首页> 外文期刊>World Journal of Gastroenterology >Mechanism of counterattack of colorectal cancer cell by Fas/Fas ligand system.
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Mechanism of counterattack of colorectal cancer cell by Fas/Fas ligand system.

机译:Fas / Fas配体系统逆转大肠癌细胞的机制。

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AIM: To determine the role of Fas/Fas ligand (FasL) in the immune escape of colon cancer cells. METHODS: Immunohistochemistry was used to observe the expression of Fas and FasL in the tissues of colon cancer patients. In situ hybridization was used to detect the localization of FasL mRNA expression in cancer tissues. Terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) assay and CD45 staining were performed to detect the apoptosis of tumor-infiltrating lymphocytes (TILs). Co-culture assays of colon cancer cells (SW480) and Jurkat cells (Fas-sensitive cells) were performed to observe the counterattack of colon cancer cells to lymphocytes. RESULTS: Of 53 cases of colon carcinomas, 23 cases (43.4%) expressed Fas which was significantly lower as compared to the normal colonic mucosa (73.3%, P<0.01), and 45 cases (84.9%) of colon carcinomas expressed FasL, whereas only two cases (3.75%) in normal mucosa expressed FasL. FasL expression in the colon cancer cells was found to be associated with increased cell death of TILs. The apoptotic rate of TIL in the FasL-positive staining regions of tumor cells was significantly higher than that in the FasL-negative staining region (54.84+/-2.79% vs 25.73+/-1.98%, P<0.01). The co-culture of SW480 cells and Jurkat cells confirmed the function of FasL on the SW480 cells. The apoptotic rates of Jurkat cells were found to be related with the amount of SW480 cells. CONCLUSION: Colon cancer cells can escape the immune surveillance and killing via decreasing Fas expression, and can counterattack the immune system via increasing FasL expression. Fas/FasL can serve as potential targets for effective antitumor therapy.
机译:目的:确定Fas / Fas配体(FasL)在结肠癌细胞免疫逃逸中的作用。方法:采用免疫组织化学方法观察结肠癌患者组织中Fas和FasL的表达。原位杂交用于检测FasL mRNA表达在癌组织中的定位。进行末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)测定和CD45染色以检测肿瘤浸润淋巴细胞(TIL)的凋亡。进行结肠癌细胞(SW480)和Jurkat细胞(Fas敏感细胞)的共培养测定,以观察结肠癌细胞对淋巴细胞的反攻。结果:在53例结肠癌中,有23例(43.4%)表达Fas,明显低于正常结肠粘膜(73.3%,P <0.01),在45例结肠癌中,表达FasL的比例为84.9%。正常黏膜中只有2例(3.75%)表达FasL。发现结肠癌细胞中的FasL表达与TIL的细胞死亡增加有关。肿瘤细胞FasL阳性染色区域的TIL凋亡率显着高于FasL阴性染色区域(54.84 +/- 2.79%vs 25.73 +/- 1.98%,P <0.01)。 SW480细胞和Jurkat细胞的共培养证实了FasL在SW480细胞上的功能。发现Jurkat细胞的凋亡率与SW480细胞的数量有关。结论:结肠癌细胞可以通过减少Fas表达来逃避免疫监视和杀伤,并可以通过增加FasL表达来抵抗免疫系统。 Fas / FasL可以作为有效抗肿瘤治疗的潜在靶点。

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