Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 472, Issue 4, Pages 643-647Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.03.004
Keywords
Cancer stem cell; Gynecologic cancer; MAPK13; Tumor-initiation
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Health and Labour Sciences Research Grants
- Ono Cancer Research Fund
- Sagawa Foundation for Promotion of Cancer Research
- Suharakinenzaidan Co., Ltd.
- Kobayashi foundation for cancer research
- Northern Advancement Center for Science & Technology of Hokkaido Japan
- Grants-in-Aid for Scientific Research [15H04722] Funding Source: KAKEN
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Cancer stem-like cells (CSCs)/cancer-initiating cells (CICs) are defined as small subpopulation of cancer cells that are endowed with higher tumor-initiating ability. CSCs/CICs are resistant to standard cancer therapies including chemotherapy and radiotherapy, and they are thus thought to be responsible for cancer recurrence and metastasis. Therefore, elucidation of molecular mechanisms of CSCs/CICs is essential to cure cancer. In this study, we analyzed the gene expression profiles of gynecological CSCs/CICs isolated as aldehyde dehydrogenase high (ALDH(high)) cells, and found that MAPK13, PTTG1IP, CAPN1 and UBQLN2 were preferentially expressed in CSCs/CICs. MAPK13 is expressed in uterine, ovary, stomach, colon, liver and kidney cancer tissues at higher levels compared with adjacent normal tissues. MAPK13 gene knockdown using siRNA reduced the ALDH(high) population and abrogated the tumor-initiating ability. These results indicate that MAPK13 is expressed in gynecological CSCs/CICs and has roles in the maintenance of CSCs/CICs and tumor-initiating ability, and MAPK13 might be a novel molecular target for treatment-resistant CSCs/CICs. (C) 2016 Elsevier Inc. All rights reserved.
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