Evidence map›Paper›PMID 32165494›Full record

ArticleThe Journal of biological chemistry2020

The cytochrome P450 enzyme CYP24A1 increases proliferation of mutant KRAS-dependent lung adenocarcinoma independent of its catalytic activity.

Wei Huang, Paramita Ray, Wenbin Ji, Zhuwen Wang, Derek Nancarrow, Guoan Chen, Stefanie Galbán, Theodore S Lawrence, David G Beer, Alnawaz Rehemtulla and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 10 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

12 authors at 1 institution in 1 country.

Wei HuangDepartment of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109.
Paramita RayDepartment of Radiation Oncology, University of Michigan Medical School, Ann Arbor, Michigan 48109.
Wenbin JiDepartment of Radiation Oncology, University of Michigan Medical School, Ann Arbor, Michigan 48109.
Zhuwen WangDepartment of Surgery, University of Michigan Medical School, Ann Arbor, Michigan 48109.
Derek NancarrowDepartment of Surgery, University of Michigan Medical School, Ann Arbor, Michigan 48109.
Guoan ChenDepartment of Surgery, University of Michigan Medical School, Ann Arbor, Michigan 48109.
Stefanie GalbánDepartment of Radiology, University of Michigan Medical School, Ann Arbor, Michigan 48109.
Theodore S LawrenceDepartment of Radiation Oncology, University of Michigan Medical School, Ann Arbor, Michigan 48109.
David G BeerDepartment of Radiation Oncology, University of Michigan Medical School, Ann Arbor, Michigan 48109; Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan 48109.
Alnawaz RehemtullaDepartment of Radiation Oncology, University of Michigan Medical School, Ann Arbor, Michigan 48109.
Nithya RamnathDepartment of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109; Veterans Administration, Ann Arbor Healthcare System, Ann Arbor, Michigan 48105. Electronic address: nithyar@umich.edu.
Dipankar RayDepartment of Radiation Oncology, University of Michigan Medical School, Ann Arbor, Michigan 48109. Electronic address: dipray@umich.edu.
University of Michigan · US

Funding

Targeting SMURF2 as a novel therapy for EGFR driven tumorsR01CA160981 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RAY, DIPANKAR · 2011 to 2015
$1.4M
The role of Vitamin D metabolism in Non-Small Cell Lung CancerI01CX000333 · VA · VETERANS HEALTH ADMINISTRATION · PI RAMNATH, NITHYA · 2011 to 2012
–
CSRD VA I01 CX000333NCI NIH HHS R01 CA160981
6 · The paper itself

Abstract

We previously reported that overexpression of cytochrome P450 family 24 subfamily A member 1 (CYP24A1) increases lung cancer cell proliferation by activating RAS signaling and that CYP24A1 knockdown inhibits tumor growth. However, the mechanism of CYP24A1-mediated cancer cell proliferation remains unclear. Here, we conducted cell synchronization and biochemical experiments in lung adenocarcinoma cells, revealing a link between CYP24A1 and anaphase-promoting complex (APC), a key cell cycle regulator. We demonstrate that CYP24A1 expression is cell cycle-dependent; it was higher in the G

Indexed as

BiocatalysisMutationAdenocarcinoma of LungCell CycleCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHumansProto-Oncogene Proteins p21(ras)Up-RegulationVitamin D3 24-HydroxylaseKRAS protein, humanProto-Oncogene Proteins p21(ras)Vitamin D3 24-Hydroxylaseanaphase promoting complex (APC)cancerCDC20-homologue 1 (CDH1)cell cyclecell cycle regulationcell division cycle 20 (CDC20)cytochrome P450cytochrome P450 family 24 subfamily A member 1 (CYP24A1)destruction box (D-box)lung adenocarcinomalung cancerRAS GTPaseubiquitin ligaseubiquitylation (ubiquitination)

Identifiers

PMID32165494
PMCPMC7196648
OpenAlexW3012258652

What OpenQuestion holds

Textmetadata
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.