| Gene information | Literature | Expression | lncRNA | Mutation | Homolog |
Basic Information | |
|---|---|
Gene ID | 6863 |
Name | TAC1 |
Synonymous | tachykinin, precursor 1;TAC1;tachykinin, precursor 1 |
Definition | PPT|neurokinin 1|neurokinin 2|neurokinin A|neurokinin alpha|neuromedin L|neuropeptide K|neuropeptide gamma|preprotachykinin|protachykinin-1|substance K|substance P|tachykinin 2|tachykinin, precursor 1 (substance K, substance P, neurokinin 1, neurokinin 2, |
Position | 7q21-q22 |
Gene type | protein-coding |
Title | Abstract |
| RE-1-silencing transcription factor shows tumor-suppressor functions and negatively regulates the oncogenic TAC1 in breast cancer cells. | Breast cancer remains the most prevalent cancer among women in the United States. Substance P, a peptide derived from the TAC1 gene, mediates oncogenic properties in breast and other cancers. TAC1 expression facilitates the entry of breast cancer cells into bone marrow. The transcriptional repressor element 1-silencing transcription factor (REST) has been implicated in both oncogenic and tumor-suppressor functions. REST binds to the 5 untranslated region of the TAC1 promoter and suppresses its expression. This study investigated a role for REST in TAC1 induction in breast cancer. Western blots and real-time PCR indicated that REST expression in breast cancer cells was inversely proportional to the cells aggressiveness, for both cell lines and primary breast cancer cells. REST knockdown in low-metastatic T47D cells and nontumorigenic MCF12A cells resulted in increases in TAC1 induction, proliferation, and migration. These parameters were negatively affected by ectopic expression of REST in highly aggressive MDA-MB-231 cells. Together, these findings show a central role for REST in the oncogenic function of TAC1 and suggest a tumor-suppressor role for REST in breast cancer. |