Evidence map›Paper›PMID 29725006›Full record

ArticleCell death & disease2018

BRD7 inhibits the Warburg effect and tumor progression through inactivation of HIF1α/LDHA axis in breast cancer.

Weihong Niu, Yanwei Luo, Xinye Wang, Yao Zhou, Hui Li, Heran Wang, Yaojie Fu, Shanshan Liu, Shanghelin Yin, Jianglei Li and 10 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 2 institutions in 4 countries.

Weihong NiuThe Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Yanwei LuoThe Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, People's Republic of China.
Xinye WangThe Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, People's Republic of China.
Yao ZhouThe Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, People's Republic of China.
Hui LiThe Second Xiang-Ya Hospital, Central South University, Changsha, Hunan, 410011, People's Republic of China.
Heran WangThe Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Yaojie FuMedical school of Xiangya, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Shanshan LiuMedical school of Xiangya, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Shanghelin YinMedical school of Xiangya, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Jianglei LiMedical school of Xiangya, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Ran ZhaoThe Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, People's Republic of China.
Yukun LiuThe Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, People's Republic of China.
Songqing FanThe Second Xiang-Ya Hospital, Central South University, Changsha, Hunan, 410011, People's Republic of China.
Zheng LiThe Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, People's Republic of China.
Wei XiongThe Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, People's Republic of China.
Xiaoling LiThe Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, People's Republic of China.
Guiyuan LiThe Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, Hunan, 410013, People's Republic of China.
Caiping RenCancer Research Institute, Central South University, Changsha, Hunan, 410078, People's Republic of China.
Ming TanMitchell Cancer Institute, University of South Alabama, Mobile, AL, 36604, USA. mtan@health.southalabama.edu.ORCID 0000-0003-2007-9898
Ming ZhouThe Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, Hunan, 410013, People's Republic of China. zhouming2001@163.com.
Central South University · CNUSA Mitchell Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The bromodomain-containing protein 7 (BRD7) was first identified as a tumor suppressor in nasopharyngeal carcinoma and has critical roles in cancer development and progression. However, the regulatory roles and mechanisms of BRD7 in cancer metabolism are still unknown. In this study, we demonstrated that BRD7 was lowly expressed in breast cancer tissues and was identified as a poor prognostic factor in breast cancer. Meanwhile, BRD7 could suppress cell proliferation, initiate cell apoptosis and reduce aerobic glycolysis, suggesting that BRD7 plays a tumor suppressive roles in breast cancer. Mechanistically, BRD7 could negatively regulate a critical glycolytic enzyme LDHA through directly interaction with its upstream transcription factor, HIF1α, facilitating degradation of HIF1α mediated by ubiquitin-proteasome pathway. Moreover, restoring the expression of LDHA in breast cancer cells could reverse the effect of BRD7 on aerobic glycolysis, cell proliferation, and tumor formation, as well as the expression of cell cycle and apopotosis related molecules such as cyclin D1, CDK4, P21, and c-PARP both in vitro and in vivo. Taken together, these results indicate that BRD7 acts as a tumor suppressor in breast cancer and represses the glycolysis and tumor progression through inactivation of HIF1α/LDHA transcription axis.

Identifiers

PMID29725006
PMCPMC5938698
OpenAlexW2801137679

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.