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Int J Mol Sci. 2015 Mar 24;16(4):6677-93. doi: 10.3390/ijms16046677.

Long noncoding RNA MALAT-1 enhances stem cell-like phenotypes in pancreatic cancer cells.

Jiao F1,2, Hu H3,4, Han T5,6, Yuan C7, Wang L8,9, Jin Z10, Guo Z11, Wang L12,13.

Author information

1
Department of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. jiao_f@outlook.com.
2
Shanghai Key Laboratory of Pancreatic Diseases, Shanghai 201620, China. jiao_f@outlook.com.
3
Department of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. huhai87@126.com.
4
Shanghai Key Laboratory of Pancreatic Diseases, Shanghai 201620, China. huhai87@126.com.
5
Department of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. yyhanwh@163.com.
6
Shanghai Key Laboratory of Pancreatic Diseases, Shanghai 201620, China. yyhanwh@163.com.
7
Department of Pathology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. blkcun@126.com.
8
Department of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. wang_lei744@hotmail.com.
9
Shanghai Key Laboratory of Pancreatic Diseases, Shanghai 201620, China. wang_lei744@hotmail.com.
10
Shanghai Key Laboratory of Pancreatic Diseases, Shanghai 201620, China. jzl920222@126.com.
11
Shanghai Key Laboratory of Pancreatic Diseases, Shanghai 201620, China. guozhenzhen@126.com.
12
Department of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. yzwlw@hotmail.com.
13
Shanghai Key Laboratory of Pancreatic Diseases, Shanghai 201620, China. yzwlw@hotmail.com.

Abstract

Cancer stem cells (CSCs) play a vital role in tumor initiation, progression, metastasis, chemoresistance, and recurrence. The mechanisms that maintain the stemness of these cells remain largely unknown. Our previous study indicated that MALAT-1 may serve as an oncogenic long noncoding RNA in pancreatic cancer by promoting epithelial-mesenchymal transition (EMT) and regulating CSCs markers expression. More significantly, there is emerging evidence that the EMT process may give rise to CSCs, or at least cells with stem cell-like properties. Therefore, we hypothesized that MALAT-1 might enhance stem cell-like phenotypes in pancreatic cancer cells. In this study, our data showed that MALAT-1 could increase the proportion of pancreatic CSCs, maintain self-renewing capacity, decrease the chemosensitivity to anticancer drugs, and accelerate tumor angiogenesis in vitro. In addition, subcutaneous nude mouse xenografts revealed that MALAT-1 could promote tumorigenicity of pancreatic cancer cells in vivo. The underlying mechanisms may involve in increased expression of self-renewal related factors Sox2. Collectively, we for the first time found the potential effects of MALAT-1 on the stem cell-like phenotypes in pancreatic cancer cells, suggesting a novel role of MALAT-1 in tumor stemness, which remains to be fully elucidated.

PMID:
25811929
PMCID:
PMC4424983
DOI:
10.3390/ijms16046677
[Indexed for MEDLINE]
Free PMC Article

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