{Reference Type}: Journal Article
{Title}: Circular ZDHHC11 supports Burkitt lymphoma growth independent of its miR-150 binding capacity.
{Author}: Liu Y;Zhao X;Seitz A;Hooijsma AA;Ravanbakhsh R;Sheveleva S;de Jong D;Koerts J;Dzikiewicz-Krawczyk A;van den Berg A;Ziel-Swier LJYM;Kluiver J;
{Journal}: Sci Rep
{Volume}: 14
{Issue}: 1
{Year}: 2024 04 16
{Factor}: 4.996
{DOI}: 10.1038/s41598-024-59443-3
{Abstract}: We previously showed that MYC promoted Burkitt lymphoma (BL) growth by inhibiting the tumor suppressor miR-150, resulting in release of miR-150 targets MYB and ZDHHC11. The ZDHHC11 gene encodes three different transcripts including a mRNA (pcZDHHC11), a linear long non-coding RNA (lncZDHHC11) and a circular RNA (circZDHHC11). All transcripts contain the same region with 18 miR-150 binding sites. Here we studied the relevance of circZDHHC11, including this miR-150 binding site region, for growth of BL cells. CircZDHHC11 was mainly present in the cytoplasmic fraction in BL cells and its localization was not altered upon miR-150 overexpression. Knockdown of circZDHHC11 caused a strong inhibition of BL growth without affecting the expression levels of MYC, MYB, miR-150 and other genes. Overexpression of circZDHHC11 neither affected cell growth, nor rescued the phenotype induced by miR-150 overexpression. Genomic deletion of the miR-150 binding site region did not affect growth, nor did it change the effect of circZDHHC11 knockdown. This indicated that the miR-150 binding site region is dispensable for the growth promoting role of circZDHHC11. To conclude, our results show that circZDHHC11 is a crucial factor supporting BL cell growth independent of its ability to sponge miR-150.