{'fraction_non_alphanumeric': 0.04204753199268738, 'fraction_numerical': 0.029859841560024376, 'mean_word_length': 5.870292887029288, '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}}
Malignant rhabdoid tumor shows incomplete neural characteristics as revealed by expression of SNARE complex

To elucidate the biological differences in neural phenotype between malignant rhabdoid tumor (MRT) and neuroblastoma cell lines, we examined the expression of solube N‐ethylmaleimide‐sensitive fusion protein attachment protein receptor (SNARE) complex proteins in MRT cell lines under differentiation induction with 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA). Six MRT cell lines (TM87‐16, STM91‐01, TTC642, TTC549, YAM‐RTK1, and TTC1240) and six neuroblastoma cell lines (IMR‐32, NH12, SCCH26, TGW, NB‐1, and NB‐NR) were used in this study. Expression of SNAREs: the vesicle SNARE (synaptotagmin, synaptophysin, and synaptobrevin‐2) and the target SNARE (syntaxin 1A, SNAP‐25A/B) was examined. Our results showed that in MRT cells, only two cell lines (TM87‐16, TTC642) expressed the vesicle SNARE and the target SNARE with the exception of SNAP‐25B, while all neuroblastoma cells expressed the entire SNARE complex. During differentiation, synaptotagmin was upregulated in these two MRT cell lines. Interestingly, synaptophysin was downregulated in these MRT cell lines in contrast with the neuroblastoma cell lines. SNAP‐25B was not expressed in MRT cells after differentiation with TPA. MRT cells having a neural phenotype morphologically looked like neuroblastoma cells after treatment with TPA. However, the expression of SNARE complex was incomplete in MRT cells. Our results suggest that the biological characteristics of MRT cells with neural phenotype are distinct from those of neuroblastoma cells. © 2002 Wiley‐Liss, Inc.