| Gene information | Literature | Expression | lncRNA | Mutation | Homolog |
Basic Information | |
|---|---|
Gene ID | 283149 |
Name | BCL9L |
Synonymous | B-cell CLL/lymphoma 9-like;BCL9L;B-cell CLL/lymphoma 9-like |
Definition | B-cell CLL/lymphoma 9-like protein|B-cell lymphoma 9-like protein|BCL9-like protein|nuclear co-factor of beta-catenin signalling|protein BCL9-2 |
Position | 11q23.3 |
Gene type | protein-coding |
Title | Abstract |
| The BCL9-2 proto-oncogene governs estrogen receptor alpha expression in breast tumorigenesis. | The majority of human breast cancers express estrogen receptor alpha (ER), which is important for therapy with anti-estrogens. Here we describe the role of BCL9-2, a proto-oncogene previously characterized as co-activator of Wnt/ss-catenin signaling, for mammary tumorigenesis in mice and human. ER positive human breast cancers showed overexpression of BCL9-2 and tamoxifen treated patients with high BCL9-2 demonstrated a better survival. BCL9-2 was upregulated during puberty and pregnancy in normal mammary epithelia, but downregulated in the involuted gland. BCL9-2 overexpression in vivo delayed the mammary involution and induced alveolar hyperplasia. Moreover, aged BCL9-2 transgenic mice developed ductal-like mammary tumors with high nuclear ER expression. We found, that primary cell cultures of BCL9-2 breast tumors responded to tamoxifen treatment. Moreover, BCL9-2 regulated the expression of ER and the proliferation of human breast cancer cells independently of ss-catenin. Finally, we describe a novel mechanism, how BCL9-2 regulates ER transcription by interaction with Sp1 through the proximal ESR1 gene promoter. In summary, BCL9-2 induces ER positive breast cancers in vivo, regulates ER expression by a novel ss-catenin independent mechanism in breast cancer cells, and might predict the therapy response to tamoxifen treatment. |