Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Protein kinase Cα suppresses the expression of STC1 in MDA-MB-231 breast cancer cells

Cornmark, Louise LU ; Kalstad Lönne, Gry LU ; Jögi, Annika LU and Larsson, Christer LU (2011) In Tumour Biology 32(5). p.1023-1030
Abstract
Several protein kinase C (PKC) isoforms have been shown to influence different cellular processes that may contribute to the malignancy of breast cancer cells. To obtain insight into mechanisms mediating the PKC effects, global gene expression was analyzed in MDA-MB-231 breast cancer cells in which PKCα, PKCδ or PKCε had been down-regulated with siRNA. Gene set enrichment analyses revealed that hypoxia-induced genes were enriched among genes that increased in PKCα-down-regulated cells. The STC1 mRNA, encoding stanniocalcin 1, was particularly up-regulated following depletion of PKCα and was also induced by hypoxia. Both hypoxia and PKCα down-regulation also led to increased STC1 protein levels. The results demonstrate that PKCα suppresses... (More)
Several protein kinase C (PKC) isoforms have been shown to influence different cellular processes that may contribute to the malignancy of breast cancer cells. To obtain insight into mechanisms mediating the PKC effects, global gene expression was analyzed in MDA-MB-231 breast cancer cells in which PKCα, PKCδ or PKCε had been down-regulated with siRNA. Gene set enrichment analyses revealed that hypoxia-induced genes were enriched among genes that increased in PKCα-down-regulated cells. The STC1 mRNA, encoding stanniocalcin 1, was particularly up-regulated following depletion of PKCα and was also induced by hypoxia. Both hypoxia and PKCα down-regulation also led to increased STC1 protein levels. The results demonstrate that PKCα suppresses the expression of STC1 in breast cancer cells (Less)
Please use this url to cite or link to this publication:
author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Gene expression, Stanniocalcin 1, Protein kinase C, Breast cancer cells
in
Tumour Biology
volume
32
issue
5
pages
1023 - 1030
publisher
Springer
external identifiers
  • wos:000293962800020
  • pmid:21720730
  • pmid:21720730
  • scopus:80052337002
ISSN
1423-0380
DOI
10.1007/s13277-011-0205-2
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Molecular Medicine (013031200), Tumour Cell Biology (013017530)
id
97169cbb-3b30-40ef-94bf-014dc63af35e (old id 2059176)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/21720730?dopt=Abstract
date added to LUP
2016-04-01 14:42:42
date last changed
2021-03-16 01:54:16
@article{97169cbb-3b30-40ef-94bf-014dc63af35e,
  abstract     = {Several protein kinase C (PKC) isoforms have been shown to influence different cellular processes that may contribute to the malignancy of breast cancer cells. To obtain insight into mechanisms mediating the PKC effects, global gene expression was analyzed in MDA-MB-231 breast cancer cells in which PKCα, PKCδ or PKCε had been down-regulated with siRNA. Gene set enrichment analyses revealed that hypoxia-induced genes were enriched among genes that increased in PKCα-down-regulated cells. The STC1 mRNA, encoding stanniocalcin 1, was particularly up-regulated following depletion of PKCα and was also induced by hypoxia. Both hypoxia and PKCα down-regulation also led to increased STC1 protein levels. The results demonstrate that PKCα suppresses the expression of STC1 in breast cancer cells},
  author       = {Cornmark, Louise and Kalstad Lönne, Gry and Jögi, Annika and Larsson, Christer},
  issn         = {1423-0380},
  language     = {eng},
  number       = {5},
  pages        = {1023--1030},
  publisher    = {Springer},
  series       = {Tumour Biology},
  title        = {Protein kinase Cα suppresses the expression of STC1 in MDA-MB-231 breast cancer cells},
  url          = {http://dx.doi.org/10.1007/s13277-011-0205-2},
  doi          = {10.1007/s13277-011-0205-2},
  volume       = {32},
  year         = {2011},
}