Abstract：AIM:To investigate the clinical significance of signal transducer and activator of transcription 1(STAT1) and intercellular adhesion molecule-1(ICAM-1) in non-small-cell lung cancer(NSCLC). METHODS:The expression of STAT1 and ICAM-1 at mRNA and protein levels was detected by real-time PCR and Western blotting in the fresh samples from 40 cases of NSCLC to analyze the correlation between STAT1, ICAM-1 and clinical characteristics(sex, age, histological type, cell differentiation, TNM stage and distant metastasis). Forty cases of non-malignant tissues from lung lesion(adjacent normal lung tissues) were used for control. RESULTS:STAT1 and ICAM-1 were evidently and more strongly expressed in lung cancer than non-malignant tissues(P<0.05). In lung cancer, the expression of ICAM-1 in adenocarcinoma was stronger than that in squamous cell carcinoma. ICAM-1 expression in lung cancer with lymph node metastasis was stronger than that in lung cancer without lymph node metastasis(P<0.05). STAT1 expression in lung cancer in the early stage was stronger than that in the late stage. ICAM-1 expression in lung cancer in the late stage was stronger than that in early stage. STAT1 expression in poorly differentiated cancer was also stronger than that in well differentiated one(P<0.05). The expression of STAT1 and ICAM-1 was not correlated with age and sex(P>0.05). CONCLUSION:The expression levels of STAT1 and ICAM-1 are closely related to the invasion, metastasis and different stages of lung cancer.
Yang L, Yang G, Zhou M, et al. Body mass index and mortality from lung cancer in smokers and nonsmokers:a nationally representative prospective study of 220,000 men in China[J]. Int J Cancer, 2009, 125(9):2136-2143.
[2]
Mitsudomi T, Takahashi T. Genetic abnormalities in lung cancer and their prognostic implication[J]. Gan To Kaqaku Ryoho, 1996, 23(8):990-996.
Stahl N, Farruggella TJ, Boulton TG, et al. Choice of STATs and other substrates specified by modular tyrosine-based motifs in cytokine receptors[J]. Science, 1995,267(5202):1349-1353.
[5]
Ihle JN.The Stat family in cytokine signaling[J]. Curr Opin Cell Biol, 2001, 13(2):211-217.
[6]
Niu G, Heller R, Catlett-Falcone R, et al. Gene therapy with dominant-negative Stat3 suppresses growth of the murine melanoma B16 tumor in vivo[J]. Cancer Res, 1999, 59(20):5059-5063.
[7]
Lim S, Caramori G, Tomita K, et al. Differential expression of IL-10 receptor by epithelial cells and alveolar macrophages[J]. Allergy, 2004, 59(5):505-514.
[8]
Levy DE, Darnell JE. Stats:transcriptional control and biological impact[J]. Nat Rev Mol Cell Biol, 2002, 3(9):651-662.
[9]
Townsend PA, Scarabelli TM, Davidson SM, et al. STAT-1 interacts with p53 to enhance DNA damage induced apoptosis[J]. J Biol Chem, 2004, 279(7):5811-5820.
[10]
Meraz MA, White JM, Sheehan KC, et al. Targeted disruption of the Stat1 gene in mice reveals unexpected physiologic specificity in the JAK-STAT signaling pathway[J]. Cell, 1996, 84(3):431-442.
[11]
Durbin JE, Hackenmiller R, Simon MC, et al. Targeted disruption of the mouse Stat1 gene results in compromised innate immunity to viral disease[J]. Cell, 1996, 84(3):443-450.
[12]
Constantinescu SN, Girardot M, Pecquet C. Mining for JAK-STAT mutations in cancer[J]. Trends Biochem Sci, 2008,33(3):122-131.
[13]
Esposito V, Groeger AM, De Luca L, et al. Expression of surface protein receptors in lung cancer[J]. Anticancer Res, 2002, 22(6C):4039-4043.
[14]
Benekli M, Güllü IH, Tekuzman G, et al. Circulating intercellular adhesion molecule-1 and E-selectin levels in gastric cancer[J]. Br J Cancer, 1998,78(2):267-271.
[15]
O Hanlon DM, Fitzsimons H, Lynch J, et al. Soluble adhesion molecules(E-selectin, ICAM-1 and VCAM-1) in breast carcinoma[J]. Eur J Cancer, 2002,38(17):2252-2257.
[16]
Burt AD, Le Bail B, Balabaud C, et al. Morphologic investigation of sinusoidal cells[J]. Semin Liver Dis, 1993. 13(1):21-38.
