderm markers appearing prior to loss of muscle cell morphology, and a lack of mesoderm, ectoderm, dedifferentiation, and pluripotency gene activation, together, suggests that reprogramming is endoderm specific and occurs via direct transdifferentiation. Our work demonstrates that within a living vertebrate animal, differentiated cells can be induced to directly adopt the identity of a completely unrelated cell lineage, while remaining in a distinct microenvironment, suggesting that differentiated cells in vivo may be more amenable to lineage conversion than previously appreciated. This discovery of extensive lineage potential of differentiated cells, in vivo, challenges our understanding of cell lineage restriction and may pave the way towards new in vivo sources of replacement cells for degenerative diseases such as diabetes.
- Published
- 2020
4. Wnt/β‑catenin signaling pathway regulates asthma airway remodeling by influencing the expression of c‑Myc and cyclin D1 via the p38 MAPK‑dependent pathway
- Author
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Tingting Zhu, Wei‑Xi Zhang, Xin‑Xin Zeng, Yue Huang, Hong Zhang, and Xiao‑Xiao Jia
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,Cancer Research ,Chemistry ,p38 mitogen-activated protein kinases ,Wnt signaling pathway ,p38 mitogen-activated protein kinase ,Articles ,General Medicine ,asthma ,β-catenin ,Cell cycle ,Cell biology ,airway remodeling ,Wnt ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Cyclin D1 ,Immunology and Microbiology (miscellaneous) ,030220 oncology & carcinogenesis ,Signal transduction ,Protein kinase A ,Transcription factor - Abstract
Airway remodeling is the main characteristic of asthma; however, the mechanisms underlying this pathophysiological change have not been fully elucidated. Previous studies have indicated that the Wnt/β-catenin and mitogen-activated protein kinase (MAPK) signaling pathway are involved in the development of airway remodeling during asthma. Therefore, the present study established an airway remodeling rat model, after which β-catenin, cyclin D1 and c-Myc protein expressions were analyzed via western blotting in the lung tissue and airway smooth muscle cells (ASMCs) of rats. The mRNA expression of the aforementioned proteins were evaluated via reverse transcription-quantitative PCR. β-catenin, cyclin D1 and c-Myc are core transcription factors and target genes of the Wnt/β-catenin and MAPK signaling pathways. Furthermore, β-catenin, c-Myc and cyclin D1 protein expression were determined following blocking of the p38 MAPK signaling pathway in vitro. The results demonstrated that higher expressions of β-catenin, cyclin D1 and c-Myc were detected in lung tissues and ASMCs in the asthma group compared with the control. Blocking the p38 MAPK signaling pathway with a specific inhibitor SB203580 also downregulated the expressions of β-catenin, cyclin D1 and c-Myc in vitro. Taken together, these results indicated that the Wnt/β-catenin signaling pathway may regulate the process of airway remodeling via the p38 MAPK-dependent pathway.
- Published
- 2019
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