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| Status |
Public on Jun 27, 2024 |
| Title |
KAT7 promotes malignant phenotypes of colorectal cancer via MRAS-mediated activation of the MAPK/ERK pathway |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Histone acetyltransferases (HATs) play a crucial role in transcriptional regulation by acetylating histones. Dysregulation of HAT activity is implicated in developmental disorders and cancer. In this study, we discovered an upregulated KAT7 signaling pathway in colorectal cancer (CRC) and its association with poor patient survival. Knockdown of KAT7 suppressed CRC cell viability, proliferation, migration, and invasion while promoting apoptosis. Conversely, KAT7 overexpression enhanced these cellular processes. In vivo experiments demonstrated that KAT7 knockdown inhibited CRC growth and lung metastasis. Mechanistically, KAT7 acetylated histone H3 at lysine 14 (H3K14) to enhance MRAS transcription, which activated the MAPK/ERK pathway and promoted tumorigenesis. Overexpression of MRAS or treatment with the ERK activator C6 Ceramide rescued the tumor inhibition caused by KAT7 silencing. The acetyltransferase activity of KAT7 is essential for CRC progression. Reexpression of KAT7, but not KAT7 acetyltransferase activity-deficient mutants, rescued MRAS expression, ERK phosphorylation, and CRC tumorigenesis in KAT7 knockdown CRC cells. Taken together, our results define the essential role of KAT7 in CRC tumorigenesis, rationalizing its potential as a therapeutic target for CRC treatment.
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| Overall design |
To investigate the molecular mechanism underlying the contribution of KAT7 to CRC progression, we established HCT116 cell lines in which KAT7 has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq. We identified a total of 1708 differentially expressed genes in KAT7 silenced HCT116 cells compared to the control group.
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| Contributor(s) |
Wang H, Guan T, Hu R, Huang Z |
| Citation missing |
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| Submission date |
Jun 20, 2024 |
| Last update date |
Jun 27, 2024 |
| Contact name |
Zhongjie Huang |
| E-mail(s) |
hzj2212819718@outlook.com
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| Phone |
18902571893
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| Organization name |
Zhuujiang hospital
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| Street address |
No. 253, Middle Industrial Avenue
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| City |
Guangzhou |
| State/province |
Guangdong |
| ZIP/Postal code |
510280 |
| Country |
China |
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| Platforms (1) |
| GPL24676 |
Illumina NovaSeq 6000 (Homo sapiens) |
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| Samples (6)
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| Relations |
| BioProject |
PRJNA1126153 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE270298_processed_data.txt.gz |
6.6 Mb |
(ftp)(http) |
TXT |
SRA Run Selector |
| Raw data are available in SRA |
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