Comparison of protein kinase C activity and isoform expression in cisplatin-sensitive and -resistant ovarian carcinoma cells
โ Scribed by Alakananda Basu; Kelly M. Weixel
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- French
- Weight
- 514 KB
- Volume
- 62
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
โฆ Synopsis
Cellular sensitivity to cis-diamminedichloroplatinum(ll) (cDDP) can be regulated by protein kinase C (PKC) signal transduction pathway. Activators of PKC were shown to enhance the sensitivity of human ovarian carcinoma 2008 cells to cDDP. We have examined whether or not the PKC signal transduction pathway is affected during development of resistance by tumor cells to cDDP. A 2-fold decrease in PKC activity was observed in cDDP-resistant ovarian carcinoma 2008/ C 13.5.25 cells compared with the drug-sensitive 2008 cells. Subcellular distribution studies revealed a reduction in both cytosolic and particulate PKC activities in 2008/CI 3.5.25 cells. The pattern of PKC isoform expression was compared in cDDP-sensitive and -resistant cell lines by Western blot analysis with isoform-specific antibodies to PKC. The parental cells expressed PKCa, -c, and -6 isoforms. The abundance of PKCo: decreased significantly in 2008/C I3*5.25 cells, whereas the amount of PKCe increased moderately in the resistant variant, with no alteration in PKC< content. Therefore, a reduction in PKCa and/or an increase in PKCc expression may be associated with the drug-resistant phenotype.
๐ SIMILAR VOLUMES
## Abstract ## Background Resistance to chemotherapy is a major limitation in the treatment of head and neck squamous cell carcinomas (HNSCCs), accounting for high mortality rates in patients. Here, we investigated the role of replication protein A (RPA) in cisplatin and etoposide resistance. ##
Determinations of mRNA and enzyme protein analyses for the protein kinase C (PKC) isoforms, alpha, epsilon and zeta, representing the classical, novel and atypical groups, respectively, in murine erythroleukaemic (MEL) cells revealed the occurrence of cyclic behaviour in expression. Such rhythmicity
Retinoic acid inhibits proliferation of hormone-dependent, but not hormone-independent breast cancer cells. Retinoic acid-induced changes in cellular proliferation and differentiation are associated with disturbances in growth factor signaling and frequently with changes in protein kinase C expressi
## Abstract Tumor cells chronically exposed to cisplatin (cDDP) acquire cDDP resistance that impacts tumor therapy. To elucidate the mechanism of acquired cDDP resistance (ACR), we compared HeLa cells that gained ACR upon chronic cDDP treatment with the parental strain. We show that ACR is due to a
The expression of different protein kinase C (PKC) isoenzymes has been shown to vary with proliferation rates, differentiation or apoptosis in normal colon crypts. In addition, the activity of some PKC isoenzymes appears to be reduced in colorectal cancer. The aim of the present work was to determin