ArticleAmerican journal of translational research2016
Molecular mechanism of prostate cancer cell apoptosis induced by busulfan via adjustment of androgen receptor phosphatization.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 2 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo probe killing effect of busulfan to prostate cancer cell without androgen and the influence of androgen receptor phosphatization and analyze its molecular mechanism.
methodsprostate cancer cell line 22RV1, LAPC4 and LNCaP treated with busulfan under androgen-free condition underwent CCK-8 examination to probe killing ability of the medicine. Flow cytometry was used to check the influence of busulfan on apoptosis rate of prostate cancer cell line LAPC4. Expression level of androgen receptor (AR), Src and Ack1 and change in phosphatization of AR after busulfan treatment were measured by RT-PCR and Western blotting. Finally, influence o proliferation ability and apoptosis of LAPC4 were measured using EGF-busulfan co-processing.
resultsSignificant dose-dependency was observed as killing ability rises with higher busulfan concentration (p<0.05). Significant improvement in prostate cancer cell inhibition ability of busulfan was also observed with prolonging of time (p<0.05). Then we discovered, as indicated by flow cytometry, that busulfan inhibits prostate cancer cell LAPC4 proliferation by strengthening its apoptosis (p<0.05), which showed significant dose- and time-dependency. Detection of AR expression and phosphatization level showed no significant influence on mRNA and protein expression level of AR made by busulfan. However, decline of phosphatization level at AR Y534 site was positively related to busulfan treatment time. Busulfan was found to be inhibitory to Src kinase induced by EGF and level of resulting AR phosphatization in our further probe into the mechanism of busulfan influence on phosphatization level at AR Y534 site. Nude mice experiment indicated that busulfan was inhibitory to protein expression of AR downstream target gene prostate specific antigen (PSA) and human tissue kallikrein2 (hk-2), thus inhibited in vivo tumorigenic ability of prostate cancer cells.
conclusionBusulfan was significantly inhibitory to prostate cancer cell proliferation by inhibiting phosphatization of Src kinase at AR Y534 site.
Indexed as
Identifiers
27904688PMC5126330W2560635870What 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.