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. 2022 Jan 31;14(3):749. doi: 10.3390/cancers14030749

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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MALAT1-fusions are abundant and regulate resistance towards androgen receptor inhibition in TRAMP tumor cells. (A) Circos plot showing the most frequently detected gene fusions found in 12 organoid lines derived from three individual TRAMP tumors as well as the TRAMPC1 cell line (n = 13 samples; raw data provided in Supplementary File S1). (B) Lentiviral knockdown of MALAT1 (MALAT1sh) in the TRAMPC1 cell line as shown by qRT-PCR (upper bar graph) leads to downregulation of the AR (lower bar graph) in TRAMPC1 cells on the mRNA level. Values normalized to scrambled control (SCRsh). Representative experiment with three technical replicates shown. (C) Knockdown of MALAT1 causes downregulation of the AR in the protein level in the TRAMPC1 cell line when compared to scrambled control (SCRsh) as shown by representative western blot. Original Western blot can be found at File S1. (D) MALAT1 knockdown sensitizes TRAMPC1 cells to enzalutamide when compared to scrambled control, as seen through lowered relative absorbance in viability assays. Representative experiment with three technical replicates shown.