ArticleAmerican journal of translational research2015
Normal peripheral prostate stromal cells stimulate prostate cancer development: roles of c-kit signal.
Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Comparative Pathobiology of Canine and Human Prostate Cancer: State of the Art and Future Directions.Cancers · 2022Review
- The Effects of Resveratrol on Prostate Cancer through Targeting the Tumor Microenvironment.Journal of xenobiotics · 2021Review
- Investigation of c-KIT and Ki67 expression in normal, preneoplastic and neoplastic canine prostate.BMC veterinary research · 2017Article
- Role of prostatic interstitial cells in prostate motility.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo investigated the peripheral stromal cell conditioned medium (CM) -stimulated c-kit-JAK2-STAT1 pathway in prostate cancer.
methodsCM harvested from normal prostate peripheral stromal cells was added to DU145 cells. DU145 cell viability and migration were measured by cell counting kit-8 reagent and Transwell analysis respectively. Colony and sphere formation efficiencies of DU145 cells co-cultured with CM from human prostate stromal cells were also measured. DU145cells were stably transfected with lentivirus-mediated shRNA for c-kit silencing.
resultsC-kit expression in prostate cancer was found to be significantly higher than in benign prostatic hyperplasia and positively associated with Gleason scores. The growth, migration and capacity of clonogenic property of DU145 cells significantly increased upon exposure to peripheral stromal CM and then were inhibited after silencing the expression of c-kit. The levels of c-kit, pJAK2 and pSTAT1 were significantly induced by peripheral zone stromal CM compared with controls in serum free medium and the levels of pJAK2 and pSTAT1 decreased after c-kit silencing.
conclusionsC-kit hyper-expression promotes the development of prostate cancer. The peripheral stromal cell CM stimulated c-kit-JAK2-STAT1 pathway in prostate cancer cell viability, migration, and capacity of clonogenic property. This may lead to a greater understanding of the role of c-kit in prostate cancer and provide a potential therapeutic target for prostate cancer.
Indexed as
Identifiers
26045890PMC4448190W643528344What 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.