Evidence map›Paper›PMID 24858037›Full record

ArticleOncogene2014

Loss of presenilin 2 is associated with increased iPLA2 activity and lung tumor development.

H-M Yun, M H Park, D H Kim, Y J Ahn, K-R Park, T M Kim, N Y Yun, Y S Jung, D Y Hwang, D Y Yoon and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  15. The phospholipase AJournal of lipid research · 2018
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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 3 institutions in 1 country.

H-M YunCollege of Pharmacy and Medical Research Center, Chungbuk National University, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
M H ParkCollege of Pharmacy and Medical Research Center, Chungbuk National University, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
D H KimCollege of Pharmacy and Medical Research Center, Chungbuk National University, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
Y J AhnCollege of Pharmacy and Medical Research Center, Chungbuk National University, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
K-R ParkCollege of Pharmacy and Medical Research Center, Chungbuk National University, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
T M KimCollege of Veterinary Medicine, Chungbuk National University, 12, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
N Y YunCollege of Pharmacy and Medical Research Center, Chungbuk National University, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
Y S JungCollege of Pharmacy, Pusan National University, San 30, Jangjeon-dong, Geumjeung-gu, Busan, Republic of Korea.
D Y HwangDepartment of Biomaterial Science, Pusan National University, Miryang, Kyungnam, Republic of Korea.
D Y YoonDepartment of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Gwangjin-gu, Seoul, Republic of Korea.
S B HanCollege of Pharmacy and Medical Research Center, Chungbuk National University, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
J T HongCollege of Pharmacy and Medical Research Center, Chungbuk National University, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
Chungbuk National University · KRPusan National University · KRKonkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Presenilins are the enzymatic components of γ-secretase complex that cleaves amyloid precursor protein, Notch and β-catenin, which has critical roles in the development of Alzheimer's disease and cancer cell growth. Therefore, in the present study, we studied the effects and mechanisms of PS2 knockout on lung cancer development and possible mechanisms as a key regulator of lung tumor development. We compared carcinogen-induced tumor growth between PS2 knockout mice and wild-type mice. PS2 knockout mice showed increased urethane (1 mg/g)-induced lung tumor incidence when compared with that of wild-type mice with decreased activity of γ-secretase in the lung tumor tissues. Consequently, iPLA2 activities in lung tumor tissues of PS2 knockout mice were much higher than in tumor tissues of wild-type mice. Furthermore, knockdown of PS2 using PS2 siRNA decreased γ-secretase activity with increased iPLA2 activity in the lung cancer cells (A549 and NCI-H460), leading to increased lung cancer cell growth. PS2 knockout mice and PS2 knockdown lung cancer cells showed increased DNA-binding activities of nuclear factor kappa-beta, signal transducer and activator of transcription 3 (STAT3) and AP-1 which are critical transcriptional factors of iPLA2 than those of PS2 wild-type mice and control lung cancer cells. Taken together, these results suggest that the loss of PS2 could have a critical role in lung tumor development through the upregulation of iPLA2 activity by reducing γ-secretase.

Indexed as

AnimalsCell Line, TumorGroup VI Phospholipases A2HumansLung NeoplasmsMice, Inbred C57BLMice, KnockoutNF-kappa BPeroxiredoxin VIPresenilin-2STAT3 Transcription FactorTranscription Factor AP-1Group VI Phospholipases A2NF-kappa BPeroxiredoxin VIPLA2G6 protein, humanPla2g6 protein, mousePrdx6 protein, mousePresenilin-2PSEN2 protein, humanPsen2 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorTranscription Factor AP-1

Identifiers

PMID24858037
PMCPMC4287650
OpenAlexW1998790126

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.