Cancer stem cells with increased metastatic potential as a therapeutic target for esophageal cancer

被引:61
作者
Wang, D. [1 ,2 ,3 ]
Plukker, J. Th. M. [3 ]
Coppes, R. P. [1 ,2 ]
机构
[1] Univ Groningen, Univ Med Ctr Groningen, Dept Cell Biol, NL-9700 RB Groningen, Netherlands
[2] Univ Groningen, Univ Med Ctr Groningen, Dept Radiat Oncol, NL-9700 RB Groningen, Netherlands
[3] Univ Groningen, Univ Med Ctr Groningen, Dept Surg, NL-9700 RB Groningen, Netherlands
关键词
Cancer stem cells; Metastases and esophageal cancer; EPITHELIAL-MESENCHYMAL TRANSITION; ACUTE MYELOID-LEUKEMIA; PROGNOSTIC VALUE; POOR-PROGNOSIS; SOX2; PROMOTES; TUMOR-GROWTH; EXPRESSION; CARCINOMA; AUTOPHAGY; HYPOXIA;
D O I
10.1016/j.semcancer.2017.03.010
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Esophageal cancers (EC) are highly aggressive tumors, commonly presented in a locally advanced stage with a poor prognosis and survival. Up to 50% of the patients are eligible for treatment with curative intent and receive the standard treatment with neoadjuvant chemoradiotherapy (nCRT) and surgery. Currently, pathologic complete response to nCRT is 20-30%, with a partial or no response in about 50% and 20%, respectively. EC recurrences occur frequently even after successful anti-cancer treatment, suggesting high aggressiveness with increased metastatic potential. A tumor sub-population of so-called cancer stem cells (CSCs), is known to display a high metastatic potential and resistance to conventional anti-cancer therapy, hereby being responsible for the unbeneficial clinical features. In this review, a concise overview will be given of the current literature on esophageal CSCs and related metastases. Esophageal CSC markers will be discussed followed by the pathways that initiate and sustain these cells. In addition, the cellular processes, epithelial-mesenchymal transition (EMT), hypoxia and autophagy, known to contribute to cancer stemness and metastasis will be explained. Finally, potential options for treatment also related to cancer genome atlas (TCGA) data on EC will be discussed.
引用
收藏
页码:60 / 66
页数:7
相关论文
共 112 条
[1]   Prognostic relevance of autophagy markers LC3B and p62 in esophageal adenocarcinomas [J].
Adams, Olivia ;
Dislich, Bastian ;
Berezowska, Sabina ;
Schlafli, Anna M. ;
Seiler, Christian A. ;
Kroell, Dino ;
Tschan, Mario P. ;
Langer, Rupert .
ONCOTARGET, 2016, 7 (26) :39241-39255
[2]   ALDH-1 expression levels predict response or resistance to preoperative chemoradiation in resectable esophageal cancer patients [J].
Ajani, J. A. ;
Wang, X. ;
Song, S. ;
Suzuki, A. ;
Taketa, T. ;
Sudo, K. ;
Wadhwa, R. ;
Hofstetter, W. L. ;
Komaki, R. ;
Maru, D. M. ;
Lee, J. H. ;
Bhutani, M. S. ;
Weston, B. ;
Baladandayuthapani, V. ;
Yao, Y. ;
Honjo, S. ;
Scott, A. W. ;
Skinner, H. D. ;
Johnson, R. L. ;
Berry, D. .
MOLECULAR ONCOLOGY, 2014, 8 (01) :142-149
[3]   A New Method for Identifying Stem-Like Cells in Esophageal Cancer Cell Lines [J].
Almanaa, Taghreed N. ;
Geusz, Michael E. ;
Jamasbi, Roudabeh J. .
JOURNAL OF CANCER, 2013, 4 (07) :536-548
[4]  
[Anonymous], J CANC RES CLIN ONCO
[5]   Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell [J].
Bonnet, D ;
Dick, JE .
NATURE MEDICINE, 1997, 3 (07) :730-737
[6]  
Böttger TG, 1998, CANCER-AM CANCER SOC, V83, P1074, DOI 10.1002/(SICI)1097-0142(19980915)83:6<1074::AID-CNCR4>3.0.CO
[7]  
2-8
[8]   TGF-β1 induces epigenetic silence of TIP30 to promote tumor metastasis in esophageal carcinoma [J].
Bu, Fangfang ;
Liu, Xing ;
Li, Jingjing ;
Chen, Shukun ;
Tong, Xin ;
Ma, Chunsheng ;
Mao, Hui ;
Pan, Fei ;
Li, Xiaoyan ;
Chen, Bo ;
Xu, Liyan ;
Li, Enmin ;
Kou, Geng ;
Han, Jun ;
Guo, Shangjing ;
Zhao, Jian ;
Guo, Yajun .
ONCOTARGET, 2015, 6 (04) :2120-2133
[9]   The hypoxic microenvironment: A determinant of cancer stem cell evolution [J].
Carnero, Amancio ;
Lleonart, Matilde .
BIOESSAYS, 2016, 38 :S65-S74
[10]   Interleukin-23 promotes the epithelial-mesenchymal transition of oesophageal carcinoma cells via the Wnt/β-catenin pathway [J].
Chen, Deyu ;
Li, Wei ;
Liu, Shenzha ;
Su, Yuting ;
Han, Guohu ;
Xu, Chenchen ;
Liu, Hongli ;
Zheng, Tingting ;
Zhou, Yuepeng ;
Mao, Chaoming .
SCIENTIFIC REPORTS, 2015, 5