mProX™ Human SPHK1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Patrick Liam (Creative Biolabs Scientific Support)
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Published Data
Fig.1 Knockdown SPHK1 inhibits cell growth in colorectal cancer cell lines.
Cell number was quantified through the MTT assay, and cell proliferation of SW480 and HCT116 cells was impeded by SphK1 knockdown.
Ref: Long, Jianting, et al. "SphK1 promotes tumor cell migration and invasion in colorectal cancer." Tumor Biology 37 (2016): 6831-6836.
Pubmed: 26662312
DOI: 10.1007/s13277-015-4542-4
Research Highlights
Zhong, Rong-Fang. et al. "Establishment of a prostate cancer prognostic risk model based on the TCGA database and inflammation-related genes." Zhonghua nan ke xue = National journal of andrology, 2022.
This study aims to examine the impact of inflammation-related genes on the likelihood of recovery for individuals with prostate cancer (PCa). A comprehensive literature review was conducted to identify relevant genetic markers and their potential association with prognosis in PCa patients. Data will be collected and analyzed from patient medical records to determine any correlations between specific genetic variants and disease outcomes. Findings from this research have the potential to contribute to the development of personalized treatment approaches for PCa.
Zhong, Rong-Fang. et al. "Establishment of a prostate cancer prognostic risk model based on the TCGA database and inflammation-related genes." Zhonghua nan ke xue = National journal of andrology, 2022.
Pubmed:
37846114
DOI:
No
Epshtein, Yulia. et al. "UCHL1 Regulates Radiation Lung Injury via Sphingosine Kinase-1." Cells, 2023.
In the study, the researchers previously identified the gene GADD45a to play a role in responding to acute lung injury. In GADD45a-/- mice, decreased activity of Akt and increased ubiquitination of Akt were observed due to decreased expression of UCHL1, a deubiquitinating enzyme. Additionally, these mice showed increased susceptibility to radiation-induced lung injury (RILI). Separate research has also suggested a link between RILI and sphingolipids, as evidenced by increased susceptibility in SphK1-/- mice lacking the enzyme sphingosine kinase 1. The study's hypothesis was that UCHL1, which regulates SphK1 ubiquitination, may mediate RILI. Results from experiments on human lung endothelial cells (EC) confirmed increased UCHL1 and SphK1 expression after radiation exposure. Further, ECs transfected with UCHL1-specific siRNA or treated with LDN-5744, a UCHL1 inhibitor, showed decreased SphK1 ubiquitination. The inhibition of UCHL1 also attenuated the increase in EC barrier enhancement typically seen with sphingolipid treatment. In mice, pretreatment with LDN-5744 worsened the severity of RILI. These findings suggest that UCHL1 plays a role in regulating SphK1 expression after radiation and that targeting UCHL1 could potentially be a novel therapeutic approach for RILI.
Epshtein, Yulia. et al. "UCHL1 Regulates Radiation Lung Injury via Sphingosine Kinase-1." Cells, 2023.
Pubmed:
37830619
DOI:
10.3390/cells12192405