Evidence map›Paper›PMID 29286126›Full record

ArticleOncology reports2018

Bcl-2 overexpression reduces cisplatin cytotoxicity by decreasing ER-mitochondrial Ca2+ signaling in SKOV3 cells.

Lu Xu, Qi Xie, Ling Qi, Chunyan Wang, Na Xu, Weimin Liu, Yang Yu, Songyan Li, Ye Xu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.3field-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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  5. Mitochondria-ER crosstalk via MAMS: Bridging cellular homeostasis and cancer progression.Apoptosis : an international journal on programmed cell death · 2026
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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

9 authors at 3 institutions in 1 country.

Lu XuKey Laboratory of Colleges and Universities of Jilin, College of Basic Medicine, Jilin Medical University, Jilin, Jilin 132013, P.R. China.
Qi XieDepartment of Pathophysiology, College of Basic Medicine, Jilin University, Changchun, Jilin 130021, P.R. China.
Ling QiKey Laboratory of Colleges and Universities of Jilin, College of Basic Medicine, Jilin Medical University, Jilin, Jilin 132013, P.R. China.
Chunyan WangKey Laboratory of Colleges and Universities of Jilin, College of Basic Medicine, Jilin Medical University, Jilin, Jilin 132013, P.R. China.
Na XuKey Laboratory of Colleges and Universities of Jilin, College of Basic Medicine, Jilin Medical University, Jilin, Jilin 132013, P.R. China.
Weimin LiuDepartment of Intervention, Jilin Municipal People's Hospital, Jilin, Jilin 132000, P.R. China.
Yang YuKey Laboratory of Colleges and Universities of Jilin, College of Basic Medicine, Jilin Medical University, Jilin, Jilin 132013, P.R. China.
Songyan LiKey Laboratory of Colleges and Universities of Jilin, College of Basic Medicine, Jilin Medical University, Jilin, Jilin 132013, P.R. China.
Ye XuKey Laboratory of Colleges and Universities of Jilin, College of Basic Medicine, Jilin Medical University, Jilin, Jilin 132013, P.R. China.
Jilin Medical University · CNJilin University · CNPeople 's Hospital of Jilin Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have revealed that a small amount of cisplatin can penetrate into the nucleus and induce intranuclear DNA damage. Specifically, most cisplatin accumulates in and stresses different organelles, including mitochondria, endoplasmic reticulum (ER) and the cytosol, where apoptosis signaling is activated and magnified. Bcl-2, which is mainly localized to ER and mitochondria, is identified as a key regulator of survival and apoptosis. Bcl-2 is reported to block cisplatin-induced apoptosis via regulating Ca2+ signaling in a variety of cancer cell lines. However, its target molecule and the mechanism responsible for its inhibitory effect in ovarian cancer are undefined. The present study revealed that Bcl-2 overexpression reduced cisplatin-induced growth inhibition and apoptosis in SKOV3 human ovarian cancer cells. Furthermore, Bcl-2 inhibited cisplatin-induced Ca2+ release from the ER to the cytoplasm and mitochondria, which reduced cisplatin-induced ER stress-mediated apoptosis through the mitochondrial apoptotic pathway. The overexpression of Bcl-2 inhibited the cisplatin-induced increase in the number of ER-mitochondrial contact sites in SKOV3 human ovarian cancer cells. In addition, the present study provided evidence that Bcl-2 reduced the anticancer activity of cisplatin towards ovarian cancer cells in vivo. These results revealed that Bcl-2 attenuates cisplatin cytotoxicity via downregulating ER-mitochondrial Ca2+ signaling transduction. Thus, Bcl-2 which may be a potential therapeutic target for ovarian cancer.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsApoptosisBiomarkers, TumorCalciumCell ProliferationCisplatinEndoplasmic ReticulumEndoplasmic Reticulum StressFemaleHumansMembrane Potential, MitochondrialMiceMice, Inbred BALB CMice, NudeAntineoplastic AgentsBCL2 protein, humanBiomarkers, TumorCalciumCisplatinProto-Oncogene Proteins c-bcl-2

Identifiers

PMID29286126
PMCPMC5802038
OpenAlexW2780776584

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.