Evidence map›Paper›PMID 34136492›Full record

ReviewFrontiers in cell and developmental biology2021

Endoplasmic Reticulum Stress and Tumor Microenvironment in Bladder Cancer: The Missing Link.

Zhenyu Nie, Mei Chen, Xiaohong Wen, Yuanhui Gao, Denggao Huang, Hui Cao, Yanling Peng, Na Guo, Jie Ni, Shufang Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 41 citations in OpenAlex.

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  20. Mechanism ofCancers · 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

10 authors at 3 institutions in 2 countries.

Zhenyu NieCentral Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
Mei ChenCentral Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
Xiaohong WenCentral Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
Yuanhui GaoCentral Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
Denggao HuangCentral Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
Hui CaoCentral Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
Yanling PengCentral Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
Na GuoCentral Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
Jie NiCancer Care Center, St. George Hospital, Sydney, NSW, Australia.
Shufang ZhangCentral Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
Hainan Medical University · CNCentral South University · CNSutherland Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bladder cancer is a common malignant tumor of the urinary system. Despite recent advances in treatments such as local or systemic immunotherapy, chemotherapy, and radiotherapy, the high metastasis and recurrence rates, especially in muscle-invasive bladder cancer (MIBC), have led to the evaluation of more targeted and personalized approaches. A fundamental understanding of the tumorigenesis of bladder cancer along with the development of therapeutics to target processes and pathways implicated in bladder cancer has provided new avenues for the management of this disease. Accumulating evidence supports that the tumor microenvironment (TME) can be shaped by and reciprocally act on tumor cells, which reprograms and regulates tumor development, metastasis, and therapeutic responses. A hostile TME, caused by intrinsic tumor attributes (e.g., hypoxia, oxidative stress, and nutrient deprivation) or external stressors (e.g., chemotherapy and radiation), disrupts the normal synthesis and folding process of proteins in the endoplasmic reticulum (ER), culminating in a harmful situation called ER stress (ERS). ERS is a series of adaptive changes mediated by unfolded protein response (UPR), which is interwoven into a network that can ultimately mediate cell proliferation, apoptosis, and autophagy, thereby endowing tumor cells with more aggressive behaviors. Moreover, recent studies revealed that ERS could also impede the efficacy of anti-cancer treatment including immunotherapy by manipulating the TME. In this review, we discuss the relationship among bladder cancer, ERS, and TME; summarize the current research progress and challenges in overcoming therapeutic resistance; and explore the concept of targeting ERS to improve bladder cancer treatment outcomes.

Indexed as

bladder cancerendoplasmic reticulum stresstherapeutic targettumor microenvironmentunfolded protein response

Identifiers

PMID34136492
PMCPMC8201605
OpenAlexW3172605771

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.