| Lung cancer was the majority of malignancies, whose mortality ranked the first in developed countries. Consequently, many scholars paid more attention to it. Most of patients with lung cancer died from its metastasis. If metastasis of lung cancer were controlled, survival rate and quality of patients with hmg cancer were greatly improved. A lot of evidences indicated that plenty of genetic alterations were involved in carcinogenesis and progression of lung cancer and underlay the molecular mechanisms of metastasis of lung cancer. Except activation of oncogenes, inactivation of tumor suppressor genes, altered cell adhesion and dysfunction of metalloproteinases and its inhibitors, loss or down - regulated expression of metastasis suppressor genes played an important role in progression of lung cancer.Kail is one of transmembrane 4 superfamily (TM4SF) , which encodes a cell glycoprotein with 4 conservative transmembrane domain. It is located on cell membrande and regulates cell proliferation, adhesion and mobility. Recent studies showed that Kail protein had inhibitory effects on tumor metastasis and its down - regulated expression was closely correlated with progression and prognosis of tumor. Fas ligand(FasL) was one of tumor necrosis factor (TNF) family. When membrane FasL(mFasL) crosslinks with membrane Fas(mFas) , Fas -associated death domain ( FADD) was activated and release of cytochrome C was iniated, leading to activation of Caspase - 3 - a key proteinase in cell apoptosis. Soluble Fas was released into tumor microenviroment to neutralize the mFasL on lymphocyte membrane, which inhibits the apoptosis induction of lymphocytes and then forms immune escape. Shinohara et aL found that TNFa could up -regulate the NF kappaB expression by autocrine and paracrine, resulting highexpression of Kail in lung cancer cells. FasL Bclongs to TNF family, so our study observed the expression of Kail and FasL in non - small cell lung cancer (NSCLC), compared their expression with clinicopathological features of NSCLC and analyze the relationship between their expression in NSCLC in order to explore the role of encoding protein of Kail and FasL genes in carcinogenesis and progression of NSCLC and its relevant molecular mechanisms.Materials and Methods1. Specimens 79 cases of primary non - small cell lung cancer were collected from Iiaoning province Tumor Hospital between February 2003 and July 2003, including 53 males and 26 females, with an age range from 32 to 76 year (mean= 51.8 years). According to histological classification, there were 49 cases of squamous cell carcinoma, 21 adenocarcinoma, 5 adenosquamous carcinoma and 4 bronchioalveolar carcinoma. Among them, 29 cases were accompanied with lymph node metastasis, others without lymph node metastasis. Tissues of primary cancers and the adjacent normal tissues from each case were fixed in 10% formalin; embedded in paraffin, and 4 m sections were prepared. Two professional pathologists diagnosed all 79 cases according to standard criteria.2. Immunohistochemistry: S - P immunohistochemistry ( S - P kit from Zhongshan Biotech Co. Ltd. ) was employed in this study to detect expressions of Kail protein(rabbit anti -human Kail polyclonal antibody, dilution 1:50, Santa Cruz Biotech. ) and FasL protein ( rabbit anti - human FasL polyclonal antibody, ready to use, Maixin Biotech. ). All procedures were implemented according to the product illustrations. For negative control, sections were processed as above but treated with PBS (0.01mol/L, pH7.4) , instead of primary antibodies. Known positive sections were used for positive control.3. Evaluation of Kail and FasL: The immnoreactivity to Kail and FasL was localized in the cytoplasm. According to the proportion of positive ones in counted cells, the degree of immunostaining was graded as follows: negative ( - ) , < 5% ; weakly positive ( + ) , 5 ~ 25% ; moderately positive ( ++ ) ,25 -50%; and strongly positive( +++ ) ,>50%4. Statistical analysis. Chi - square test was used to differentiate th...
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