Protein kinase D2 silencing reduced motility of doxorubicin-resistant MCF7 cells

Date

2015-06-01

Author

Alpsoy, Aktan
Gündüz, Ufuk

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Success of chemotherapy is generally impaired by multidrug resistance, intrinsic resistance, or acquired resistance to functionally and structurally irrelevant drugs. Multidrug resistance emerges via distinct mechanisms: increased drug export, decreased drug internalization, dysfunctional apoptotic machinery, increased DNA damage repair, altered cell cycle regulation, and increased drug detoxification. Several reports demonstrated that multidrug resistance is a multifaceted problem such that multidrug resistance correlates with increased aggressiveness and metastatic potential. Here, we tested the involvement of protein kinase D2, a serine/threonine kinase that was previously implicated in proliferation, drug resistance, and motility in doxorubicin-resistant MCF7 (MCF7/DOX) cell line, which served as an in vitro model for drug resistance and invasiveness. We showed that basal level activity of protein kinase D2 (PKD2) was higher in MCF7/DOX cells than parental MCF7 cells. To elucidate the roles of PKD2 MCF7/DOX, PKD2 expression was reduced via small interfering RNA (siRNA)-mediated knockdown. Results showed that acquired resistance of MCF7/DOX to doxorubicin was not affected by PKD2 silencing, while motility of MCF7/DOX cells was reduced. The results implied that PKD2 silencing might inhibit migration of MCF7/DOX cells without affecting chemoresistance significantly.

Subject Keywords

Multidrug resistance, Breast cancer, Migration, Protein kinase D2

URI

https://hdl.handle.net/11511/30142

Journal

TUMOR BIOLOGY

DOI

https://doi.org/10.1007/s13277-015-3081-3

Collections

Graduate School of Natural and Applied Sciences, Article

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Citation Formats

A. Alpsoy and U. Gündüz, “Protein kinase D2 silencing reduced motility of doxorubicin-resistant MCF7 cells,” TUMOR BIOLOGY, pp. 4417–4426, 2015, Accessed: 00, 2020. [Online]. Available: https://hdl.handle.net/11511/30142.