Evidence map›Paper›PMID 33041328›Full record

ArticleOncogenesis2020

Inhibition of Chk1 by miR-320c increases oxaliplatin responsiveness in triple-negative breast cancer.

Sera Lim, Yesol Kim, Soo-Been Lee, Hyeok-Gu Kang, Da-Hyun Kim, Jee Won Park, Daeun Chung, Hyunkyung Kong, Kyung Hyun Yoo, Yonghwan Kim and 3 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 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

13 authors at 3 institutions in 1 country.

Sera Lim *Department of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0003-3583-0410
Yesol Kim *Department of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.
Soo-Been LeeDepartment of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.
Hyeok-Gu KangDepartment of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Da-Hyun KimDepartment of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jee Won ParkDepartment of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.
Daeun ChungDepartment of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.
Hyunkyung KongDepartment of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.
Kyung Hyun YooDepartment of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.
Yonghwan KimDepartment of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.
Wonshik HanCancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea.
Kyung-Hee ChunDepartment of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jong Hoon ParkDepartment of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea. parkjh@sookmyung.ac.kr.ORCID http://orcid.org/0000-0002-8082-0214
Sookmyung Women's University · KRYonsei University · KRSeoul National University · KR

Funding

National Research Foundation of Korea (NRF) 2015M3A9B6027555National Research Foundation of Korea (NRF) 2016R1A5A1011974National Research Foundation of Korea (NRF) 2019R1A2B5B03069738
6 · The paper itself

Abstract

Checkpoint kinase 1 (Chk1) expression is enhanced in most cancers owing to oncogenic activation and constant replicative stress. Chk1 inactivation is a promising cancer therapy, as its inactivation leads to genomic instability, chromosomal catastrophe, and cancer cell death. Herein, we observed that miR-320c, downregulated in triple-negative breast cancer (TNBC) patients, can target Chk1. In addition, downregulated miR-320c expression was associated with poor overall survival in TNBC patients. As Chk1 was associated with the DNA damage response (DDR), we investigated the effect of miR-320c on DDR in TNBC cells. To induce DNA damage, we used platinum-based drugs, especially oxaliplatin, which is most effective with miR-320c. We observed that overexpression of miR-320c in TNBC regulated the oxaliplatin responsiveness by mediating DNA damage repair through the negative regulation of Chk1 in vitro. Furthermore, using a xenograft model, a combination of miR-320c mimic and oxaliplatin effectively inhibited tumor progression. These investigations indicate the potential of miR-320c as a marker of oxaliplatin responsiveness and a therapeutic target to increase the efficacy of chemotherapy in TNBC.

Identifiers

PMID33041328
PMCPMC7548284
OpenAlexW3091838596

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.