Evidence map›Paper›PMID 31428587›Full record

ArticleFrontiers in oncology2019

LSD1 Activates PI3K/AKT Signaling Through Regulating p85 Expression in Prostate Cancer Cells.

Zifeng Wang, Shuai Gao, Dong Han, Wanting Han, Muqing Li, Changmeng Cai

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Zifeng WangCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Shuai GaoCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Dong HanCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Wanting HanCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Muqing LiCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
Changmeng CaiCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA, United States.
University of Massachusetts Boston · US

Funding

Study the Mechanism of Retinoblastoma Protein Mediated Androgen Receptor Transcriptional Repression Activity on DNA ReplicationR01CA211350 · NCI · UNIVERSITY OF MASSACHUSETTS BOSTON · PI CAI, CHANGMENG · 2017 to 2021
$1.7M
Molecular basis of androgen receptor mediated gene transcriptional repressionR00CA166507 · NCI · UNIVERSITY OF MASSACHUSETTS BOSTON · PI CAI, CHANGMENG · 2015 to 2017
$726k
NCI NIH HHS R00 CA166507NCI NIH HHS R01 CA211350
6 · The paper itself

Abstract

Lysine specific demethylase 1 (LSD1) functions as a transcriptional repressor through demethylating active histone marks such as mono- or di-methylated histone 3 lysine 4 (H3K4) and interacting with histone deacetylases. However, LSD1 can also act as an activator through demethylating repressive histone marks and possibly non-histone proteins. In prostate cancer (PCa) cells, LSD1 mediates the transcriptional activity of androgen receptor (AR), a ligand dependent nuclear transcription factor that drives PCa initiation and progression to the castration-resistant prostate cancer (CRPC). However, it is unclear whether LSD1 also regulates other growth promoting pathways independent of AR signaling in PCa cells. In this study, we show that LSD1 can activate PI3K/AKT pathways in absence of androgen stimulation, and we further demonstrate that LSD1 transcriptionally regulates the expression of PI3K regulatory subunit, p85, possibly through epigenetic reprogramming of enhancer landscape in PCa cells. Our study suggests that LSD1 has dual functions in promoting PCa development, that it enhances AR signaling through its coactivator function, and that it activates PI3K/AKT signaling through increasing p85 gene expression.

Indexed as

AKTandrogen-deprivation therapyKDM1ALSD1p85PI3KPI3K regulatory subunitsprostate cancer

Identifiers

PMID31428587
PMCPMC6688199
OpenAlexW2962717375

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.