{'fraction_non_alphanumeric': 0.020335985853227233, 'fraction_numerical': 0.022104332449160036, 'mean_word_length': 5.185792349726776, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Induction of p53-Dependent Apoptosis in HCT116 Tumor Cells by RNA Viruses and Possible Implications in Virus-Mediated Oncolysis

Recent findings showed that type I interferons (IFN-?/?) induce the transcription of tumor suppressor p53 and sensitize primary mouse embryonic fibroblasts (MEFs) to p53-mediated apoptosis by oncolytic viruses. However, the ability of RNA viruses to induce a p53-mediated apoptotic response may differ between primary and tumor cells and may be dependent upon the virus type. We have investigated this hypothesis by analyzing the apoptotic effects of various oncolytic viruses on the human colon carcinoma HCT116 cells and their derivatives lacking either p53 or bax gene. We show that HCT116 cells are resistant to the apoptotic effects of vesicular stomatitis virus, reovirus or poliovirus but activate the p53/Bax apoptotic pathway after infection with Sendai virus. These data substantiate the role of p53 in virus-mediated apoptosis and show that, unlike primary cells, tumor cells may be more selective in the activation of p53 pathway in response to the infection with specific types of viruses.