Evidence map›Paper›PMID 34743414›Full record

ArticleMolecular oncology2022

Calsequestrin 2 overexpression in breast cancer increases tumorigenesis and metastasis by modulating the tumor microenvironment.

Ju Hee Kim, Eun-Shin Lee, Jihui Yun, Han Suk Ryu, Hong Kyu Kim, Young Wook Ju, Kwangsoo Kim, Jong-Il Kim, Hyeong-Gon Moon

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

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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

9 authors at 2 institutions in 3 countries.

Ju Hee KimBiomedical Research Institute, Seoul National University Hospital, South Korea.ORCID 0000-0002-5583-3857
Eun-Shin LeeBiomedical Research Institute, Seoul National University Hospital, South Korea.
Jihui YunGenomic Medicine Institute, Medical Research Center, Seoul National University, Korea.
Han Suk RyuDepartment of Pathology, Seoul National University Hospital, South Korea.
Hong Kyu KimDepartment of Surgery, Seoul National University Hospital, Korea.
Young Wook JuDepartment of Surgery, Seoul National University Hospital, Korea.
Kwangsoo KimDivision of Clinical Bioinformatics, Seoul National University Hospital, Korea.
Jong-Il KimGenomic Medicine Institute, Medical Research Center, Seoul National University, Korea.
Hyeong-Gon MoonDepartment of Surgery, Seoul National University Hospital, Korea.
Seoul National University · KRSeoul National University Hospital · KR

Funding

NTP INFORMATION SYSTEMS SUPPORT27305C0011 · NIEHS · Z-TECH CORPORATION · 2007 to 2009
$4.3M
PROVIDE RABBITS, RATS, MICE, HAMSTERS, GERBILS, GUINEA PIGS27307C0011 · NIEHS · PI BOLEN, WAYNE · 2007 to 2007
$500k
NIEHS NIH HHS 27305C0011NIEHS NIH HHS 27307C0011NIEHS NIH HHS 27398C0011
6 · The paper itself

Abstract

The spatial tumor shape is determined by the complex interactions between tumor cells and their microenvironment. Here, we investigated the role of a newly identified breast cancer-related gene, calsequestrin 2 (CASQ2), in tumor-microenvironment interactions during tumor growth and metastasis. We analyzed gene expression and three-dimensional tumor shape data from the breast cancer dataset of The Cancer Genome Atlas (TCGA) and identified CASQ2 as a potential regulator of tumor-microenvironment interaction. In TCGA breast cancer cases containing information of three-dimensional tumor shapes, CASQ2 mRNA showed the highest correlation with the spatial tumor shapes. Furthermore, we investigated the expression pattern of CASQ2 in human breast cancer tissues. CASQ2 was not detected in breast cancer cell lines in vitro but was induced in the xenograft tumors and human breast cancer tissues. To evaluate the role of CASQ2, we established CASQ2-overexpressing breast cancer cell lines for in vitro and in vivo experiments. CASQ2 overexpression in breast cancer cells resulted in a more aggressive phenotype and altered epithelial-mesenchymal transition (EMT) markers in vitro. CASQ2 overexpression induced cancer-associated fibroblast characteristics along with increased hypoxia-inducible factor 1α (HIF1α) expression in stromal fibroblasts. CASQ2 overexpression accelerated tumorigenesis, induced collagen structure remodeling, and increased distant metastasis in vivo. CASQ2 conferred more metaplastic features to triple-negative breast cancer cells. Our data suggest that CASQ2 is a key regulator of breast cancer tumorigenesis and metastasis by modulating diverse aspects of tumor-microenvironment interactions.

Indexed as

CarcinogenesisNeoplasm MetastasisTumor MicroenvironmentCalsequestrinCell Line, TumorEpithelial-Mesenchymal TransitionExtracellular MatrixFemaleGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitModels, BiologicalPhenotypeSignal TransductionTriple Negative Breast NeoplasmsCalsequestrinCASQ2 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha Subunitbreast cancercalsequestrin 2metastasistumor microenvironment

Identifiers

PMID34743414
PMCPMC8763655
OpenAlexW3212573215

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.