Evidence map›Paper›PMID 27246979›Full record

ArticleOncotarget2016

Cdc6 contributes to cisplatin-resistance by activation of ATR-Chk1 pathway in bladder cancer cells.

Sansan Chen, Xinglu Chen, Gui'e Xie, Yue He, Daoyu Yan, Dianpeng Zheng, Shi Li, Xinyang Fu, Yeping Li, Xiang Pang and 4 more

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 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

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  13. ORChestra coordinates the replication and repair music.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
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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

14 authors at 3 institutions in 1 country.

Sansan ChenDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Xinglu ChenInstitute of Biotherapy, School of Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Gui'e XieKingMed School of Laboratory Medicine, Guangzhou Medical University, Guangzhou, Guangdong, China.
Yue HeInstitute of Biotherapy, School of Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Daoyu YanInstitute of Biotherapy, School of Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Dianpeng ZhengInstitute of Biotherapy, School of Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Shi LiDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Xinyang FuDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Yeping LiDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Xiang PangDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Zhiming HuInstitute of Biotherapy, School of Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Hongwei LiInstitute of Biotherapy, School of Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Wanlong TanDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Jinlong LiInstitute of Biotherapy, School of Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Southern Medical University · CNNanfang Hospital · CNKingmed Diagnostics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High activation of DNA damage response is implicated in cisplatin (CDDP) resistance which presents as a serious obstacle for bladder cancer treatment. Cdc6 plays an important role in the malignant progression of tumor. Here, we reported that Cdc6 expression is up-regulated in bladder cancer tissues and is positively correlated to high tumor grade. Cdc6 depletion can attenuate the malignant properties of bladder cancer cells, including DNA replication, migration and invasion. Furthermore, higher levels of chromatin-binding Cdc6 and ATR were detected in CDDP-resistant bladder cancer cells than in the parent bladder cancer cells. Intriguingly, down-regulation of Cdc6 can enhance sensitivity to CDDP both in bladder cancer cells and CDDP-resistant bladder cancer cells. Cdc6 depletion abrogates S phase arrest caused by CDDP, leading to aberrant mitosis by inactivating ATR-Chk1-Cdc25C pathway. Our results indicate that Cdc6 may be a promising target for overcoming CDDP resistance in bladder cancer.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisAtaxia Telangiectasia Mutated Proteinscdc25 PhosphatasesCell Cycle ProteinsCell Line, TumorCell SurvivalCheckpoint Kinase 1ChromatinCisplatinDisease ProgressionDNA DamageDNA ReplicationDown-RegulationDrug Resistance, NeoplasmHumansAtaxia Telangiectasia Mutated ProteinsATR protein, humanCDC25C protein, humancdc25 PhosphatasesCDC6 protein, humanCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanChromatinCisplatinNuclear ProteinsRNA, Small InterferingATRbladder cancerCdc6cisplatin-resistance

Identifiers

PMID27246979
PMCPMC5130013
OpenAlexW2395383112

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.