Evidence map›Paper›PMID 26716515›Full record

ArticleOncotarget2016

Mitotic cell death caused by follistatin-like 1 inhibition is associated with up-regulated Bim by inactivated Erk1/2 in human lung cancer cells.

Kieun Bae, Kyoung Eun Park, Jihye Han, Jongkwang Kim, Kyungtae Kim, Kyong-Ah Yoon

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

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  8. Follistatin-like 1 in development and human diseases.Cellular and molecular life sciences : CMLS · 2018
    Review
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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.

Kieun BaeResearch Institute and Hospital, National Cancer Center, Goyang, Gyeonggi, Korea.
Kyoung Eun ParkResearch Institute and Hospital, National Cancer Center, Goyang, Gyeonggi, Korea.
Jihye HanResearch Institute and Hospital, National Cancer Center, Goyang, Gyeonggi, Korea.
Jongkwang KimResearch Institute and Hospital, National Cancer Center, Goyang, Gyeonggi, Korea.
Kyungtae KimResearch Institute and Hospital, National Cancer Center, Goyang, Gyeonggi, Korea.
Kyong-Ah YoonResearch Institute and Hospital, National Cancer Center, Goyang, Gyeonggi, Korea.
National Cancer Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Follistatin-like 1 (FSTL1) was identified as a novel pro-inflammatory protein showing high-level expression in rheumatoid arthritis. The protective effect of FSTL1 via the inhibition of apoptosis was reported in myocardial injury. However, the functional mechanism of FSTL1 in cancer is poorly characterized, and its proliferative effects are ambiguous. Here, we examined the effects of FSTL1 on cellular proliferation and cell cycle checkpoints in lung cancer cells. FSTL1 inhibition induced the cellular portion of G2/M phase in human lung cancer cells via the accumulation of regulators of the transition through the G2/M phase, including the cyclin-dependent kinase 1 (Cdk1)-cyclin B1 complex. An increase in histone H3 phosphorylation (at Ser10), another hallmark of mitosis, indicated that the knockdown of FSTL1 in lung cancer cells stimulated a mitotic arrest. After that, apoptosis was promoted by the activation of caspase-3 and -9. Protein level of Bim, a BH3 domain-only, pro-apoptotic member and its isoforms, BimL, BimS, and BimEL were up-regulated by FSTL1 inhibition. Degradation of Bim was blocked in FSTL1-knockdown cells by decreased phosphorylation of Bim. Increased BimEL as well as decreased phosphorylated Erk1/2 is essential for cell death by FSTL1 inhibition in NCI-H460 cells. Taken together, our results suggest that the knockdown of FSTL1 induces apoptosis through a mitotic arrest and caspase-dependent cell death. FSTL1 plays the important roles in cellular proliferation and apoptosis in lung cancer cells, and thus can be a new target for lung cancer treatment.

Indexed as

A549 CellsApoptosisBcl-2-Like Protein 11Carcinoma, Non-Small-Cell LungCaspase 3Caspase 9CDC2 Protein KinaseCell Line, TumorCell ProliferationCyclin B1Cyclin-Dependent KinasesExtracellular Signal-Regulated MAP KinasesFollistatin-Related ProteinsG2 Phase Cell Cycle CheckpointsHistonesHumansBcl-2-Like Protein 11Caspase 3Caspase 9CCNB1 protein, humanCDC2 Protein KinaseCDK1 protein, humanCyclin B1Cyclin-Dependent KinasesExtracellular Signal-Regulated MAP KinasesFollistatin-Related ProteinsFSTL1 protein, humanHistonesRNA, Small InterferingapoptosisBimErk1/2FSTL1lung cancer

Identifiers

PMID26716515
PMCPMC4951272
OpenAlexW2197239674

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.