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KRAS activation in gastric cancer stem-like cells promotes tumor angiogenesis and metastasis
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yoon, Changhwan | - |
dc.contributor.author | Lu, Jun | - |
dc.contributor.author | Jun, Yukyung | - |
dc.contributor.author | Suh, Yun-Suhk | - |
dc.contributor.author | Kim, Bang-Jin | - |
dc.contributor.author | Till, Jacob E. | - |
dc.contributor.author | Kim, Jong Hyun | - |
dc.contributor.author | Keshavjee, Sara H. | - |
dc.contributor.author | Ryeom, Sandra | - |
dc.contributor.author | Yoon, Sam S. | - |
dc.date.accessioned | 2023-08-11T05:01:56Z | - |
dc.date.available | 2023-08-11T14:02:37Z | - |
dc.date.issued | 2023-07-22 | - |
dc.identifier.citation | BMC Cancer, Vol.23(1):690 | ko_KR |
dc.identifier.issn | 1471-2407 | - |
dc.identifier.uri | https://hdl.handle.net/10371/195362 | - |
dc.description.abstract | Abstract
Our previous work showed that KRAS activation in gastric cancer cells leads to activation of an epithelial-to-mesenchymal transition (EMT) program and generation of cancer stem-like cells (CSCs). Here we analyze how this KRAS activation in gastric CSCs promotes tumor angiogenesis and metastasis. Gastric cancer CSCs were found to secrete pro-angiogenic factors such as vascular endothelial growth factor A (VEGF-A), and inhibition of KRAS markedly reduced secretion of these factors. In a genetically engineered mouse model, gastric tumorigenesis was markedly attenuated when both KRAS and VEGF-A signaling were blocked. In orthotropic implant and experimental metastasis models, silencing of KRAS and VEGF-A using shRNA in gastric CSCs abrogated primary tumor formation, lymph node metastasis, and lung metastasis far greater than individual silencing of KRAS or VEGF-A. Analysis of gastric cancer patient samples using RNA sequencing revealed a clear association between high expression of the gastric CSC marker CD44 and expression of both KRAS and VEGF-A, and high CD44 and VEGF-A expression predicted worse overall survival. In conclusion, KRAS activation in gastric CSCs enhances secretion of pro-angiogenic factors and promotes tumor progression and metastasis. | ko_KR |
dc.description.sponsorship | This study was funded by NIH/NCI grant P30 CA008748, the DeGregorio Family Foundation, and Stand Up To Cancer. | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | BMC | ko_KR |
dc.subject | Gastric adenocarcinoma | - |
dc.subject | KRAS | - |
dc.subject | Epithelial-to-mesenchymal transition | - |
dc.subject | Cancer stem cells | - |
dc.title | KRAS activation in gastric cancer stem-like cells promotes tumor angiogenesis and metastasis | ko_KR |
dc.type | Article | ko_KR |
dc.identifier.doi | 10.1186/s12885-023-11170-0 | ko_KR |
dc.citation.journaltitle | BMC Cancer | ko_KR |
dc.language.rfc3066 | en | - |
dc.rights.holder | The Author(s) | - |
dc.date.updated | 2023-07-23T03:11:31Z | - |
dc.citation.number | 1 | ko_KR |
dc.citation.volume | 23 | ko_KR |
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