Evidence map›Paper›PMID 31423257›Full record

ArticleOncology letters2019

CDS-1548 induces apoptosis in HeLa cells by activating caspase 3.

Yuanxin Zhang, Yakun Ge, Wei Shi, Chenming Hu, Xu Bai, Jimin Rong, Ming Yu

Abstract read
In one paragraph

Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Yuanxin ZhangCollege of Biology and Food Engineering, Jilin Institute of Chemical Technology, Jilin, Jilin 132022, P.R. China.
Yakun GeCollege of Biology and Food Engineering, Jilin Institute of Chemical Technology, Jilin, Jilin 132022, P.R. China.
Wei ShiKey Laboratory for Molecular Enzymology and Engineering of The Ministry of Education, School of Life Science, Jilin University, Changchun, Jilin 130012, P.R. China.
Chenming HuThe Center for Combinatorial Chemistry and Drug Discovery, College of Pharmacy, Jilin University, Changchun, Jilin 130012, P.R. China.
Xu BaiThe Center for Combinatorial Chemistry and Drug Discovery, College of Pharmacy, Jilin University, Changchun, Jilin 130012, P.R. China.
Jimin RongCollege of Biology and Food Engineering, Jilin Institute of Chemical Technology, Jilin, Jilin 132022, P.R. China.
Ming YuCollege of Biology and Food Engineering, Jilin Institute of Chemical Technology, Jilin, Jilin 132022, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical cancer continues to be a threat to female health globally. In the present study, the potential anticancer activity of 2-[2-hydroxyl-1-(4-methoxy phenyl) ethyl]-3-(4-benzyloxy phenyl) isoindolin-1-one (CDS-1548), was evaluated in HeLa cells. CDS-1548 is an organic small-molecule compound characterized by two chiral centers, with the nuclear parent 1H-isoindolin-1-one. CDS-1548 administration significantly elevated the transcriptional activity of p53 and its downstream target genes in a dose-dependent manner. Additionally, CDS-1548 treatment increased the expression levels of p53 and mouse double minute 2 homolog, as well as inducing apoptosis in HeLa cells. Furthermore, CDS-1548 treatment downregulated the expression of B-cell lymphoma 2, upregulated Bcl-2 homologous antagonist killer, promoted the release of cytochrome c from mitochondria to cytoplasm, and activated the production of caspase 3 and 9. Collectively, these results suggested that CDS-1548 inhibited HeLa cell proliferation by promoting G

Indexed as

apoptosisG2/M arrestHeLap53small-molecule inhibitor

Identifiers

PMID31423257
PMCPMC6614674

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Registered trials

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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.