SPRY4 and miR-411 mRNA levels correlated with TGF-β1 expression levels in RMS tissues, which was confirmed by immunohistochemical staining for TGF-β1, SPRY4, and phosphorylated p38MAPK proteins.
Taken together, these results suggest that disrupting the TGF-β1 suppression of miR-450b-5p, or knockdown of ENOX2 and PAX9, are effective approaches in inducing RMS MyoD.
These data suggest that chitosan nanoparticle-mediated delivery of an shRNA produces efficient TGFB1 knockdown in rhabdomyosarcoma cells and may be a method of choice for shRNA delivery for gene therapy.
To study the role of the TGF-beta1 autocrine loop in regulating growth and myogenic differentiation in the human rhabdomyosarcoma cell line, RD, an attempt was made to establish a framework for the expression of several components of TGF-beta1/Smad signalling pathway at the mRNA and protein levels by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis in RD cells compared with the normal myoblasts.