Evidence map›Paper›PMID 35442158›Full record

ArticleBioengineered2022

Inhibition of endoplasmic reticulum stress alleviates triple-negative breast cancer cell viability, migration, and invasion by Syntenin/SOX4/Wnt/β-catenin pathway via regulation of heat shock protein A4.

Jinniang Nan, Xuguang Hu, Binbin Guo, Meiyun Xu, Yufeng Yao

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

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  18. Inhibition of DNAJC12 Inhibited Tumorigenesis of Rectal Cancer via Downregulating HSPA4 Expression.Evidence-based complementary and alternative medicine : eCAM · 2022
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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 3 institutions in 1 country.

Jinniang NanSchool of Clinical Medicine, Nanchang Medical College, Jiangxi Province, Nanchang, P.R.China.
Xuguang HuDepartment of Organ Transplantation, Jiangxi Provincial People's Hospital, Nanchang, Jiangxi Province, P.R.China.
Binbin GuoSchool of Clinical Medicine, Nanchang Medical College, Jiangxi Province, Nanchang, P.R.China.
Meiyun XuSchool of Clinical Medicine, Nanchang Medical College, Jiangxi Province, Nanchang, P.R.China.
Yufeng YaoDepartment of General Surgery, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & the Affiliated Cancer Hospital of Nanjing Medical University, Nanchang, Jiangxi Province, P.R.China.
First Affiliated Hospital of Jiangxi Medical College · CNJiangxi Provincial People's Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum stress (ER stress) is a double-edged sword in the occurrence and development of malignant cancer. The aim of this study was to explore the roles of ER stress in metastasis and epithelial-mesenchymal transitionin triple-negative breast cancer (TNBC) and potential mechanisms. In this study, 4-PBA was administrated to inhibit the ER stress. Cell viability was evaluated using a cell counting kit-8 assay. Cell migration and invasion were identified by wound healing and transwell assay, respectively. Levels of MMP2 and MMP9 were measured by enzyme-linked immunosorbent assay and immunohistochemical staining. Western blot assay was used to assess the levels of ER stress-related proteins, Syndecan-1 (SDC-1)/Syntenin-1 (SDCBP-1)/SRY-related HMG-box 4 (SOX4) signaling and Wnt/β-catenin signaling. Moreover, a xenograft mice model was conducted to confirm the role of ER stress in TNBC. The data indicate that the ability of viability and metastasis of breast cancer cells were stronger than normal mammary epithelial cells. More aggressiveness was manifested in TNBC cells than that in non-TNBC cells. 4-PBA significantly suppressed the viability, migration, and invasion in BC cells and inhibited the SDC/SDCBP/SOX4 axis and Wnt/β-catenin signaling. Furthermore, heat shock protein A4 (HSPA4) overexpression stimulated ER stress and activated the SDC-1/SDCBP-1/SOX4 pathway and Wnt/β-catenin signaling. Animal experiments showed similar results that 4-PBA repressed tumor growth and inactivated the two pathways, while HSPA4 overexpression reversed the effects of 4-PBA. In summary, inhibition of ER stress inhibited TNBC viability, migration, and invasion by Syntenin/SOX4/Wnt/β-catenin pathway via regulation of HSPA4 in vivo and in vitro.

Indexed as

HSP110 Heat-Shock ProteinsTriple Negative Breast NeoplasmsWnt Signaling PathwayAnimalsbeta CateninCell Line, TumorCell MovementCell ProliferationCell SurvivalEndoplasmic Reticulum StressHumansMiceSOXC Transcription FactorsSynteninsbeta CateninHSP110 Heat-Shock ProteinsHSPA4 protein, humanSDCBP protein, humanSOX4 protein, humanSOXC Transcription FactorsSynteninsEndoplasmic reticulum stressHSPA4Syntenin/SOX4triple-negative breast cancer (TNBC)Wnt/β-catenin pathway

Identifiers

PMID35442158
PMCPMC9161907
OpenAlexW4224219217

What OpenQuestion holds

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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.