mProX™ Human SGK1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 Colonic tumor cell proliferation is promoted by SGK1.
The EdU assay was performed on HCT116 cells, and treatment with SGK1 overexpression plasmids (SGK1) and an SGK1 inhibitor (GSK650394) was administered. The cells were subjected to analysis, with the resulting data based on four replicates, and the scale bars for the measurements were set at 200 μm.
Ref: Liang, Xuchun, et al. "Therapeutic inhibition of SGK1 suppresses colorectal cancer." Experimental & molecular medicine 49.11 (2017): e399-e399.
Pubmed: 29170478
DOI: 10.1038/emm.2017.184
Research Highlights
Song, Shuting. et al. "miR-3200 accelerates the growth of liver cancer cells by enhancing Rab7A." Non-coding RNA research, 2023.
Recent studies have shown a close correlation between miR-3200 and tumorigenesis. However, the exact impact of miR-3200 on human hepatocarcinogenesis remains uncertain. Through this research, it has been illustrated that miR-3200 promotes the proliferation of liver cancer cells. These findings highlight the significant role of miR-3200 in the development and progression of liver cancer.
Song, Shuting. et al. "miR-3200 accelerates the growth of liver cancer cells by enhancing Rab7A." Non-coding RNA research, 2023.
Pubmed:
37860266
DOI:
10.1016/j.ncrna.2023.10.005
Mayayo-Peralta, Isabel. et al. "Proteomics on malignant pleural effusions reveals ERα loss in metastatic breast cancer associates with SGK1-NDRG1 deregulation." Molecular oncology, 2023.
Breast cancer (BCa) is a highly heterogeneous disease that affects a large number of individuals. A key factor in the prognosis and treatment of BCa is the status of hormone receptors. The majority of primary tumors are positive for estrogen receptor alpha (ERα), which is crucial in the development and progression of the disease. However, approximately one third of patients with ERα-positive BCa experience relapse and progression to the metastatic stage, with 20% of metastatic cases exhibiting ERα loss after endocrine treatment, termed ERα-conversion. The extent to which ERα-converted cancers resemble true ERα-negative disease and the pathways that drive tumor growth in this context are not fully understood. To gain insight into the molecular changes that occur in metastatic BCa following ERα loss, a (phospho)proteomics analysis was performed on 47 malignant pleural effusions from 37 breast cancer patients, comparing ERα-positive, ERα-converted and ERα-negative cases. The results showed that the loss of ERα-dependency at this advanced stage of the disease results in a partial shift to an ERα-negative molecular profile, while maintaining a luminal-like proteomic landscape. Additionally, a decrease in the activity of several key kinases, including serum/glucocorticoid regulated kinase 1 (SGK1), was observed in ERα-converted metastases. This potential compensatory mechanism for the loss of ERα may offer a new therapeutic target for treating these patients.
Mayayo-Peralta, Isabel. et al. "Proteomics on malignant pleural effusions reveals ERα loss in metastatic breast cancer associates with SGK1-NDRG1 deregulation." Molecular oncology, 2023.
Pubmed:
37854018
DOI:
10.1002/1878-0261.13540
