Evidence map›Paper›PMID 30592293›Full record

ArticleOncology reports2019

Bromodomain‑containing protein 7 sensitizes breast cancer cells to paclitaxel by activating Bcl2‑antagonist/killer protein.

Jinqi Ma, Weihong Niu, Xinye Wang, Yao Zhou, Heran Wang, Fengxia Liu, Yukun Liu, Jie Guo, Wei Xiong, Zhaoyang Zeng and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

20 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

17 authors at 1 institution in 1 country.

Jinqi MaThe Key Laboratory of Carcinogenesis of The Chinese Ministry of Health and The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan 410078, P.R. China.
Weihong NiuCancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, Hunan 410078, P.R. China.
Xinye WangCancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, Hunan 410078, P.R. China.
Yao ZhouCancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, Hunan 410078, P.R. China.
Heran WangCancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, Hunan 410078, P.R. China.
Fengxia LiuDepartment of Blood Transfusion, The Third Xiang‑Ya Hospital, Central South University, Changsha, Hunan 410013, P.R. China.
Yukun LiuCancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, Hunan 410078, P.R. China.
Jie GuoNational Institution of Drug Clinical Trial, Xiangya Hospital, Central South University, Changsha, Hunan 410078, P.R. China.
Wei XiongCancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, Hunan 410078, P.R. China.
Zhaoyang ZengCancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, Hunan 410078, P.R. China.
Songqing FanDepartment of Pathology, The Second Xiang‑Ya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.
Xiaoling LiCancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, Hunan 410078, P.R. China.
Xinmin NieDepartment of Blood Transfusion, The Third Xiang‑Ya Hospital, Central South University, Changsha, Hunan 410013, P.R. China.
Guiyuan LiCancer Research Institute and School of Basic Medical Sciences, Central South University, Changsha, Hunan 410078, P.R. China.
Rong GuiDepartment of Blood Transfusion, The Third Xiang‑Ya Hospital, Central South University, Changsha, Hunan 410013, P.R. China.
Yanwei LuoThe Key Laboratory of Carcinogenesis of The Chinese Ministry of Health and The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan 410078, P.R. China.
Ming ZhouThe Key Laboratory of Carcinogenesis of The Chinese Ministry of Health and The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan 410078, P.R. China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous study demonstrated that bromodomain‑containing protein 7 (BRD7) inhibits cell proliferation and tumor growth, restoring the expression of B‑cell lymphoma 2 antagonist/killer (Bak) sensitized breast cancer cells to paclitaxel. However, the association between BRD7 and paclitaxel sensitization, as well as BRD7 and Bak in breast cancer remains unknown. In the present study, immunochemical staining was performed to measure the expression of BRD7 and Bak in breast cancer tissues. Cell Counting Kit‑8 assay, flow cytometry and tumor xenograft procedures were performed to evaluate the biological role of BRD7 and Bak in breast cancer cells. Western blotting, reverse transcription‑quantitative polymerase chain reaction, chromatin immunoprecipitation and luciferase reporter assays were also performed. BRD7 was positively correlated with Bak levels in breast cancer tissues, and the survival rate of patients with low Bak and BRD7 expression was significantly lower than that of patients with high Bak and BRD7 expression. In addition, BRD7 activated Bak promoter activity and induced Bak expression in an indirect manner. Furthermore, ectopic expression of BRD7 inhibited cell proliferation, tumor growth and sensitized cancer cells to paclitaxel, while knockdown of Bak abolished BRD7‑mediated inhibitory effects on cell proliferation and paclitaxel sensitization in breast cancer cells whether in vitro and in vivo. The results demonstrated that BRD7 inhibits cell proliferation and sensitizes breast cancer cells to paclitaxel by activating Bak; they also provide promising targets for the diagnosis and treatment of breast cancer.

Indexed as

Antineoplastic Agents, PhytogenicApoptosisbcl-2 Homologous Antagonist-Killer ProteinBreastBreast NeoplasmsBreast Neoplasms, MaleBromodomain Containing ProteinsCell ProliferationChromosomal Proteins, Non-HistoneDrug Resistance, NeoplasmFemaleGene Knockdown TechniquesHumansMaleMCF-7 CellsMiddle AgedAntineoplastic Agents, PhytogenicBAK1 protein, humanbcl-2 Homologous Antagonist-Killer ProteinBRD7 protein, humanBromodomain Containing ProteinsChromosomal Proteins, Non-HistonePaclitaxel

Identifiers

PMID30592293
PMCPMC6365691
OpenAlexW2906520367

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.