SOCS1 overexpression

CASC9 overexpression ameliorated the sepsis-induced liver injury, and the probable underlying mechanism may be that CASC9 stabilized the SOCS-1 mRNA by interacting with FUS.

SOCS1 inhibits the progression and chemotherapy resistance of TNBC by regulating GPX4 expression.

This study demonstrated for the first time the association between the T allele of the rs767649 T>A polymorphism in the pre-MIR155 gene and higher expression of miR-155, lower expression of SOCS-1, and swift latent progression in newly diagnosed BC patients. Thus, miR-155 may play a critical role in BC pathogenesis.

Overexpression of SOCS1 has a potent antitumor effect on HNSCC, suggesting the potential for clinical use. The varying effectiveness among cancer cells by over expression of SOCS1 may contribute to efficacy of SOCS 1 gene therapy for clinical use.

SOCS1 gene therapy may be a beneficial approach for the treatment of OSCC.

Co-administration of the STAT3 activator, colivelin, partially abolished the effect of PIAS3 and SOCS1 overexpression in these processes. Therefore, oxidative stress in HCC cells may improve their migration and reduce proliferation through STAT3 activation through the repression of PIAS3 and SOCS1 expression.

BMSC-derived exosomal miR-19b-3p promotes progression of EC through targeting SOCS1. This study provides a novel understanding on molecular mechanisms of EC.

To the best of our knowledge, this is the first article reporting dysregulation of the JAK/STAT pathway in cholesteatoma-adjacent mucosa. The main finding is that important players of the aforementioned pathway are significantly altered, namely SOCS1 is upregulated and STAT5B is downregulated compared with healthy controls.

It was found that enhanced cell proliferation induced by miR‑210‑5p inhibitors was attenuated by the knockdown of SOCS1, while the influences triggered by miR‑210‑5p mimics were reversed by SOCS1 overexpression. Collectively, the present findings provided a novel insight into the crucial regulatory functions of circ_400068 in RCC, and the circ_400068/miR‑210‑5p/SOCS1 axis could be a candidate therapeutic target for the treatment of patients with RCC.

Therefore, MAGI2-AS3 upregulates cytokine signaling 1 by sponging miR-155 to inhibit NSCLC cell proliferation.

The results demonstrate that ROS signal acts as a mediator of the FIR-induced EMT. The data also suggest a potential anti-tumor function of SOCS1 by blocking the FIR therapy-induced resistance through the counter-regulation of ROS generating and scavenging systems.