Article Sidebar
Published:
Feb 13, 2023Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Knockdown of FK506-binding proteins 14 enhances tamoxifen-sensitivity of breast cancer through PI3K/AKT and ERK signaling
Abstract
Purpose: To investigate the effect of FK506-binding proteins 14 (FKBP14) in the development of chemoresistance of breast cancer.
Methods: Breast cancer cell lines (MCF-7 and T47D) were exposed to 4-hydroxytamoxifen over a long period to establish tamoxifen-resistant (TamR) cells. Cell proliferation was evaluated by MTT and colony formation assays, while Transwell assay was used to investigate cell migration and invasion.
Results: TamR cells showed resistance to 4-hydroxytamoxifen through increase in IC50 for 4-hydroxytamoxifen in MCF-7 and T47D. The FKBP14 was significantly up-regulated in TamR cells (p < 0.05). Knockdown of FKBP14 reduced the IC50 for 4-hydroxytamoxifen in TamR cells. The number of colony formation in TamR cells was also significantly decreased by silencing of FKBP14 (p < 0.01). Knockdown of FKBP14 inhibited the migration and invasion of TamR cells. Protein expression of p-AKT, p-PI3K and p-ERK in TamR cells were down-regulated by silencing of FKBP14.
Conclusion: Loss of FKBP14 enhances sensitivity to tamoxifen in TamR MCF-7 and T47D cells through inactivation of PI3K/AKT and ERK signaling. The role of FKBP14 in tamoxifen-resistant animal models needs further investigation.
