ArticleInternational journal of clinical and experimental pathology2018
PKCδ reveals a tumor promoter function by promoting cell proliferation and migration in somatotropinomas.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Regulation of pro-apoptotic and anti-apoptotic factors in obesity-related esophageal adenocarcinoma.Molecular biology reports · 2024Article
- The miR-19a/Cylindromatosis Axis Regulates Pituitary Adenoma Bone Invasion by Promoting Osteoclast Differentiation.Cancers · 2024Article
- PKCθ Regulates Pituitary Adenoma Bone Invasion by Activating Osteoclast in NF-κB/IL-1β-Dependent Manner.Cancers · 2023Article
- Inhibition of protein kinase C isozymes causes immune profile alteration and possibly decreased tumorigenesis in bladder cancer.American journal of cancer research · 2023Article
- PLOD3 regulates the expression of YAP1 to affect the progression of non-small cell lung cancer via the PKCδ/CDK1/LIMD1 signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Functional proteomic analysis reveals roles for PKCδ in regulation of cell survival and cell death: Implications for cancer pathogenesis and therapy.Advances in biological regulation · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein kinase C δ (PKCδ), a subtype of PKC family, has been recognized as a tumor promoter or suppressor depending on different tissue specificities in various tumor types. However, the effects of PKCδ on somatotropinomas are poorly understood. This study aims to explore the precise role of PKCδ in promoting tumor progression in somatotropinomas. In the present study, we examined the expression levels of PKCδ in clinical specimens of human somatotropinomas to show that PKCδ overexpression correlated with invasive properties of somatotropinomas. Furthermore, we employed rat anterior pituitary GH3 cells as the experiment model to demonstrate that PKCδ activation by PKC agonist (Phorbol-12-myristate-13-acetate, PMA) significantly promoted the proliferation and migration potential of GH3 cells, and these effects could be abolished following PKCδ inhibition by specific inhibitor Rottlerin. Mechanistically, PKCδ activated ERK1/2 signaling, which was responsible for PKCδ-induced promotion of GH3 cell proliferation and migration. Taken together, our results indicated that PKCδ functions as a tumor promoter by promoting cell proliferation and migration in somatotropinomas.
Indexed as
Identifiers
31938102PMC6957976W3011058103What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.