Evidence map›Paper›PMID 31076571›Full record

ArticleCell death & disease2019

Cancer-associated fibroblasts promote cisplatin resistance in bladder cancer cells by increasing IGF-1/ERβ/Bcl-2 signalling.

Xingbo Long, Wei Xiong, Xiting Zeng, Lin Qi, Yi Cai, Miao Mo, Huichuan Jiang, Bisong Zhu, Zhi Chen, Yuan Li

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

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
13.7field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 125 citations in OpenAlex.

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  14. Unraveling the Therapeutic Potential ofCurrent pharmaceutical design · 2025
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20 more citing papers are in PubMed but not listed here.

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.

Xingbo LongDepartment of Urology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Wei XiongDepartment of Urology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Xiting ZengDepartment of Ophthalmology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Lin QiDepartment of Urology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yi CaiDepartment of Urology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Miao MoDepartment of Urology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Huichuan JiangDepartment of Urology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Bisong ZhuDepartment of Urology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Zhi ChenDepartment of Urology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yuan LiDepartment of Urology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. yuanlixy@csu.edu.cn.ORCID http://orcid.org/0000-0002-5249-3172
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While cancer-associated fibroblasts (CAFs) in the tumour microenvironment may play important roles in bladder cancer (BCa) progression, their impacts on BCa chemoresistance remain unclear. Using human BCa samples, we found that tumour tissues possessed more CAFs than did adjacent normal tissues. Both the presence of CAFs in the BCa stroma and the expression of ERβ in BCa contribute to chemoresistance, and CAFs and BCa cells interact to affect ERβ expression. In vitro co-culture assays demonstrated that compared with normal bladder cells, BCa cells had a higher capacity to induce the transformation of normal fibroblasts into CAFs. When BCa cells were co-cultured with CAFs, their viability, clone formation ability and chemoresistance were increased, whereas their apoptotic rates were downregulated. Dissection of the mechanism revealed that the recruited CAFs increased IGF-1/ERβ signalling in BCa cells, which then led to the promotion of the expression of the anti-apoptotic gene Bcl-2. Blocking IGF-1/ERβ/Bcl-2 signalling by either an shRNA targeting ERβ or an anti-IGF-1 neutralizing antibody partially reversed the capacity of CAFs to increase BCa chemoresistance. The in vivo data also confirmed that CAFs could increase BCa cell resistance to cisplatin by increasing ERβ/Bcl-2 signalling. The above results showed the important roles of CAFs within the bladder tumour microenvironment, which could enhance BCa chemoresistance.

Indexed as

Drug Resistance, NeoplasmAnimalsApoptosisCancer-Associated FibroblastsCell LineCisplatinEstrogen Receptor betaFemaleHumansInsulin-Like Growth Factor IJNK Mitogen-Activated Protein KinasesKaplan-Meier EstimateMiceMice, NudeProto-Oncogene Proteins c-bcl-2RNA InterferenceBCL2 protein, humanCisplatinEstrogen Receptor betaIGF1 protein, humanInsulin-Like Growth Factor IJNK Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-bcl-2RNA, Small Interfering

Identifiers

PMID31076571
PMCPMC6510780
OpenAlexW2943881236

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.