RT Journal
A1 Zhang, Lei
A1 He, Anshun
A1 Chen, Bohan
A1 Bi, Jinfang
A1 Chen, Jun
A1 Guo, Dianhao
A1 Qian, Yuyang
A1 Wang, Wenbin
A1 Shi, Tengfei
A1 Zhao, Zhongfang
A1 Shi, Jiandang
A1 An, Woojin
A1 Attenello, Frank
A1 Lu, Wange
T1 A HOTAIR regulatory element modulates glioma cell sensitivity to temozolomide through long-range regulation of multiple target genes
JF Genome Research 
JO Genome Research 
YR 2020 
FD February 01 
VO 30 
IS 2 
SP 155 
OP 163 
DO 10.1101/gr.251058.119 
UL http://genome.cshlp.org/content/30/2/155.abstract 
AB Temozolomide (TMZ) is a frequently used chemotherapy for glioma; however, chemoresistance is a major problem limiting its effectiveness. Thus, knowledge of mechanisms underlying this outcome could improve patient prognosis. Here, we report that deletion of a regulatory element in the HOTAIR locus increases glioma cell sensitivity to TMZ and alters transcription of multiple genes. Analysis of a combination of RNA-seq, Capture Hi-C, and patient survival data suggests that CALCOCO1 and ZC3H10 are target genes repressed by the HOTAIR regulatory element and that both function in regulating glioma cell sensitivity to TMZ. Rescue experiments and 3C data confirmed this hypothesis. We propose a new regulatory mechanism governing glioma cell TMZ sensitivity.