YY1-induced LncRNA-TUG1 elevates YOD1 to promote cell proliferation and inhibit bortezomib sensitivity in multiple myeloma

Abstract

Taurine upregulated gene 1 (TUG1) has been implicated in the onset and progression of various malignancies. The current study aimed to evaluate the biological function and potential mechanisms of TUG1 in multiple myeloma (MM) progression. TUG1 knockdown in MM cells was investigated in vitro and in vivo to evaluate the role of TUG1. We also predicted the transcription factor (TF) that bound to TUG1 together with the downstream target genes of the TUG1-TF interaction, and evaluated the regulatory mechanism of TUG1 in cell assays. TUG1 knockdown reduced the cell’s proliferative and migratory capabilities while increasing apoptosis and bortezomib sensitivity in vitro and inhibiting tumorigenesis in vivo. TUG1 was found in the nucleus of MM cells and was found to be positively regulated by the TF-YY1. Further in vitro mechanistic investigations indicated that the YY1-TUG1 complex targeted YOD1 to regulate MM progression.

Keywords:

• lncRNA TUG1
• multiple myeloma
• bortezomib
• YOD1

Ethics approval

This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of the Affiliated Hospital of Nantong University.

Author contributions

All authors contributed to the study conception and design. Shaoqing Ju conceived and supervised the study; Qingqing Yin designed the research study; Qingqing Yin, Honglei Xu, Wei Feng and Xiuying Shi performed experiments; Qingqing Yin and Xianjuan Shen analyzed data; Qingqing Yin wrote the paper; Shaoqing Ju made manuscript revisions. All authors read and approved the final manuscript.

Disclosure statement

The authors report there are no competing interests to declare.

Additional information

Funding

This project was supported by the National Nature Science Foundation of China under Grant No.81871720 and No.82072363; and Municipal Science and Technology Plan of Nantong under Grant JCZ20009.