Establishment of Hepatocellular Cancer Induced Pluripotent Stem Cells Using a Reprogramming Technique.
- Author:
Han Joon KIM
1
;
Jaemin JEONG
;
Sunhoo PARK
;
Young Woo JIN
;
Seung Sook LEE
;
Seung Bum LEE
;
Dongho CHOI
Author Information
- Publication Type:Original Article
- Keywords: Liver neoplasms; Induced pluripotent stem cells; Reprogramming
- MeSH: Carcinoma, Hepatocellular; Cell Line; Genetic Background; Induced Pluripotent Stem Cells*; Liver Neoplasms*; Pluripotent Stem Cells; Transcription Factors; Zidovudine
- From:Gut and Liver 2017;11(2):261-269
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/AIMS: Cancer is known to be a disease by many factors. However, specific results of reprogramming by pluripotency-related transcription factors remain to be scarcely reported. Here, we verified potential effects of pluripotent-related genes in hepatocellular carcinoma cancer cells. METHODS: To better understand reprogramming of cancer cells in different genetic backgrounds, we used four liver cancer cell lines representing different states of p53 (HepG2, Hep3B, Huh7 and PLC). Retroviral-mediated introduction of reprogramming related genes (KLF4, Oct4, Sox2, and Myc) was used to induce the expression of proteins related to a pluripotent status in liver cancer cells. RESULTS: Hep3B cells (null p53) exhibited a higher efficiency of reprogramming in comparison to the other liver cancer cell lines. The reprogrammed Hep3B cells acquired similar characteristics to pluripotent stem cells. However, loss of stemness in Hep3B-iPCs was detected during continual passage. CONCLUSIONS: We demonstrated that reprogramming was achieved in tumor cells through retroviral induction of genes associated with reprogramming. Interestingly, the reprogrammed pluripotent cancer cells (iPCs) were very different from original cancer cells in terms of colony shape and expressed markers. The induction of pluripotency of liver cancer cells correlated with the status of p53, suggesting that different expression level of p53 in cancer cells may affect their reprogramming.
