肠型胃癌与癌前病变中α-SMA和TGF-β的表达及其与Ki-67的相关性研究
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摘要
目的探究肠型胃癌与癌前病变中α-平滑肌肌动蛋白(α-SMA)、转化生长因子-β(TGF-β)的表达及其与Ki-67的相关性。方法回顾性分析2016年4月至2018年6月确诊为肠型胃癌患者78例(观察组)和癌前病变患者33例(对照组)。分别检测胃黏膜组织细胞内α-SMA、TGF-β及Ki-67的表达水平和阳性细胞表达情况并分析三个指标的相关性及其与各病理因素的关系。结果观察组患者胃黏膜组织细胞中α-SMA、TGF-β和Ki-67阳性表达均明显高于对照组(P <0. 01),观察组患者胃黏膜组织细胞中α-SMA、TGF-β和Ki-67阳性细胞分布最高比率分别为41. 03%、37. 18%和42. 31%;不同分化程度癌细胞中α-SMA、TGF-β阳性表达差异无显著性(P> 0. 05),但分化程度越高,癌细胞中Ki-67阳性表达越少(P <0. 05);淋巴结是否转移、浸润程度不同和TNM分期不同细胞中α-SMA、TGF-β和Ki-67阳性表达数均存在明显差异(P <0. 05);α-SMA、TGF-β和Ki-67阳性表达相关系数分别为4. 791和4. 657,均呈正相关。结论胃黏膜组织细胞中在癌前病变至癌症发生过程中,α-SMA、TGF-β和Ki-67表达均呈正相关,为其作为标志物表征在胃癌发展过程提供理论依据。
Objective To investigate the expression of α-smooth muscle actin( α-SMA) and transforming growth factor-β( TGF-β) in intestinal type gastric cancer and precancerous lesions and its correlation with Ki-67. Methods A retrospective analysis with 78 cases of intestinal type gastric cancer( observation group) and 33 cases of precancerous lesions( control group) diagnosed in our hospital from April 2016 to June 2018 were performed to detect α-SMA in gastric mucosa. The expression levels of TGF-β and Ki-67 were analyzed and their correlation was analyzed. Results The positive expressions of α-SMA,TGF-β and Ki-67 in the gastric mucosa of the observation group were significantly higher than those in the control group( P < 0. 01). The α-SMA,TGF-β and the gastric mucosal cells in the observation group were observed. The highest proportion of Ki-67 positive cells were 41. 03%,37. 18% and 42. 31%,respectively. The positive expressions of α-SMA and TGF-β were not significantly different in different degrees of differentiation( P > 0. 05),but the higher the degree of differentiation,the positive expression of Ki-67 in the cells was less( P < 0. 05). There were significant differences in the expression of α-SMA,TGF-β and Ki-67 in different lymph node metastasis,infiltration degree and TNM stage( P < 0. 05). The correlation coefficients of α-SMA,TGF-β and Ki-67 positive expression were 4. 791 and 4. 657,respectively,which were positively correlated. Conclusion The expressions of α-SMA,TGF-β and Ki-67 are positively correlated in the pathogenesis of gastric mucosal cells from precancerous lesions to cancer,which provides a theoretical basis for the development of gastric cancer.
Objective To investigate the expression of α-smooth muscle actin( α-SMA) and transforming growth factor-β( TGF-β) in intestinal type gastric cancer and precancerous lesions and its correlation with Ki-67. Methods A retrospective analysis with 78 cases of intestinal type gastric cancer( observation group) and 33 cases of precancerous lesions( control group) diagnosed in our hospital from April 2016 to June 2018 were performed to detect α-SMA in gastric mucosa. The expression levels of TGF-β and Ki-67 were analyzed and their correlation was analyzed. Results The positive expressions of α-SMA,TGF-β and Ki-67 in the gastric mucosa of the observation group were significantly higher than those in the control group( P < 0. 01). The α-SMA,TGF-β and the gastric mucosal cells in the observation group were observed. The highest proportion of Ki-67 positive cells were 41. 03%,37. 18% and 42. 31%,respectively. The positive expressions of α-SMA and TGF-β were not significantly different in different degrees of differentiation( P > 0. 05),but the higher the degree of differentiation,the positive expression of Ki-67 in the cells was less( P < 0. 05). There were significant differences in the expression of α-SMA,TGF-β and Ki-67 in different lymph node metastasis,infiltration degree and TNM stage( P < 0. 05). The correlation coefficients of α-SMA,TGF-β and Ki-67 positive expression were 4. 791 and 4. 657,respectively,which were positively correlated. Conclusion The expressions of α-SMA,TGF-β and Ki-67 are positively correlated in the pathogenesis of gastric mucosal cells from precancerous lesions to cancer,which provides a theoretical basis for the development of gastric cancer.
