mProX™ Human AURKA Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 hnRNP K is required for AURKA to activate MYC transcription and enhance BCSC phenotype.
HA-tagged AURKA overexpressed in MDA-MB-231 cells was transfected using NCsiRNA or hnRNP K. Cells were transfected with pRL-TK for an additional 24 hours along with either the basic reporter (Vec) or the MYC promoter reporter (MYC).
Ref: Zheng, Feimeng, et al. "Nuclear AURKA acquires kinase-independent transactivating function to enhance breast cancer stem cell phenotype." Nature communications 7.1 (2016): 10180.
Pubmed: 26782714
DOI: 10.1038/ncomms10180
Research Highlights
Preclinical research has been conducted on several AURKA inhibitors (AKIs), and a number of them have undergone clinical trials either as monotherapies or in conjunction with conventional chemotherapy or other targeted therapies.
Du, Ruijuan, et al. "Targeting AURKA in Cancer: molecular mechanisms and opportunities for Cancer therapy." Molecular cancer 20 (2021): 1-27.
Pubmed:
33451333
DOI:
10.1186/s12943-020-01305-3
These results uncover a hitherto unidentified carcinogenic characteristic of the spatially dysregulated AURKA in carcinogenesis and offer a possible treatment avenue to overcome kinase inhibitor resistance.
Zheng, Feimeng, et al. "Nuclear AURKA acquires kinase-independent transactivating function to enhance breast cancer stem cell phenotype." Nature communications 7.1 (2016): 10180.
Pubmed:
26782714
DOI:
10.1038/ncomms10180