Immunofluorescence was used to observe changes in transforming growth factor β1 (TGF-β1) protein expression levels in the osteosarcoma cells following drug administration.
The study demonstrated that circ_0051079 could act as an oncogene via regulating miR-26a-5p/TGF-β1 and a potential biomarker for osteosarcoma diagnose.
Our findings implied that the novel identified NEAT1/miR-339-5p/TGF-β1 axis might be a new molecular pathway or therapeutic target for OS diagnosis and treatment.
Our results suggest that PDCD5 may attenuate EMT by inhibiting TGF-β1/Smad signaling pathway to inhibit OS metastasis and may be a potential adjuvant genetic therapy for OS.
Serum miRNA-21 may be used to effectively diagnose osteosarcoma and predict the prognosis of the disease. miRNA-21 knockdown inhibited the proliferation of osteosarcoma and promoted the expression of PTEN and TGF-β1 proteins in the osteosarcoma cells.
In conclusion, our study demonstrated that oridonin inhibited EMT and TGF-β1-induced EMT by inhibiting TGF-β1/Smad2/3 signaling pathway in osteosarcoma.
Chimaphilin inhibits human osteosarcoma cell invasion and metastasis through suppressing the TGF-β1-induced epithelial-to-mesenchymal transition markers via PI-3K/Akt, ERK1/2, and Smad signaling pathways.
Our subgroup analysis showed a significant association between IL-6 174G/C and IL-10 1082A/G and OS risk in Asians, while no such significant correlation was observed with TNF-α 308G/A, TNF-α 238G/A, TNF-β 252A/G and TGF-β129T/C polymorphisms.
In addition, targeting TGF-β1 to induce osteogenic differentiation might represent a novel therapeutic strategy to treat osteosarcoma with minimal side effects.
Further results suggested that miR-210 promoted the expression of TGF-β1 and its downstream effectors Snail1 and Slug which were highly elevated in the process of OS dedifferentiation.
Furthermore, the co-culturing with MSC stimulated the migratory capacity of OS via TGFβ1 and IL-6 secretion, and the neutralizing antibody anti-IL-6 impaired this effect.
Targeting miR-29 exhibits significant in vivo and in vitro anti-tumor activities in OS through a novel mechanism resulting in inhibition of TGF-β1 expression and inducing PUMA expression.
We found that miR-202 is overexpressed in osteosarcoma tissues when compared with normal human osteoblasts and TGF-β1 can induce the expression of miR-202.
TGFbeta was found to induce marked elongation of TSP-1 mRNA longevity in osteosarcoma cells when mRNA degradation was assayed in the presence of alpha-amanitin.
Similarly, mRNA levels of TGF beta 1 detected by in situ hybridization were significantly higher (p = 0.04, Fisher's exact test) in high-grade osteosarcoma variants, while no differences were found for TGF beta 2 and -3 mRNA (p = 1.0; p = 0.2, respectively; Fisher's exact test).