Epithelial-to-mesenchymal transition (EMT) activation is important in cancer progression and metastasis. Evidence indicates that

nc886

is a representative Pol III gene that processes microRNA products via Dicer and further downregulates its target gene transforming growth factor- β1 (TGF-β1)

which is the most prominent inducer of EMT in prostate cancer (PC). Consistent with the previous literature

we found that

nc886

downregulation was strongly associated with metastatic behavior and showed worse outcomes in PC patients. However

little is known about the association between

nc886

and the EMT signaling pathway. We developed a PC cell model with stable overexpression of

nc886

and found that

nc886

changed cellular morphology and drove MET. The underlying mechanism may be related to its promotion of SNAIL protein degradation via ubiquitination

but not to its neighboring genes

TGFβ-induced protein (

TGFBI

) and

SMAD5

which are Pol II-transcribed. TGF-β1 also override nc886 promotion of MET via transient suppression the transcription of

nc886

promotion of

TGFBI

or increase in SMAD5 phosphorylation. Both

nc886

inhibition and

TGFBI

activation occur regardless of their methylation status. The literature suggests that MYC inhibition by TGF-β1 is attributed to

nc886

downregulation. We incidentally identified MYC-associated zinc finger protein (MAZ) as a suppressive transcription factor of TGFBI

which is controlled by TGF-β1. We elucidate a new mechanism of TGF-β1 differential control of Pol II and the transcription of its neighboring Pol III gene and identify a new EMT unit consisting of

nc886

and its neighboring genes.