| General information | Literature | Expression | Regulation | Mutation | Homolog | Interaction |
Basic Information | |
|---|---|
Gene ID | 9462 |
Name | RASAL2 |
Synonymous | RAS protein activator like 2;RASAL2;RAS protein activator like 2 |
Definition | RAS protein activator-like 2|Ras protein activator like 1|ras GTPase-activating protein nGAP |
Position | 1q24 |
Gene type | protein-coding |
Title | Abstract |
| breast cancer | RAS genes are commonly mutated in cancer; however, RAS mutations are rare in breast cancer, despite frequent hyperactivation of Ras and ERK. Here, we report that the RasGAP gene, RASAL2, functions as a tumor and metastasis suppressor. RASAL2 is mutated or suppressed in human breast cancer, and RASAL2 ablation promotes tumor growth, progression, and metastasis in mouse models. In human breast cancer, RASAL2 loss is associated with metastatic disease; low RASAL2 levels correlate with recurrence of luminal B tumors; and RASAL2 ablation promotes metastasis of luminal mouse tumors. Additional data reveal a broader role for RASAL2 inactivation in other tumor types. These studies highlight the expanding role of RasGAPs and reveal an alternative mechanism of activating Ras in cancer. |
| lung cancer | It was reported that genetically-engineered RASAL2 knockout mice are prone to development of several sporadic tumor, including lung adenocarcinoma. However, a causative relationship between RASAL2 deficiency and lung adenocarcinoma development still remains unknown. In the present study, RASAL2 level was determined in patients with lung adenocarcinoma and control subjects in an attempt to explore its potential clinical diagnostic and prognostic value. Low RASAL2 expression levels were found in 71% (37 of 52) of lung adenocarcinoma, which were correlated with lymph node metastasis in lung adenocarcinoma. Moreover, Low RASAL2 expression levels were correlated with reduced overall survival (OS) in lung adenocarcinoma. We find that inactivation of RASAL2 promotes lung cancer cell migration through the induction of epithelial mesenchymal transition (EMT) and promoted lung metastasis in nude mice. Our results suggest that the down-regulation of RASAL2 promotes metastatic progression of lung adenocarcinoma, hence it could serve as a potential target for the development of lung cancer therapies. |