mProX™ Human PKN3 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
To download a Certificate of Analysis, please enter a lot number in the search box below. Note: Certificate of Analysis not available for kit components.
Lot Number
Made to Order Inquiry
InquiryProduct Information
Product Properties
Protocols
Please visit our protocols page.
Customer Reviews
There are currently no Customer reviews or questions for mProX™ Human PKN3 Stable Cell Line (S01YF-1023-PY75). Click the button above to contact us or submit your feedback about this product.
Cameron Miller (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Cameron Brown (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 Primary tumor growth and metastasis are facilitated by the mediation of PKN3 in an orthotopic mouse model of prostate cancer.
Stably engineered C-3 cells for Dox-dependent expression of PKN3, p110β, or control shRNAs were cultivated in the presence or absence of Dox (250 ng/ml) for 72 hours, and subsequent analyses were conducted via immunoblotting using the indicated antibodies, with Akt expression employed as a loading control. Subsequently, stable PC-3 cells expressing shRNAs targeting PKN3 (represented by orange bars), p110β (represented by blue bars), or PC-3 control cells (represented by white bars) were intraprostatically transplanted into nude mice. Two groups of animals were administered either Dox (+) or standard food without Dox (−) (consisting of 7 animals per cohort). Following 49 days, the mice were euthanized and subjected to primary tumor development evaluation, with the mean tumor volume ± S.E. being represented by each bar.
Ref: Unsal-Kacmaz, Keziban, et al. "The interaction of PKN3 with RhoC promotes malignant growth." Molecular oncology 6.3 (2012): 284-298.
Pubmed: 22217540
DOI: 10.1016/j.molonc.2011.12.001
Research Highlights
Chu, Nan. et al. "ANP promotes HTR-8/SVneo cell invasion by upregulating protein kinase N 3 via autophagy inhibition." FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2023.
Preeclampsia is a gestational disease caused by shallow trophoblast invasion and impaired spiral artery remodeling. The involvement of atrial natriuretic peptide (ANP) in regulating blood pressure has been linked to the pathogenesis of preeclampsia. However, the precise mechanism by which ANP affects trophoblast function is unknown. In this study, researchers identified Protein Kinase 3 (PKN3) as a downstream factor of ANP in HTR-8/SVneo cells, which was found to be downregulated in preeclamptic placenta. Through isobaric tags for relative and absolute quantification (iTRAQ) experiments, the research team also determined that ANP treatment in HTR-8/SVneo cells upregulated PKN3 by promoting the transcription factor NFYA, which was confirmed by chromatin immunoprecipitation analysis and luciferase assays. Using transmission electron microscopy and Western Blotting, the study further revealed that ANP inhibits autophagy through the AMPK-mTORC1 signaling pathway, while preeclamptic placenta displayed excessive autophagy. Additionally, ANP was found to enhance trophoblast invasion through upregulation of PKN3 via NFYA promotion and inhibition of autophagy in an AMPK/mTORC1 signaling-dependent manner. These findings provide evidence that ANP plays a crucial role in the regulation of trophoblast function and may contribute to the development of preeclampsia.
Chu, Nan. et al. "ANP promotes HTR-8/SVneo cell invasion by upregulating protein kinase N 3 via autophagy inhibition." FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2023.
Pubmed:
36723798
DOI:
10.1096/fj.202200833RRR
Temme, Louisa. et al. "PKN3: a target in cancer metastasis." Nature reviews. Drug discovery, 2022.
This article is about the role and potential of PKN3, a protein kinase, as an anticancer drug target. It reviews the evidence that PKN3 is involved in cancer processes such as metastasis and neovascularization, and that its inhibition could have therapeutic benefits. It also describes some of the existing chemical tool inhibitors for PKN3, such as Atu027, JZ128 and UNC-CA94, and their modes of action.
Temme, Louisa. et al. "PKN3: a target in cancer metastasis." Nature reviews. Drug discovery, 2022.
Pubmed:
36104477
DOI:
10.1038/d41573-022-00154-7
