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  • Title: Overexpression of activated leukocute cell adhesion molecule in gastric cancer is associated with advanced stages and poor prognosis and miR-9 deregulation.
    Author: Ye M, Du YL, Nie YQ, Zhou ZW, Cao J, Li YF.
    Journal: Mol Med Rep; 2015 Mar; 11(3):2004-12. PubMed ID: 25395097.
    Abstract:
    Activated leukocyte cell adhesion molecule (ALCAM) has been identified as a novel potential molecular marker of human tumors. The present study aimed to assess ALCAM as a prognostic marker for gastric cancer (GC), and to explore the mRNA deregulation underlying the abnormal expression of ALCAM. The mRNA and protein expression of ALCAM in GC and adjacent non‑tumor tissues from 66 patients with GC were analyzed. The association between miR‑9 and ALCAM mRNA expression was determined by quantitative polymerase chain reaction. Serum soluble ALCAM (sALCAM) was analyzed by ELISA in 72 patients with GC, 82 patients with gastric precancerous lesions and 73 controls. ALCAM and sALCAM levels were associated with certain clinicopathological variables, including overall survival. Compared with the non‑tumor tissues, the expression of ALCAM mRNA in the GC tissues was significantly upregulated (P=0.013). The expression of miR‑9 was reduced and inversely correlated with ALCAM mRNA levels in GC tissues and cell lines. The ALCAM mRNA level was reduced following ectopic overexpression of miR‑9 in SGC‑7901 human gastric cancer cells. The rates of membranous and cytoplasmic expression of ALCAM in GC tissues were 59.1 and 48.48%, respectively, and the serum sALCAM levels were significantly elevated in patients with GC. Elevated ALCAM mRNA, membranous ALCAM expression in GC tissues and high sALCAM levels are associated with advanced tumor stage, lymphatic invasion and shorter overall survival duration. The results of the current study indicated that membranous ALCAM expression and high serum sALCAM levels are independent prognostic markers of poor survival for patients with GC, and that the overexpression of ALCAM may be due to the downregulation of miR‑9.
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