유방암 세포에서 종양억제 유전자로서 알려지고있는 Rb 단백질의 스테로이드 수용체 활성에 대한 영향과 작용기전을 규명할 목적으로 실시된 연구로서 인간의 유방암 계대세포인 MCF 7에 wild type과 mutant type의 Rb expression vector를 도입한후 스테로이드 수용체 활성에 따른 CAT 활성의 변화를 thin layer chromatography를 통해 분석하였으며 스테로이드 호르몬 반응을 유발하는 Kil-GRE sequence를 P32로 labeling한 소식자로서 Rb expr-ession vector를 도입한 사람의 유방암 세포주 MCF7 혹은 도입되지않은 MCF7 세포로부터 핵단백질을 제조하여 gel mobility shift assay 실시하여 핵단백질의 결합양상을 비교하고자 시도하였으며 다음의 결과를 확인하였다. 1. 유방암 세포내에서 Rb 단백질의 과표현은 스테로이드 수용체 작용을 억제함을 확인하였다. 2. exon 22가 deletion된 mutant type Rb expre-ssion vector를 도입하였을 때는 이러한 억제작용은 유발되지 않았다. 3. Rb 단백질과 복합체를 형성하는 E2F expres-sion vector를 도입하였을 때는 Rb 단백질에 의한 스테로이드 수용체의 억제 작용은 상쇄되었다.

Cancer results from mutations that disrupt the harmonious checks and balances that regulate normal cellular growth and development. These mutations arise in two classes of interacting genes：those that facilitate cell growth and tumor formation(oncogenes), in which mutation or overexpression is oncogenic, and those that inhibit these processes(tumor supp-ressor genes) whose loss is oncogenic. The human retinoblastoma(Rb) protein, a tumor suppressor, acts as transcription factor or/and cell cycle regulator. Heterogenous expression of the Rb gene product contributes to the genesis of a diverse group of human neoplasma such as breast, prostate, small cell lu- ng, bladder carcinoma and leukemia. Its structural aberrations were observed in 25% of br- east tumor cell lines studied and 7% of the primary tumors, such as homozygous internal deletions and total deletion. These observations suggest that Rb protein is involved in bre- ast cancer development. Here we report that Rb protein represses steroid receptor function and its involvement of cell cycle process in human breast cancer cell line, MCF7 cells. 1. The overexpression of Rb protein repressed the steroid receptor function in breast cancer cell line, MCF 7. 2. When we introduced the mutant type Rb expression vector(deletion of exon 22), such repression was not observed. 3. By introducing E2F expression vector, the action of Rb protein was repressed. 4. Rb protein modulated the binding patterns of proteins to Kil-GRE site. 5. Flow cytometry analysis showed that Rb protein acts on G0/G1 stage of cell cycle process. These findings provide the molecular basis of breast cancer therapy using Rb protein.