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유방암 세포주에 에스트로겐 및 항에스트로겐 처치에 따른 Coregulators, MAP Kinase 활성도 및 세포주기 조절인자 p27/kip1의 변화

Other Titles
 Changes of Coregulators, MAP Kinase Activity and p27/kip1 with Estrogen or Antiestrogen Treatment in Breast Cancer Cell Line 
 박세호  ;  허민규  ;  이미정  ;  김주희  ;  박병우 
 JOURNAL OF BREAST CANCER, Vol.11(2) : 56-63, 2008 
Journal Title
Issue Date
Estrogen receptor ; Coregulatory protein ; Tamoxifen ; p27/kip1 ; MAP kinase
PURPOSE: Estrogen, various polypeptide hormones and growth factors are associated with the development and progression of breast cancer. Coregulatory proteins are also associated with estrogen receptor (ER) transcriptional activity and tamoxifen resistance. Therefore, it is necessary to investigate the change of coregulator mRNAs and various cell proliferation proteins and cell cycle-related proteins after treatment with estrogen or antiestrogen. METHODS: MCF-7 cells were maintained in dextran-coated charcoal stripped 10% Dulbecco's Modified Eagle Medium (DMEM). To measure the change of the coactivators' (src-1, P/CAF, CBP, AIB1) mRNAs and corepressors' (SMRT, N-coR) mRNAs, multiple PCR was carried out using specific primers. In addition, intracellular proteins related to cell proliferation and cell cycle regulation were measured by performing Western blotting after treatment with estrogen or tamoxifen. The change of mitogen activated protein kinases was also measured by performing Western after tamoxifen treatment for 4 weeks. RESULTS: Coactivator mRNAs expression rapidly decreased in 15 min after estrogen treatment but this recovered to the initial level in 3 hr. The pattern was similar for the case of tamoxifen treatment. Corepressor mRNAs expression rapidly decreased in 15 min after estrogen treatment and it remained at a lower level until 24 hr after estrogen treatment. With tamoxifen treatment, the initial response was similar to the cases of estrogen treatment, but the xpression gradually increased 3 hr after tamoxifen treatment. Treatment of estrogen induced intracellular concentrations of c-myc and Ki-67 and it increased nuclear translocation of NF-kappaB and phosphor-ERK and it decreased the intracellular cell cycle suppressor p27/kip1. Tamoxifen treatment increased nuclear p27/kip1 but it decreased c-myc, NF-kappaB and phosphor-ERK. Long-term (4 weeks) treatment of tamoxifen was associated with decrease of activated ERK and p38 but there was no change in phospho-Akt level. CONCLUSION: Estrogen induced cell proliferation and the survival pathway-related factors, but it decreased the cell cycle suppressor p27/kip1. Long-term treatment with antiestrogen tamoxifen might decrease the MAPK activities in ERalpha-expressing tumor cells.
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1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Joo Hee(김주희)
Park, Byeong Woo(박병우) ORCID logo https://orcid.org/0000-0003-1353-2607
Park, Se Ho(박세호) ORCID logo https://orcid.org/0000-0001-8089-2755
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