引文
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[16]Wang X,Li M,Hu M,et al.BAMBI overexpression together withβ-sitosterol ameliorates NSCLC via inhibiting autophagy and inactivating TGF-β/Smad2/3 pathway[J].Oncol Rep,2017,37(5):3046-3054.
[17]Chatterjee A,Mukhopadhyay S,Tung K,et al.Rapamycin-induced G1 cell cycle arrest employs both TGF-βand Rb pathways[J].Cancer Lett,2015,360(2):134-140.
[18]Sundqvist A,Zieba A,Vasilaki E,et al.Specific interactions between Smad proteins and AP-1 components determine TGFβ-induced breast cancer cell invasion[J].Oncogene,2013,32(31):3606-3615.
[19]Huh JW,Lee JH,Kim HR.Expression of p16,p53,and Ki-67 in colorectal adenocarcinoma:a study of 356 surgically resected cases[J].Hepatogastroenterology,2010,57(101):734-740
[2]章真,李桂超.新辅助放化疗用于局部进展期胃癌治疗临床价值[J].中国实用外科杂志,2017,37(10):1109-1114.
[3]施慧,王震凯,汪芳裕,等.早期胃癌的多学科联合诊治[J].医学研究生学报,2016,29(5):529-532.
[4]邹文斌,李兆申.中国胃癌发病率及死亡率研究进展[J].中国实用内科杂志,2014,34(4):408-415.
[5]Di Sabatino A,Pickard KM,Rampton D,et al.Blockade of transforming growth factor beta upregulates T-box transcription factor T-bet,and increases T helper cell type 1 cytokine and matrix metalloproteinase-3 production in the human gut mucosa[J].Gut,2016,57(5):605-612.
[6]Dejanovic D,Shuai Z,Cruise MW,et al.626-Selective Deletion of MYD88 Signaling inα-SMA Positive Cells Ameliorates Experimental Intestinal Fibrosis via Posttranscriptional Regulation[J].Gastroenterology,2018,154(6):S130-S131.
[7]隋燕霞,柳雨,蒋娜,等.142例恶性胸水细胞蜡块的免疫组化检测及分子病理检测[J].临床与实验病理学杂志,2017,33(3):292-296.
[8]梅丽红.早期胃癌的临床病理特点与内镜下的表现分析[J].中国内镜杂志,2018,24(2):75-79.
[9]Zhong Q,Sun Q,Xu G F,et al.Differential analysis of lymph node metastasis in histological mixed-type early gastric carcinoma in the mucosa and submucosa[J].World J Gastroenterol,2018,24(1):87-95.
[10]Soga J,Tazawa K,Aizawa O,et al.Argentaffin cell adenocarcinoma of the stomach:an atypical carcinoid[J]?Cancer,2015,28(4):999-1003.
[11]Segura DI,Montero C.Histochemical characterization of different types of intestinal metaplasia in gastric mucosa[J].Cancer,2015,52(3):498-503.
[12]Chen B,Luo QC,Chen JB,et al.Efficient isolation and proteomic analysis of cell plasma membrane proteins in gastric cancer reveal a novel differentiation and progression related cell surface marker,R-cadherin[J].Tumor Biol,2016,37(9):11775-11787.
[13]Mcm WE.Smooth Muscle Differentiation Control Comes Full Circle:The Circular Noncoding RNA,circ Acta2,Functions as a miRNA Sponge to Fine-Tuneα-SMA Expression[J].Circulation Res,2017,121(6):591-593.
[14]车明文,胡晋平,唐亚为,等.miR-143-3p在人腹膜间皮细胞转分化过程中的作用及机制[J].细胞与分子免疫学杂志,2015,31(4):496-499.
[15]Prunotto M,Bruschi M,Gunning P,et al.Stable incorporation ofα-smooth muscle actin into stress fibers is dependent on specific tropomyosin isoforms[J].Cytoskeleton(Hoboken),2015,72(6):257-267.
[16]Wang X,Li M,Hu M,et al.BAMBI overexpression together withβ-sitosterol ameliorates NSCLC via inhibiting autophagy and inactivating TGF-β/Smad2/3 pathway[J].Oncol Rep,2017,37(5):3046-3054.
[17]Chatterjee A,Mukhopadhyay S,Tung K,et al.Rapamycin-induced G1 cell cycle arrest employs both TGF-βand Rb pathways[J].Cancer Lett,2015,360(2):134-140.
[18]Sundqvist A,Zieba A,Vasilaki E,et al.Specific interactions between Smad proteins and AP-1 components determine TGFβ-induced breast cancer cell invasion[J].Oncogene,2013,32(31):3606-3615.
[19]Huh JW,Lee JH,Kim HR.Expression of p16,p53,and Ki-67 in colorectal adenocarcinoma:a study of 356 surgically resected cases[J].Hepatogastroenterology,2010,57(101):734-740