title: Activation of SNAT1/SLC38A1 in human breast cancer: correlation with p-Akt overexpression.
abstract: BACKGROUND
  SNAT1 is a subtype of the amino acid transport system A that has been implicated to play a potential role in cancer development and progression, yet its role in breast cancer remains unclear. In present study, we detected SNAT1 expression in breast cancers and explored its underlying mechanism in promoting breast carcinogenesis.
  
  
  METHODS
  RT-PCR and Western blotting were performed to analyze the transcription and protein levels of SNAT1 in breast cancer cell lines and fresh tissues. Tissue microarray blocks containing breast cancer specimens obtained from 210 patients were constructed. Expression of SNAT1 in these specimens was analyzed using immunohistochemical studies. SNAT1 was down-regulated by SNAT1-shRNA in breast cancer cells and the functional significance was measured.
  
  
  RESULTS
  SNAT1 was up-regulated in breast cancer cell lines and breast cancer tissues. Overexpression of SNAT1 was observed in 127 cases (60.5%). Expression of SNAT1 was significantly associated with tumor size, nodal metastasis, advanced disease stage, Ki-67, and ER status. Suppression of endogenous SNAT1 leads to cell growth inhibition, cell cycle arrest, and apoptosis of 4T1 cells and lowered the phosphorylation level of Akt. SNAT1 expression correlated significantly with p-Akt expression in human breast cancer samples.
  
  
  CONCLUSIONS
  The cross-talk between Akt signaling and SNAT1 might play a critical role in the development and progression of breast cancer, providing an important molecular basis for novel diagnostic markers and new attractive targets in the treatment of breast cancer patients.
authors.affiliation: Department of Surgery, The Affiliated Kunshan First People's Hospital, Jiangsu University, Kunshan 215300, Jiangsu Province, China.
authors.forename: Kuo
authors.initials: K
authors.lastname: Wang
authors.forename: Fang
authors.initials: F
authors.lastname: Cao
authors.forename: Wenzheng
authors.initials: W
authors.lastname: Fang
authors.forename: Yongwei
authors.initials: Y
authors.lastname: Hu
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Houzhong
authors.initials: H
authors.lastname: Ding
authors.forename: Guanzhen
authors.initials: G
authors.lastname: Yu
mesh_terms: D000328:Adult; D026924:Amino Acid Transport System A / Q000378:metabolism*; D015153:Blotting, Western; D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D051057:Proto-Oncogene Proteins c-akt / Q000096:biosynthesis*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000502:physiology*; D046888:Tissue Array Analysis
chemical_list: D026924:Amino Acid Transport System A; C445761:SLC38A1 protein, human; D051057:Proto-Oncogene Proteins c-akt