Data from: MFSD12, transcriptionally regulated by PLAGL2, promotes bladder cancer progression

Bladder cancer (BLCA) is one of the most common malignant tumors of the
urinary system. Identification of novel molecular signaling targets for
the tumorigenesis of BLCA is important. Data from the Gene Expression
Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases suggest that
major facilitator superfamily domain containing 12 (MFSD12) may act as an
important oncogene in BLCA. MFSD12 expression is confirmed to be elevated
in BLCA patients. Genetic manipulation of MFSD12 mediated by Tet-inducible
lentiviral expression vector is conducted in two BLCA cell lines,
including UMUC3 and 5637. Following this manipulation, the cells are
subjected to treatment with or without doxycycline. Our results show that
MFSD12 knockdown inhibits cell proliferation, migration, and invasion, and
arrests the G1 stage-induced cell cycle. Furthermore, silencing of MFSD12
reduces lung metastatic lesions and xenografted tumor formation of BLCA
cells. To further explore the effect of MFSD12 on BLCA cells,
transcriptomics and metabolomics analyses are performed on
MFSD12-overexpressing cells. Subsequently, luciferase reporters and
chromatin immunoprecipitation (ChIP)-PCR assays reveal that MFSD12 is
regulated positively by pleomorphic adenoma gene like-2 (PLAGL2), an
important transcription factor. Collectively, our results indicate that
MFSD12 exerts a tumor-promoting effect on BLCA progression, under the
modulation of transcription factor PLAGL2.