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Background  Growing evidence supports the pivotal role of long non-coding RNAs (lncRNAs) in the regulation of cancer development and progression. Their expression patterns and biological function in muscle invasive bladder cancer (MIBC) remain elusive.    Methods  Transcript levels of lncRNA miR-31 host gene ( MIR31HG ) and its splice variants were measured in our MIBC cohort ( n  = 102) by qRT-PCR, and validated in silico by the TCGA cohort ( n  = 370). Kaplan-Meier and multiple Cox regression analysis were conducted to evaluate the survival significance of  MIR31HG  and its splice variants. Functional experiments were performed to examine the proliferation and migration abilities of  MIR31HG  and its splice variants by knockdown approaches.    Results  In this study, a decreased expression of  MIR31HG  was found in bladder cancer cells and tissues, except in the basal subtype. Survival analysis showed that high expression of  MIR31HG  was associated with poor overall survival (OS) and disease-free survival (DFS) in patients with MIBC of basal subtype. Two splice variants of  MIR31HG  lacking exon 1 ( MIR31HGΔE1 ) and exon 3 ( MIR31HGΔE3 ) were identified to have specific expression patterns in different molecular subtypes of our MIBC cohort.  MIR31HGΔE3  was highly expressed in basal subtype tumors. A high expression of  MIR31HGΔE1  and  MIR31HGΔE3  was associated with worse OS and DFS in our cohort. In vitro experiments revealed that knockdown of  MIR31HG  inhibits cell proliferation, colony formation, and migration in bladder cancer. Cell proliferation and migration assays after knockdown of splice variants of  MIR31HG  showed corresponding roles for the full-length transcript.    Conclusions  Our study demonstrates that  MIR31HG  and its splice variants could serve as biomarkers for the classification and prognosis prediction of patients with MIBC.    Supplementary Information  The online version contains supplementary material available at 10.1186/s13046-020-01795-5.

Long noncoding RNA MIR31HG and its splice variants regulate proliferation and migration: prognostic implications for muscle invasive bladder cancer