Abstract | AIM: MATERIALS AND METHODS: RESULTS: PKD2 and PKD3 were two major isoforms expressed at the highest levels in tumorgenic HCC1806 triple-negative breast cancer cells. Silencing PKD2 or PKD3 significantly inhibited HCC1806 cell proliferation, and PKD3 silencing had a higher inhibitory effect than PKD2 silencing on cell growth and PKD-mediated signaling. HCC1806 breast cancer cells were highly responsive to PKD inhibitors but not to a general protein kinase C (PKC) inhibitor. CONCLUSION: We have identified PKD2 and PKD3, especially PKD3, as novel cell growth regulators in HCC1806 triple-negative breast cancer cells. Targeting PKD instead of all PKCs effectively inhibited cell proliferation in a number of breast cancer cell lines.
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Authors | Qin Hao, Raymond McKenzie, Huachen Gan, Hua Tang |
Journal | Anticancer research
(Anticancer Res)
Vol. 33
Issue 2
Pg. 393-9
(Feb 2013)
ISSN: 1791-7530 [Electronic] Greece |
PMID | 23393329
(Publication Type: Journal Article)
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Chemical References |
- Isoenzymes
- Protein Kinase D2
- Protein Kinase Inhibitors
- RNA, Small Interfering
- Protein Kinases
- protein kinase C nu
- Protein Kinase C
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Topics |
- Blotting, Western
- Breast Neoplasms
(enzymology, genetics, pathology)
- Cell Line, Tumor
- Cell Proliferation
(drug effects)
- Female
- Humans
- Isoenzymes
- Protein Kinase C
(metabolism)
- Protein Kinase D2
- Protein Kinase Inhibitors
(pharmacology)
- Protein Kinases
(metabolism)
- RNA, Small Interfering
- Reverse Transcriptase Polymerase Chain Reaction
- Signal Transduction
(drug effects, physiology)
- Transfection
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