SMAD7 overexpression

Overall, our results provide insights into the role of TGF-β-mediated epigenetic regulation in ovarian cancer metastasis and underscore the therapeutic potential of targeting TGF-β signaling and its downstream effectors. Further research is needed to elucidate the underlying mechanisms and validate these therapeutic strategies.

UHRF1 inhibition mitigates vascular endothelial cell injury and ameliorates AS progression in mice by regulating the SMAD7/YAP1 axis.

Pharmacological inhibition of NF-κB signaling decreased IL-12A expression, while blocking the Smad2/3 signaling pathway by overexpression of Smad7 and inhibiting JNK1/2 signaling with a pharmacological inhibitor, SP600125, increased its expression. The elucidated signaling pathways that regulate IL-12A gene expression potentially provide new therapeutic targets to increase IL-12 levels in the tumor microenvironment.

Our findings reveal a mechanism which underlies the contribution of the fSNP rs8085824 on the SMD7 locus to CRC susceptibility.

We demonstrated the high efficacy and resistance to negative TGFβ regulation of EGFR-SMAD7-CAR-T comparable with EGFR-DNR-CAR-T and without the systemic effect of TGFβ inhibition.

In a long-term therapeutic model for mouse dextran sodium sulfate (DSS)-induced colitis, systemic delivery of miR-497a-5p load on super carbonate apatite (sCA) nanoparticle as a vehicle restored epithelial structure of the colonic mucosa and suppressed bowel inflammation compared with negative control miRNA treatment. Our data suggest that sCA-miR-497a-5p may potentially have a therapeutic ability against IBD although further investigation is essential.

RNA-pulldown assay proved that circNDRG1 sponged miR-520h leading to the overexpression of smad7, which was a negative regulatory protein of EMT. Our research revealed that nitroxoline may suppress metastasis in bladder cancer via EGR1/circNDRG1/miR-520h/smad7/EMT signaling pathway.

The overexpression of SMAD7, a target gene of miR-21-5p, reversed the effect of miR-21-5p on curcumol-treated cells. Curcumol inhibited growth of xenograft-tumors and the biological activities of pancreatic cancer cells by regulating the miR-21-5p/SMAD7 axis.

Further mechanism study suggested that SMAD7 promoted T cells activation by decreasing regulatory T cells (Tregs) infiltrating into the tumor microenvironment. In summary, our results proved that tumor cell derived SMAD7 inhibited melanoma lung metastasis by impairing the migration capacity of Tregs.

The present data indicate that SMAD7 contributes to liver carcinogenesis by activating the YAP/NOTCH signaling cascade and by inducing a cholangiocellular and EMT signature.

Lastly, the ectopic overexpression of SMAD7 rescued the suppressive effects of LINC00858 knockdown in CRC cells. Collectively, the results from the present study, to the best of our knowledge, firstly demonstrated a novel LINC00858/miR‑25‑3p/SMAD7 regulatory axis that promoted CRC progression, indicating LINC00858 as a promising therapeutic target for CRC.

MiR-487a-3p is downregulated in pancreatic cancer samples, which is linked to metastasis and prognosis in pancreatic cancer. It inhibits the malignant development of pancreatic cancer by negatively regulating SMAD7.