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G protein signaling 1 regulator facilitate ovarian cancer development by activating NF-κB signal pathway
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Abstract
Background The RGS1 protein and its regulators are key players in the development of different malignancies. The RGS1 gene was considered as a promising biomarker for ovarian cancer prognosis, and it was hypothesized that it would encourage proliferation via the NF-κB signaling pathway.Methods The data was gathered using the Cancer Genome Atlas (TCGA) database, the Human Protein Atlas (HPA) dataset, and the gene expression omnibus (GEO) database. The role of RGS1 in the development of OC was examined utilizing the CCK-8, EDU, Transwell, real-time PCR, and Western blotting assays. In nude mice, the impact of RGS1 on OC formation was confirmed.Results RGS1 was revealed to be a major determinant of OC prognosis. Functionally, although knockdown of RGS1 had the opposite effects, ectopic expression of RGS1 increased growth capacity in vitro and triggered tumor development in vivo. Additionally, RGS1 suppression caused OC cells to stop in the G1/S phase, which is in line with changes in cell-cycle components. In terms of mechanism, RGS1 knockdown inhibited the NF-κB signaling pathway.Conclusions RGS1 can be a target for cancer treatment since it performed an oncogenic function in the development of OC, in part via controlling the NF-κB signaling pathway.
Research Square Platform LLC
Title: G protein signaling 1 regulator facilitate ovarian cancer development by activating NF-κB signal pathway
Description:
Abstract
Background The RGS1 protein and its regulators are key players in the development of different malignancies.
The RGS1 gene was considered as a promising biomarker for ovarian cancer prognosis, and it was hypothesized that it would encourage proliferation via the NF-κB signaling pathway.
Methods The data was gathered using the Cancer Genome Atlas (TCGA) database, the Human Protein Atlas (HPA) dataset, and the gene expression omnibus (GEO) database.
The role of RGS1 in the development of OC was examined utilizing the CCK-8, EDU, Transwell, real-time PCR, and Western blotting assays.
In nude mice, the impact of RGS1 on OC formation was confirmed.
Results RGS1 was revealed to be a major determinant of OC prognosis.
Functionally, although knockdown of RGS1 had the opposite effects, ectopic expression of RGS1 increased growth capacity in vitro and triggered tumor development in vivo.
Additionally, RGS1 suppression caused OC cells to stop in the G1/S phase, which is in line with changes in cell-cycle components.
In terms of mechanism, RGS1 knockdown inhibited the NF-κB signaling pathway.
Conclusions RGS1 can be a target for cancer treatment since it performed an oncogenic function in the development of OC, in part via controlling the NF-κB signaling pathway.
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