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| Status |
Public on Aug 11, 2021 |
| Title |
Stomach-specific c-Myc overexpression drives intestinal-type gastric cancer in mice via AKT/mTOR signaling |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Gastric cancer (GC) is one of the most common malignant cancers in the world. c-Myc, a well-known oncogene, is commonly amplified in many cancers, including gastric cancer. However, it is still not completely understood how c-Myc functions in GC. Here, we generated a stomach-specific c-Myc knock-in mouse model to investigate its role in GC. We found that overexpression of c-Myc in Atp4b+ gastric parietal cells could induce intestinal-type gastric cancer in mice. Mechanistically, c-Myc promoted tumorigenesis via the AKT/mTOR pathway. Furthermore, AKT inhibitor (MK-2206) or mTOR inhibitor (Rapamycin) inhibited the proliferation of c-Myc overexpressing gastric cancer cell lines. Thus, our findings highlight that gastric cancer can be induced by c-Myc overexpression through activation of the AKT/mTOR pathway.
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| Overall design |
Gastric mRNA profiles of 12-week old wild type (WT) and Atp4b-cre;MycOE mice were generated by deep sequencing, in triplicate.
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| Contributor(s) |
Liu J, Li L |
| Citation(s) |
33259779 |
| Submission date |
Feb 20, 2020 |
| Last update date |
Aug 11, 2021 |
| Contact name |
Jing Liu |
| E-mail(s) |
ljyolo0749@sjtu.edu.cn
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| Organization name |
Shanghai Jiao Tong University
|
| Street address |
Huashan Road 1954
|
| City |
Shanghai |
| ZIP/Postal code |
200030 |
| Country |
China |
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| Platforms (1) |
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| Samples (4)
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| Relations |
| BioProject |
PRJNA607660 |
| SRA |
SRP250081 |
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