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  • 尚立娜,周彰映,张城,龚川友,田世馨,安利锋,李晓琴,赵晋.Bcl2转录抑制因子1、E-钙黏蛋白在宫颈鳞状细胞癌不同区域的表达及两者与P16INK4a表达的关系[J].第二军医大学学报,2019,40(12):1317-1324    [点击复制]
  • SHANG Li-na,ZHOU Zhang-ying,ZHANG Cheng,GONG Chuan-you,TIAN Shi-xin,AN Li-feng,LI Xiao-qin,ZHAO Jin.Expression of Bcl2 inhibitor of transcription 1 and E-cadherin in different regions of cervical squamous cell carcinoma and their relationship with expression of P16INK4a[J].Acad J Sec Mil Med Univ,2019,40(12):1317-1324   [点击复制]
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Bcl2转录抑制因子1、E-钙黏蛋白在宫颈鳞状细胞癌不同区域的表达及两者与P16INK4a表达的关系
尚立娜1,周彰映1,张城1,龚川友1,田世馨1,安利锋1,李晓琴2,赵晋1*
0
(1. 西北民族大学医学院形态学教研室, 兰州 730030;
2. 甘肃省肿瘤医院, 甘肃省医学科学研究院病理科, 兰州 730030
*通信作者)
摘要:
目的 检测宫颈鳞状细胞癌肿瘤出芽区及肿瘤中央区失巢凋亡因子Bcl2转录抑制因子1(Bit1)、上皮-间质转化(EMT)标志物E-钙黏蛋白及P16INK4a的表达情况,探讨Bit1、E-钙黏蛋白在宫颈癌获得高侵袭力过程中的意义及二者与P16INK4a表达的关系。方法 收集甘肃省肿瘤医院病理科2014-2018年宫颈鳞状细胞癌石蜡包埋标本77例。采用免疫组织化学法检测宫颈鳞状细胞癌肿瘤出芽区及中央区Bit1、E-钙黏蛋白、P16INK4a的表达情况。以肿瘤中央区及出芽区各蛋白质表达评分的中位数作为分界点,将标本分为高表达组和低表达组,分析在不同P16INK4a表达情况下Bit1及E-钙黏蛋白的表达差异及二者与患者临床病理特征的关系,并进一步分析在肿瘤中央区及出芽区Bit1与E-钙黏蛋白的相关关系。统计学分析采用χ2检验或连续校正χ2检验和Spearman等级相关分析。结果 77例宫颈鳞状细胞癌标本中,肿瘤中央区P16INK4a、E-钙黏蛋白、Bit1高表达率分别为32.5%(25/77)、67.5%(52/77)、63.6%(49/77),而在肿瘤出芽区分别为67.5%(52/77)、33.8%(26/77)、37.7%(29/77),差异有统计学意义(χ2=18.935、17.561、10.391,P均<0.01)。无论在肿瘤出芽区还是中央区,P16INK4a高表达组与P16INK4a低表达组Bit1及E-钙黏蛋白的表达差异均无统计学意义(P均>0.05)。肿瘤中央区Bit1低表达与脉管内癌栓及淋巴结转移有关(χ2=5.053、4.400,P均<0.05),肿瘤出芽区E-钙黏蛋白和Bit1低表达均与淋巴结转移有关(χ2=5.580、7.573,P均<0.05)。Spearman等级相关分析显示,在肿瘤中央区及肿瘤出芽区E-钙黏蛋白与Bit1表达均呈正相关(r=0.287,P=0.011;r=0.236,P=0.039)。结论 宫颈癌侵袭力的增高与Bit1及E-钙黏蛋白表达降低及P16INK4a表达增高有关,宫颈癌细胞可能通过抑制Bit1获得失巢凋亡抗性并影响EMT的发生从而获得更高的侵袭能力,但P16INK4a并未参与此过程。
关键词:  宫颈肿瘤  鳞状细胞癌  肿瘤出芽  失巢凋亡  Bcl2 转录抑制因子1  E-钙黏蛋白  上皮-间质转化  P16INK4a
DOI:10.16781/j.0258-879x.2019.12.1317
投稿时间:2019-05-23修订日期:2019-09-18
基金项目:国家自然科学基金(81260442),中央高校基本科研业务费专项资金(31920150044).
Expression of Bcl2 inhibitor of transcription 1 and E-cadherin in different regions of cervical squamous cell carcinoma and their relationship with expression of P16INK4a
SHANG Li-na1,ZHOU Zhang-ying1,ZHANG Cheng1,GONG Chuan-you1,TIAN Shi-xin1,AN Li-feng1,LI Xiao-qin2,ZHAO Jin1*
(1. Department of Morphology, Medical College of Northwest Minzu University, Lanzhou 730030, Gansu, China;
2. Department of Pathology, Gansu Provincial Cancer Hospital, Gansu Provincial Academic Institute for Medical Research, Lanzhou 730030, Gansu, China
*Corresponding author)
Abstract:
Objective To determine the expression of anoikis factor Bcl2 inhibitor of transcription 1 (Bit1), epithelial-mesenchymal transformation (EMT) marker E-cadherin and P16INK4a in tumor budding and central tumor of cervical squamous cell carcinoma, and to explore the significance of Bit1 and E-cadherin expression in the process of obtaining high invasiveness of cervical cancer and their relationship with P16INK4a expression. Methods A total of 77 paraffin-embedded specimens of cervical squamous cell carcinoma were collected from the Department of Pathology of Gansu Provincial Cancer Hospital between 2014 and 2018. The expression levels of Bit1, E-cadherin and P16INK4a in tumor budding and central tumor of these specimens were detected by immunohistochemistry. Taking the median scores of protein expression in the central tumor and tumor budding as dividing points, the specimens were divided into high expression group and low expression group. The differences of Bit1 and E-cadherin expression under different p16INK4a expression and their relationship with the clinicopathological characteristics of the patients were analyzed. The correlation between Bit1 and E-cadherin expression in central tumor and tumor budding was explored. The χ2 test, continuous correction χ2 test and Spearman rank correlation analysis were used for statistical analysis. Results In 77 cases of paraffin-embedded specimens of cervical squamous cell carcinoma, the high expression rates of P16INK4a, E-cadherin and Bit1 in central tumor and tumor budding were 32.5% (25/77), 67.5% (52/77) and 63.6% (49/77), and 67.5% (52/77), 33.8% (26/77) and 37.7% (29/77), respectively, and the differences were significant (χ2=18.935, 17.561 and 10.391, all P<0.01). Both in central tumor and in tumor budding, there were no significant differences in Bit1 or E-cadherin expression between high and low P16INK4a expression regions (all P>0.05). In central tumor, the low expression of Bit-1 was related to lymphovascular invasion and lymph node metastasis (χ2=5.053 and 4.400, both P<0.05). In tumor budding, the low expression levels of E-cadherin and Bit-1 were both associated with lymph node metastasis (χ2=5.580 and 7.573, both P<0.05). Spearman rank correlation analysis showed that there was positive correlation between E-cadherin and Bit1 expression in central tumor and tumor budding (r=0.287, P=0.011; r=0.236, P=0.039). Conclusion The increased invasiveness of cervical cancer may be related to the decreased expression of Bit1 and E-cadherin and the increased expression of P16INK4a. Cervical cancer cells may acquire high invasiveness by inhibiting Bit1 to obtain anoikis resistance and affecting the EMT, but P16INK4a is not involved in this process.
Key words:  uterine cervical neoplasms  squamous cell carcinoma  tumor budding  anoikis  Bcl2 inhibitor of transcription 1  E-cadherin  epithelial-mesenchymal transformation  P16INK4a