Evidence map›Paper›PMID 31651209›Full record

ArticleCancer biology & therapy2020

GSK343 induces programmed cell death through the inhibition of EZH2 and FBP1 in osteosarcoma cells.

Xifeng Xiong, Jinli Zhang, Aiguo Li, Libing Dai, Shengnan Qin, Pengzhen Wang, Wei Liu, Zhi Zhang, Xiaojian Li, Zhihe Liu

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 31 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

10 authors at 1 institution in 1 country.

Xifeng XiongGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Medical Collage, Jinan University, Guangzhou, China.
Jinli ZhangGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Medical Collage, Jinan University, Guangzhou, China.
Aiguo LiGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Medical Collage, Jinan University, Guangzhou, China.
Libing DaiGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Medical Collage, Jinan University, Guangzhou, China.
Shengnan QinGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Medical Collage, Jinan University, Guangzhou, China.
Pengzhen WangGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Medical Collage, Jinan University, Guangzhou, China.
Wei LiuDepartment of Breast Surgery, Guangzhou Red Cross Hospital, Medical Collage, Jinan University, Guangzhou, China.
Zhi ZhangDepartment of Burns and Plastic Surgery, Guangzhou Red Cross Hospital, Medical Collage, Jinnan University, Guangzhou, Guangdong, China.
Xiaojian LiDepartment of Burns and Plastic Surgery, Guangzhou Red Cross Hospital, Medical Collage, Jinnan University, Guangzhou, Guangdong, China.
Zhihe LiuGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Medical Collage, Jinan University, Guangzhou, China.
Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enhancer of zeste homolog 2 (EZH2) is an important member of the epigenetic regulatory factor polycomb group proteins (PcG) and is abnormally expressed in a wide variety of tumors, including osteosarcoma. Scientists consider EZH2 as an attractive target for the treatment of osteosarcoma and have found many potential EZH inhibitors, such as GlaxoSmithKline 343 (GSK343). It has been reported that GSK343 can be used as an inhibitor in different types of cancer. This study demonstrated that GSK343 not only induced apoptosis by increasing cleaved Casp-3 and poly ADP-ribose polymerase (PARP) expression, but also induced autophagic cell death by inhibiting p62 expression. Apoptosis and autophagic cell death induced by GSK343 were confirmed by the high expression of cleaved caspase-3, LC3-II and transmission electron microscopy. GSK343 inhibited the expression of EZH2 and c-Myc. Additionally, GSK343 inhibited the expression of FUSE binding protein 1 (FBP1), which was identified by its regulatory effects on c-Myc expression. Since c-Myc is a common target of EZH2 and FBP1, and GSK343 inhibited the expression of these proliferation-promoting proteins, a mutual regulatory mechanism between EZH2 and FBP1 was proposed. The knockdown of EZH2 suppressed the expression of FBP1; similarly, the knockdown of FBP1 suppressed the expression of EZH2. These results suggest the mutual regulatory association between EZH2 and FBP1. The knockdown of either EZH2 or FBP1 accelerated the sensitivity of osteosarcoma cells to GSK343. Based on these results, this study clarified that GSK343, an EZH2 inhibitor, may have potential for use in the treatment of osteosarcoma. The underlying mechanisms of the effects of GSK343 are partly mediated by its inhibitory activity against c-Myc and its regulators (EZH2 and FBP1).

Indexed as

ApoptosisBiomarkers, TumorBone NeoplasmsCell ProliferationEnhancer of Zeste Homolog 2 ProteinEnzyme InhibitorsFructose-BisphosphataseGene Expression Regulation, NeoplasticHumansIndazolesOsteosarcomaPyridonesTumor Cells, CulturedBiomarkers, TumorEnhancer of Zeste Homolog 2 ProteinEnzyme InhibitorsEZH2 protein, humanFBP1 protein, humanFructose-BisphosphataseGSK343IndazolesPyridonesEZH2FBP1GSK343osteosarcomaprogrammed cell death

Identifiers

PMID31651209
PMCPMC7012145
OpenAlexW2981428688

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.