Evidence map›Paper›PMID 34109118›Full record

ArticleFrontiers in oncology2021

Targeting Mutated p53 Dependency in Triple-Negative Breast Cancer Cells Through CDK7 Inhibition.

Jingyu Peng, Ming Yang, Ran Bi, Yueyuan Wang, Chunxi Wang, Xue Wei, Zhihao Zhang, Xiao Xie, Wei Wei

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. 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
1.9field-weighted citation impact, top 11% 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, 27 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 1 country.

Jingyu PengDepartment of Breast Surgery, The First Hospital of Jilin University, Changchun, China.
Ming YangDepartment of Breast Surgery, The First Hospital of Jilin University, Changchun, China.
Ran BiKey Laboratory of Organ Regeneration & Transplantation of the Ministry of Education, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Yueyuan WangDepartment of Breast Surgery, The First Hospital of Jilin University, Changchun, China.
Chunxi WangDepartment of Urology, The First Hospital of Jilin University, Changchun, China.
Xue WeiDepartment of Breast Surgery, The First Hospital of Jilin University, Changchun, China.
Zhihao ZhangDepartment of Breast Surgery, The First Hospital of Jilin University, Changchun, China.
Xiao XieDepartment of Breast Surgery, The First Hospital of Jilin University, Changchun, China.
Wei WeiKey Laboratory of Organ Regeneration & Transplantation of the Ministry of Education, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Jilin University · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCyclin-dependent kinase 7 (CDK7) is crucial for cell cycle progression and gene expression transcriptional regulation, which are often not assessed in cancer developing process. CDK7 inhibitors have emerged as promising drugs for treating diverse cancers, including breast cancer. However, the mechanism behind its anticancer effect has not been well investigated. Here, the possible mechanism of CDK7 inhibitors for treating human triple-negative breast cancer (TNBC) has been studied.

methodsThe effects of CDK7 inhibitors on breast cancer cells have been identified by measuring cell viability (Cell Counting Kit-8) and cell proliferation and calculating colony formation. The short hairpin RNA and short interfering RNA were used for the construction of knockdown cells. To assess the expression of associated proteins, western blot was used.

resultsThis study confirmed that, compared to hormone receptor-positive breast cancer cells, TNBC cells were more sensitive to THZ1, a novel CDK7 inhibitor. THZ1 treatment specifically downregulated mutated p53 in a dose- and time-dependent manner in TNBC cells with p53 mutation. Another CDK7 inhibitor, LDC4297, also potently interfered with the expression of mutated p53. Furthermore, endogenous CDK7 expression was positively correlated with the levels of mutated p53 in TNBC cells with p53 mutation. Downregulating mutated p53 expression significantly suppressed the proliferation of TNBC cells with p53 mutation.

conclusionOur findings demonstrated that targeting CDK7 was an effective approach for the treatment of TNBC with p53 mutation.

Indexed as

cancer treatmentCDK7 inhibitionmutated p53targeted therapyTHZ1triple-negative breast cancer

Identifiers

PMID34109118
PMCPMC8183379
OpenAlexW3165144341

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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.