“…In glioma, the expression of NLK in glioma is inversely related to the glioma grading. NLK may be a useful independent prognostic indicator for glioma (Cui et al, 2011).…”
“…In glioma, the expression of NLK in glioma is inversely related to the glioma grading. NLK may be a useful independent prognostic indicator for glioma (Cui et al, 2011).…”
“…The Wnt/β-catenin signaling is thought to play a critical role in human carcinogenesis, so it is possible that NLK can act as a tumor suppressor by regulating the Wnt/β-catenin pathway. Cui et al (3) found that NLK induced apoptosis in glioma cells via the activation of caspases, and suggested that NLK might be a useful independent prognostic indicator for glioma. Gene therapeutic approaches aimed at upregulating NLK expression could be developed for treatment of glioma.…”
“…17 Clinical data show that NLK expression is significantly associated with the pathologic cancer grade and is correlated with cell proliferation and apoptosis. 29,30 Recently, NLK has been associated with hepatocellular malignant transformation and proliferation. 31 Thus, the precise role of NLK in tumorigenesis is still unclear and warrants further investigation.…”
The DNA damage response (DDR) acts as a protective mechanism for maintaining cell homeostasis. Nemo-like kinase (NLK) is a serine/threonine-protein kinase that has an important role in many pathways; however, its function in the DDR has not yet been defined. In our study, NLK-deficient HCT116 cells were found to be resistant to etoposide-induced cell death. We demonstrated that NLK is required for p53 activation in response to DNA damage. Remarkably, mechanistic studies revealed that NLK interacts with p53 and stabilizes p53 by blocking MDM2-mediated p53 ubiquitination and degradation. Furthermore, NLK enhances p53 activity and affects expression downstream of p53. Interestingly, these functions of NLK are not related to its kinase activity. Consistent with these results, NLK-deficient cells have a resistance effect on DNA damage. Therefore, these findings emphasize that NLK is a novel factor in DDR mechanisms.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.