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- Title
CD133+ liver cancer stem cells resist interferon-gamma-induced autophagy.
- Authors
Jian Li; Jin-Na Chen; Ting-Ting Zeng; Fan He; Shu-Peng Chen; Stephanie Ma; Jiong Bi; Xiao-Feng Zhu; Xin-Yuan Guan; Li, Jian; Chen, Jin-Na; Zeng, Ting-Ting; He, Fan; Chen, Shu-Peng; Ma, Stephanie; Bi, Jiong; Zhu, Xiao-Feng; Guan, Xin-Yuan
- Abstract
<bold>Background: </bold>Hepatocellular carcinoma (HCC) is one of the most fatal malignancies worldwide, and CD133 is a popular cancer stem cell (CSC) marker for HCC. CD133(+) CSCs have been reported to resist conventional chemo- and radiotherapy, but little is known about their response to immune surveillance. Interferon-gamma (IFN-γ) is one of key cytokines that the immune system produce to eradicate cancer cells, so we investigated the function of IFN-γ on CD133+ HCC CSCs in this study. <bold>Methods: </bold>The response of CD133(+) cells to IFN-γ was performed with functional assays (cell proliferation assay and tumor formation in nude mice), flow cytometry, immunofluorescence staining and RNA interference. <bold>Results: </bold>We found that IFN-γ inhibited the proliferation of cell lines with low percentage of CD133(+) cells (wild-type human cells, BEL7402, QGY7701) but it did not affect the proliferation of cell lines with high percentage of CD133(+) cells (wild-type human cells, Huh7, PLC8024) in vivo and in vitro (nude mice). Flow cytometry analysis demonstrated that the percentage of CD133+ cells increased after IFN-γ treatment of low CD133(+) cell lines. Furthermore, IFN-γ induced the autophagy of low CD133(+) cell lines to decrease proliferation. <bold>Conclusion: </bold>CD133(+) HCC CSCs resisted IFN-γ-induced autophagy, which might also be a mechanism through which CSCs resist immune eradication.
- Subjects
CD antigens; LIVER cancer; CANCER stem cells; INTERFERON gamma; AUTOPHAGY; ANIMAL experimentation; ANTIGENS; CELL lines; CELL physiology; GENES; GLYCOPROTEINS; HEPATOCELLULAR carcinoma; INTERFERONS; LIVER tumors; MICE; PEPTIDES; STEM cells
- Publication
BMC Cancer, 2016, Vol 16, p1
- ISSN
1471-2407
- Publication type
journal article
- DOI
10.1186/s12885-016-2050-6