The Oncogenic lncRNA HOTAIR is not Expressed in the ATRT-MYC-derived Cell Line BT12

Abstract

A typical teratoid Rhabdoid tumor (ATRT) is a highly aggressive pediatric tumor of the brain and spinal cord and is one of the most lethal neoplasms of early neonatal life, with a mortality rate exceeding 75%. Almost 95% of ATRT carry a biallelic SMARCB1 gene mutation. ATRT-MYC subgroup is distinguished by elevated levels of HOX Transcript Antisense Intergenic RNA, or HOTAIR, long non-coding RNA (LncRNA). We hypothesize that HOTAIR may play an epigenetic role in ATRT onset of tumorigenesis. In this study, we investigated the existence of potential interaction between the SMARCB1 and the HOTAIR in the non-tumor HEK-293 line, harboring a wild-type SMARCB1. First, the levels of HOTAIR in the BT-12 cell line were assessed using quantitative realtime PCR (qPCR) relative to the non-tumor HEK-293 line, harboring a wild-type SMARCB1, as a calibrator. In contrast to previous reports, our results showed that the HOTAIR expression level was below the detection limit of the qPCR assay, with a quantification cycle (Cq) of ≥ 40 cycles in the BT-12 cell line. Silencing of HOTAIR in HEK-293 cells using antisense oligonucleotides resulted in a significant 32% reduction in wound healing compared to mock-transfected cells