Evidence map›Paper›PMID 30544747›Full record

ArticleCells2018

Silencing Heat Shock Protein 27 Inhibits the Progression and Metastasis of Colorectal Cancer (CRC) by Maintaining the Stability of Stromal Interaction Molecule 1 (STIM1) Proteins.

Chien-Yu Huang, Po-Li Wei, Wei-Yu Chen, Wei-Chiao Chang, Yu-Jia Chang

Open access · goldAbstract read
In one paragraph

Article in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  3. [Effect of phosphorylated HSP27 on the proliferation and metastasis of nasopharyngeal carcinoma and its mechanism].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2024
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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

5 authors at 4 institutions in 1 country.

Chien-Yu HuangDepartment of Surgery, College of Medicine, Taipei Medical University, Taipei 110, Taiwan. cyh@tmu.edu.tw.
Po-Li WeiDepartment of Surgery, College of Medicine, Taipei Medical University, Taipei 110, Taiwan. poliwei@tmu.edu.tw.
Wei-Yu ChenDepartment of Pathology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan. wychen.patho@gmail.com.
Wei-Chiao ChangSchool of Pharmacy, Taipei Medical University, Taipei 110, Taiwan. weichiao.chang@gmail.com.
Yu-Jia ChangCancer Research Center and Translational Laboratory, Department of Medical Research, Taipei Medical University Hospital, Taipei Medical University, Taipei 110, Taiwan. r5424012@tmu.edu.tw.ORCID 0000-0003-3978-3244
Taipei Medical University Hospital · TWTaipei Medical University · TWTaipei Medical University-Shuang Ho Hospital · TWWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of colorectal cancer (CRC) has significantly increased in recent decades, and this disease has become an important health issue worldwide. Currently, there is no useful prognostic or diagnostic biomarker for CRC. Heat shock protein 27 (HSP27) is a chaperone that interacts with many proteins. HSP27 has been shown to be overexpressed in many cancers, including colon cancer, and its overexpression is related to poor disease outcome. Although the importance of HSP27 as a biomarker cannot be underrated, its detailed mechanisms in colon cancer are still unclear. In vitro studies have indicated that silencing HSP27 reduces the proliferation, migration and invasion of colon cancer cells, and xenograft models have shown that silencing HSP27 decreases tumor progression. Tissue array results showed that colon cancer patients with high expression of HSP27 exhibited poor prognosis. In addition, we found a reduction of calcium influx through a decrease in STIM1 protein after HSP27 was abolished. The formation of puncta was decreased in HSP27 knockdown (HSP27KD) cells after thapsigargin (TG) treatment. Finally, we confirmed that the reduction of STIM1 after HSP27 silencing may be due to a loss of STIM1 stability instead of transcription. HSP27 may interact with STIM1 but not Orai1, as shown by immunoprecipitation assays. HSP27 and STIM1 were co-expressed in CRC specimens. Our study showed that HSP27 is a key mediator in the progression and metastasis of CRC by regulating the store-operated calcium entry. This novel pathway may provide a new direction for development of therapeutic strategies for CRC.

Indexed as

CRCERHSP27SOCESTIM1

Identifiers

PMID30544747
PMCPMC6315635
OpenAlexW2905545423

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.