B类Ⅰ型清道夫受体在食管鳞状细胞癌中的表达与其对细胞增殖和侵袭的影响

Expression of scavenger receptor class type B1 in esophageal squamous cell carcinoma and its effects on cell proliferation and invasion

目的探讨B类Ⅰ型清道夫受体（SR-B1）在食管鳞状细胞癌中的表达，以及其表达变化对食管鳞状细胞癌细胞增殖和侵袭的影响。方法纳入2012年5月至2017年8月于河南省人民医院行手术切除治疗的63例食管鳞状细胞癌患者，收集其鳞状细胞癌组织和所对应的癌旁组织。采用免疫组织化学染色法和蛋白质印迹法检测所取组织和食管鳞状细胞癌细胞中SR-B1蛋白质的表达。使用SR-B1小干扰RNA、对照小干扰RNA、pcDNA3．1和pcDNA3．1-SR-B1分别转染食管鳞状细胞癌ECl和TEl细胞。采用蛋白质印迹法检测转染后SR-B1蛋白质的表达，采用细胞计数试剂盒8（CCK-8）、流式细胞术和Tranwell小室分别检测转染后食管鳞状细胞癌ECl和TEl细胞增殖、周期和侵袭的改变。统计学分析采用卡方检验和t检验。结果食管鳞状细胞癌组织的SR-B1蛋白质表达阳性率为60．3Z（38／63），高于癌旁组织的30．20（19／63），差异有统计学意义（X^2=11.565，P=0．001）。食管鳞状细胞癌Ecal09、EC9706、ECl、TEl和KYSE70细胞中SR-B1蛋白质的表达水平分别为0．244±0．012、0．285±0．018、0．455±0．016、0．479±0．019和0．390土0．022，均高于正常食管上皮细胞Het-1A的0．027±0．011，差异均有统计学意义（t=23．252、21．633、39．081、36．010、25．591，P均〈O．01）。SR-B1小干扰RNA下调食管鳞状细胞癌ECl和TEl细胞中SR-B1蛋白质的表达。SR-B1蛋白质的表达下调抑制食管鳞状细胞癌ECl和TEl细胞的增殖，增加ECl和TEl细胞在G0／G1期的细胞比例[分别为（64．92±1．68）O和（64．34±0．94）％]，降低ECl和TEl细胞的侵袭能力（分别为33．33±7．51和21．67±4．04）；SR-B1表达上调促进食管鳞状细胞癌ECl和TEl细胞的增殖，降低其G0／G1期的细胞比例[分别为（31．72±1．30）％和（33．12±1．04）％]，增强其侵袭能力（Yt别为285．33±28．10和247．33土28．29）。结论SR-B1在食管鳞状细胞癌中的过表达可能与食管鳞状细胞癌的发生、发展密切相关，SR—B1可能成为治疗食管鳞状细胞癌的新靶点。

Objective To explore the expression of scavenger receptor class type B1 （SR-B1） in esophageal squamous cell carcinoma （ESCC） , and its effects on proliferation and invasion of ESCC cells. Methods From May 2012 to August 2017, 63 ESCC patients who underwent surgical resection in Henan Provincial People＇s Hospital were enrolled and ESCC tissues and corresponding normal tissues were collected. The expression of SR-B1 protein in collected tissues and ESCC cells were detected by immunohistochemistry and Western blotting. ESCC EC1 cells and TEl cells were transfected with SR-B1 small interfering RNA （siRNA）, control siRNA, pcDNA3.1 and pcDNA3.1-SR-B1, respectively. After transfection, the expression of SR-B1 protein was examined by Western blotting. The cell proliferation, cell cycle and invasion ability of ESCC EC1 cells and TEl cells after transfection were determined by cell counting kit-8 （CCK-8） assay, flow cytometry and Transwell chamber. Chi-square test and t test were performed for statistical analysis. Results The positive rate of SR-B1 protein expression in ESCC tissues was 60.3% （38/63）, which was higher than that of corresponding normal tissues （30.2%, 19/63）, and the difference was statistically significant （X^2=11. 565, P=0. 001）. The expression of SR-B1 protein in ESCC cells Ecal09, EC9706, EC1, TEl and KYSET0 were 0. 244±0.012, 0. 285±0. 018, 0.4554±0. 016, 0. 479± 0. 019 and 0. 390±0. 022, respectively, which were all higher than that of normal esophageal epithelial cell Het-lA （0. 027±0. 011）, and the differences were statistically significant （t=23. 252, 21. 633, 39. 081, 36.010 and 25. 591; all P〈0. 01）. The expression of SR-B1 protein inESCC EC1 and TEl was downregulated by SR-B1 siRNA. The downregulation of SR-BI protein expression suppressed the proliferation of ESCC EC1 cells and TEl cells, increased the percentage of cells at G0/G1 phase of ESCC EC1 ceils and TEl cells （（64. 92±1. 68） % and （64. 34 ±0. 94） %）, and reduced the invasion abilities of ECI and TEl cells （33. 33±7. 51 and 21. 67±4.04）. The upregulation of SR-B1 expression promoted the proliferation of ESCC EC1 ceils and TEl cells, reduced the percentage of cells at G0/G1 phase （（31. 724±1.30）% and （33.12±1.04）%）, and enhanced cell invasion abilities （285.33±28.10 and 247.33±28.29）. Conclusions The overexpression of SR-B1 in ESCC may be associated with the occurrence and development of ESCC. Treatment targeting SRB1 may be a novel therapeutic strategy in ESCC.