Evidence map›Paper›PMID 33408886›Full record

ArticleJournal of breast cancer2020

Tryptophanyl-tRNA Synthetase Sensitizes Hormone Receptor-Positive Breast Cancer to Docetaxel-Based Chemotherapy.

Kyung-Min Lee, Eun Hye Hwang, Seong Eun Kang, Cheng Hyun Lee, Hyebin Lee, Hyeon Jeong Oh, Kwangsoo Kim, Jiwon Koh, Han Suk Ryu

Open access · goldAbstract read
In one paragraph

Article in Journal of breast cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

8 citing papers in PubMed, 9 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 3 institutions in 1 country.

Kyung-Min LeeCenter for Medical Innovation, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.ORCID 0000-0002-1359-7382
Eun Hye HwangDepartment of Pathology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea.ORCID 0000-0001-5414-821X
Seong Eun KangDepartment of Pathology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea.ORCID 0000-0003-4119-7607
Cheng Hyun LeeDepartment of Pathology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea.ORCID 0000-0003-0714-8473
Hyebin LeeDepartment of Radiation Oncology, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Korea.ORCID 0000-0001-8442-6479
Hyeon Jeong OhDepartment of Pathology, Seoul National University Bundang Hospital, 82 Gumi-ro 173, Bundang-gu, Seongnam, Korea.ORCID 0000-0002-9998-3988
Kwangsoo KimTransdisciplinary Department of Medicine & Advanced Technology, Seoul National University Hospital, Seoul, Korea.ORCID 0000-0002-4586-5062
Jiwon KohDepartment of Pathology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea.ORCID 0000-0002-7687-6477
Han Suk RyuCenter for Medical Innovation, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.ORCID 0000-0003-2508-9796
Seoul National University Hospital · KRKangbuk Samsung Hospital · KRSeoul National University Bundang Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeA relatively low response to chemotherapy has been reported for hormone receptor (HR)-positive breast cancer. In this study, we investigated the role of tryptophanyl-transfer RNA synthetase

methodsPre-chemotherapeutic needle biopsy samples of 45 HR-positive breast cancer patients undergoing the same chemotherapeutic regimen were subjected to immunohistochemistry. To investigate the biological functions of WARS in HR-positive breast cancer, we conducted cell viability assay, flow cytometry analysis, caspase activity assay, Quantitative real-time polymerase chain reaction, and western blotting using WARS gene-modulated HR-positive breast cancer cells (T47D, ZR-75-1, and MCF7).

resultsWARS overexpression in HR-positive breast cancer patients showed a significant correlation with favorable chemotherapy response. Downregulation of WARS increased cell viability following docetaxel treatment in tumor cell lines. On the other hand, WARS overexpression sensitized the therapeutic response to docetaxel. Additionally, downregulation of WARS caused a decrease in the number of apoptotic cell populations by docetaxel. Poly (ADP-ribose) polymerase cleavage and caspase 3/7 activity were increased in docetaxel-treated tumor cells with WARS overexpression.

conclusionOur results suggest that WARS might be a potential predictor for chemotherapy response in patients with HR-positive breast cancer as well as a novel molecular target to improve chemosensitivity.

Indexed as

ApoptosisBreast neoplasmsDrug resistanceNeoadjuvant therapyWARS1 protein, human

Identifiers

PMID33408886
PMCPMC7779724
OpenAlexW3113283668

What OpenQuestion holds

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Registered trials

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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.