Yang Liu, Levi Edi, Zhu Shunshi, Du Jianhua, Majumdar Adhip P N
Department of Gastroenterology, The Ninth People's Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200011, China,
J Gastrointest Cancer. 2013 Dec;44(4):428-35. doi: 10.1007/s12029-013-9534-2.
Gastric carcinogenesis is a multistep process, involving multiple molecular alterations, including changes in cancer stem cells (CSCs). The present investigation was undertaken to determine whether changes in cancer stem cells could be utilized as a marker of progression of gastric carcinogenesis by examining the expression of gastric CSCs at different stages of carcinogenesis.
Ninety-three cases with 31 in each group of chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG), or gastric cancer (GC) were analyzed immunohistochemically for proliferating cell nuclear antigen (PCNA) and Bcl-xl as biomarkers of proliferation and apoptosis, respectively, and CD44, CD166, and LGR5 levels by qRT-PCR as markers of gastric CSCs. Additionally, the levels of P53 and phosphorylated form of epidermal growth factor receptor (p-EGFR) were examined.
While the levels of each of these biomarkers were found to be low to moderate in CSG and CAG patients, they were markedly increased in GC patients, in whom co-expression of CD44 with LGR5 and CD166 with p-EGFR was found to be the highest. We have also observed that although the expression of different CSC markers as well as the levels of p-EGFR were increased in precancerous lesions (CSG and CAG), they are further augmented in GC suggesting that they may play a pivotal role in the development and progression of gastric cancer.
Our observations suggest that the progression to gastric carcinogenesis from preneoplastic lesions such as superficial gastritis and chronic atrophic gastritis is associated with induction of CSCs together with increase in cell proliferation and inhibition of apoptosis.
胃癌发生是一个多步骤过程,涉及多种分子改变,包括癌症干细胞(CSCs)的变化。本研究旨在通过检测胃癌发生不同阶段胃CSCs的表达,确定癌症干细胞的变化是否可作为胃癌发生进展的标志物。
对93例患者进行分析,其中慢性浅表性胃炎(CSG)、慢性萎缩性胃炎(CAG)或胃癌(GC)每组各31例。分别采用免疫组化法检测增殖细胞核抗原(PCNA)和Bcl-xl作为增殖和凋亡的生物标志物,通过qRT-PCR检测CD44、CD166和LGR5水平作为胃CSCs的标志物。此外,检测P53和表皮生长因子受体磷酸化形式(p-EGFR)的水平。
虽然在CSG和CAG患者中这些生物标志物的水平均为低至中度,但在GC患者中显著升高,其中发现CD44与LGR5以及CD166与p-EGFR的共表达最高。我们还观察到,尽管癌前病变(CSG和CAG)中不同CSC标志物的表达以及p-EGFR水平均升高,但在GC中进一步升高,这表明它们可能在胃癌的发生和进展中起关键作用。
我们的观察结果表明,从浅表性胃炎和慢性萎缩性胃炎等癌前病变进展为胃癌与CSCs的诱导以及细胞增殖增加和凋亡抑制有关。