Please use this identifier to cite or link to this item:
https://doi.org/10.3390/cancers12061705
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dc.title | Potential of tyrosine kinase receptor TIE-1 as novel therapeutic target in high-PI3K-expressing ovarian cancer | |
dc.contributor.author | Zhang, X. | |
dc.contributor.author | Ishibashi, M. | |
dc.contributor.author | Kitatani, K. | |
dc.contributor.author | Shigeta, S. | |
dc.contributor.author | Tokunaga, H. | |
dc.contributor.author | Toyoshima, M. | |
dc.contributor.author | Shimada, M. | |
dc.contributor.author | Yaegashi, N. | |
dc.date.accessioned | 2021-08-18T04:01:29Z | |
dc.date.available | 2021-08-18T04:01:29Z | |
dc.date.issued | 2020 | |
dc.identifier.citation | Zhang, X., Ishibashi, M., Kitatani, K., Shigeta, S., Tokunaga, H., Toyoshima, M., Shimada, M., Yaegashi, N. (2020). Potential of tyrosine kinase receptor TIE-1 as novel therapeutic target in high-PI3K-expressing ovarian cancer. Cancers 12 (6) : 1-14. ScholarBank@NUS Repository. https://doi.org/10.3390/cancers12061705 | |
dc.identifier.issn | 20726694 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/197727 | |
dc.description.abstract | Tyrosine kinase receptor TIE-1 plays a critical role in angiogenesis and blood-vessel stability. In recent years, increased TIE-1 expression has been observed in many types of cancers; however, the biological significance and underlying mechanisms remain unknown. Thus, in the present study, we investigated the tumor biological functions of TIE-1 in ovarian cancer. The treatment of SKOV3 ovarian-cancer cells with siRNA against TIE-1 decreased the expression of key molecules in the PI3K/Akt signaling pathway, such as p110? and phospho-Akt, suggesting that TIE-1 is related to the PI3K/Akt pathway. Furthermore, the knockdown of TIE-1 significantly decreased cell proliferation in high-PI3K-expressing cell lines (SKOV3, CAOV3) but not low-PI3K-expressing cell lines (TOV112D, A2780). These results suggested that inhibition of TIE-1 decreases cell growth in high-PI3K-expressing cells. Moreover, in low-PI3K-expressing TOV112D ovarian-cancer cells, TIE-1 overexpression induced PI3K upregulation and promoted a PI3K-mediated cell proliferative phenotype. Mechanistically, TIE-1 participates in cell growth and proliferation by regulating the PI3K/Akt signaling pathway. Taken together, our findings strongly implicate TIE-1 as a novel therapeutic target in high-PI3K-expressing ovarian-cancer cells. � 2020 by the authors. Licensee MDPI, Basel, Switzerland. | |
dc.publisher | MDPI AG | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.source | Scopus OA2020 | |
dc.subject | Molecular targeted therapy | |
dc.subject | Ovarian cancer | |
dc.subject | PI3K | |
dc.subject | TIE-1 | |
dc.type | Article | |
dc.contributor.department | CANCER SCIENCE INSTITUTE OF SINGAPORE | |
dc.description.doi | 10.3390/cancers12061705 | |
dc.description.sourcetitle | Cancers | |
dc.description.volume | 12 | |
dc.description.issue | 6 | |
dc.description.page | 1-14 | |
Appears in Collections: | Elements Staff Publications |
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