| Literature DB >> 31902948 |
Tingting Qian1,2, Longzhen Cui3,4, Yan Liu3,4, Zhiheng Cheng5, Liang Quan1,2, Tiansheng Zeng6, Wenhui Huang1,2, Yifeng Dai5, Jinghong Chen2, Ling Liu1, Jingqi Chen2, Ying Pang1, Guangsheng Wu7, Xu Ye1, Jinlong Shi8, Lin Fu9,10,11,12, Chaozeng Si13.
Abstract
The prognosis role of CCT3 in MM and the possible pathways it involved were studied in our research. By analyzing ten independent datasets (including 48 healthy donors, 2220 MM, 73 MGUS, and 6 PCL), CCT3 was found to express higher in MM than healthy donors, and the expression level was gradually increased from MGUS, SMM, MM to PCL (all P < 0.01). By analyzing three independent datasets (GSE24080, GSE2658, and GSE4204), we found that CCT3 was a significant indicator of poor prognosis (all P < 0.01). KEGG and GSEA analysis showed that CCT3 expression was associated with JAK-STAT3 pathway, Hippo signaling pathway, and WNT signaling pathway. In addition, different expressed genes analysis revealed MYC, which was one of the downstream genes regulated by JAK-STAT3 pathway, was upregulated in MM. This confirms that JAK-STAT3 signaling pathway may promote the progress of disease which was regulated by CCT3 expression. Our study revealed that CCT3 may play a supporting role at the diagnosis of myeloid, and high expression of CCT3 suggested poor prognosis in MM. CCT3 expression may promote the progression of MM mainly by regulating MYC through JAK-STAT3 signaling pathway.Entities:
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Year: 2020 PMID: 31902948 DOI: 10.1038/s41397-019-0145-6
Source DB: PubMed Journal: Pharmacogenomics J ISSN: 1470-269X Impact factor: 3.550