基底样亚型乳腺癌增殖活力高、抗药性强、复发率高、侵袭力和转移能力强、预后差，是恶性程度最高的乳腺癌亚型。目前，基底样乳腺癌的代谢调控机制尚不清楚。γ-氨基丁酸转氨酶(Gamma-aminobutyrate aminotransferase，ABAT）是γ-氨基丁酸(GABA)代谢过程中的一个关键酶。我们前期研究发现基底样乳腺癌细胞和组织标本的ABAT表达水平明显低于其它的亚型。此外，我们也发现Snail能够显著抑制ABAT的表达。在本申请项目中，我们将重点研究ABAT介导的代谢改变对基底样乳腺癌发生及转移的作用与分子机制，明确Snail对ABAT表达的调控机制，从体外和体内研究Snail/ABAT与基底样乳腺癌的内在联系。本项目的开展将不仅有助于理解ABAT介导的代谢改变对基底样乳腺癌的发生与转移的影响，也有助于为早期预防和治疗该型乳腺癌提供理论依据和潜在的标记分子。

Basal-like breast cancer (BLBC) is the most aggressive subtype with a poor clinical outcome; however the molecular mechanisms underlying aggressiveness in BLBC remain poorly understood. Here, we found that in contrast to other subtypes, gamma-aminobutyrate aminotransferase (ABAT) was dramatically downregulated in BLBC. We also noticed ABAT expression was remarkably downregulated by Snail, a transcriptional repressor of E-cadherin. Based on these findings, we propose that ABAT may associate with breast cancer cell proliferation and metastasis by regulating metabolic reprogramming. The objective of this proposal is to explore the potential roles of ABAT in tumorigenicity and metastasis of breast cancer cells. This study will uncover the important role of ABAT loss induced by Snail in regulating metabolic reprogramming in BLBC cells. Elucidating the correlation between ABAT and Snail will contribute to our understanding of how metabolic reprogramming regulating tumorigenicity and metastasis in BLBC, providing potential prognostic indicators and therapeutic targets for BLBC.