EMT in cervical cancer: Its role in tumour progression and response to therapy

被引:253
作者
Qureshi, Rehana [1 ]
Arora, Himanshu [2 ]
Rizvi, M. A. [1 ]
机构
[1] Jamia Millia Islamia, Dept Biosci, Genome Biol Lab, New Delhi 110025, India
[2] Univ Strasbourg, ESBS API Pole, CNRS, IREBS UMR7242, F-67412 Illkirch Graffenstaden, France
关键词
Epithelial Mesenchymal Transition; Mesenchymal transition (EMT); Therapeutics; Oncogene; Tumour-suppressor; Cervical cancer; EPITHELIAL-MESENCHYMAL TRANSITION; ASTROCYTE-ELEVATED GENE-1; NF-KAPPA-B; GROWTH-FACTOR RECEPTOR; LYMPH-NODE METASTASIS; FUSED TOES HOMOLOG; CELL-MIGRATION; E-CADHERIN; DOWN-REGULATION; MIR-200; FAMILY;
D O I
10.1016/j.canlet.2014.09.021
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The prognosis of cervical patients significantly decreases as the cancer metastasizes to other parts of the body. The epithelial to mesenchymal transition (EMT) plays an important role in cervical cancer progression and metastasis. Recurrence is the primary cause of the increased number of deaths due to cervical cancer. Oncogenes, such as AEG1, Sam-68, FTS and miR-361-5p, induce EMT in cervical cancer. Tumour suppressors, such as LMX-1, SFRP1, klotho, and miR-155, suppress EMT in cervical cancer. Factors such as hypoxia, the radiation dose, cytokines, proteins, transcription factors, and signalling pathways also play an important role in the induction, progression and maintenance of EMT in cervical cancer. Overall, this review describes a wide range of factors with potential roles in EMT that have been identified to date, and this information could be important for the development of new and more effective therapeutics that ameliorate the negative impact of cervical pathogenesis via EMT. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:321 / 331
页数:11
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