WT-CLS1 is a rhabdoid tumor cell line and can be inhibited by miR-16

Emily Kunce Stroup, Yunku Yeu, Albert Budhipramono, Tae Hyun Hwang, Dinesh Rakheja, Anat Erdreich-Epstein, Theodore W. Laetsch, James F. Amatruda, Kenneth S. Chen

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


Background: Wilms tumor and rhabdoid tumor can have similar clinical presentations, but they have distinct histological and biological features. For instance, Wilms tumors commonly bear mutations in kidney differentiation or microRNA processing genes, whereas rhabdoid tumor is characterized by loss of SMARCB1. Aims: We initially set out to characterize and identify tumor suppressor microRNAs in WT-CLS1, which had been described as a Wilms tumor cell line. Methods and Results: We characterized the cell line WT-CLS1 by whole exome sequencing, RNA-seq, and xenograft histology. We measured the effect of microRNA overexpression on WiT49, WT-CLS1, BT-12, and CHLA-06-ATRT. We found that miR-16 significantly impairs cell proliferation in WT-CLS1 by repressing numerous cell cycle genes, including the D-type cyclins. In addition, we found that the WT-CLS1 cell line demonstrates the classic histological, mutational, and transcriptional hallmarks of rhabdoid tumor, including SMARCB1 loss. Lastly, miR-16 also represses cell cycle genes and impairs proliferation in the BT-12 and CHLA-06-ATRT rhabdoid tumor cell lines. Conclusions: The loss of SMARCB1 warrants reclassification of WT-CLS1 as rhabdoid tumor. Overexpression of miR-16 significantly abrogates proliferation of WT-CLS1 and other rhabdoid tumor cell lines. Further studies are necessary to gain insight into the potential for miR-16 to be a tumor suppressor or a novel therapeutic in rhabdoid tumor.

Original languageEnglish (US)
Article numbere1110
JournalCancer Reports
Issue number3
StatePublished - Jun 2019


  • WT-CLS1
  • miR-16
  • rhabdoid tumor

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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