Evidence map›Paper›PMID 26701852›Full record

ArticleOncotarget2016

miR-101 reverses hypomethylation of the PRDM16 promoter to disrupt mitochondrial function in astrocytoma cells.

Qianqian Lei, Xiaoping Liu, Haijuan Fu, Yingnan Sun, Liping Wang, Gang Xu, Wei Wang, Zhibin Yu, Changhong Liu, Peiyao Li and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Fumonisin BEpigenetics · 2025
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  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Multifaceted Role of PRDM Proteins in Human Cancer.International journal of molecular sciences · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. LINC00470 Coordinates the Epigenetic Regulation of ELFN2 to Distract GBM Cell Autophagy.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    Article
  16. Article
  17. Epigenetics and MicroRNAs in Cancer.International journal of molecular sciences · 2018
    Review
  18. Article
  19. Article
  20. Review
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 4 institutions in 1 country.

Qianqian LeiHunan Provincial Tumor Hospital and The Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha 410013, Hunan, China.
Xiaoping LiuDepartment of Breast Oncology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, Guangdong, China.
Haijuan FuCancer Research Institute, School of Basic Medical Science, Central South University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Yingnan SunHunan Provincial Tumor Hospital and The Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha 410013, Hunan, China.
Liping WangDepartment of Oncology, The First Hospital of Chenzhou City, 423000, Hunan, China.
Gang XuCancer Research Institute, School of Basic Medical Science, Central South University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Wei WangCancer Research Institute, School of Basic Medical Science, Central South University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Zhibin YuCancer Research Institute, School of Basic Medical Science, Central South University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Changhong LiuCancer Research Institute, School of Basic Medical Science, Central South University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Peiyao LiCancer Research Institute, School of Basic Medical Science, Central South University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Jianbo FengCancer Research Institute, School of Basic Medical Science, Central South University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Guiyuan LiHunan Provincial Tumor Hospital and The Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha 410013, Hunan, China.
Minghua WuCancer Research Institute, School of Basic Medical Science, Central South University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Central South University · CNChenzhou First People's Hospital · CNHunan Cancer Hospital · CNSun Yat-sen University Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous report identified PR domain containing 16 (PRDM16), a member of the PR-domain gene family, as a new methylation associated gene in astrocytoma cells. This previous study also reported that miR-101 is a tumor suppressor in glioma. The present study confirms that PRDM16 is a hypomethylated gene that can be overexpressed in astrocytoma patients and demonstrates that the hypomethylation status of the PRDM16 promoter can predict poor prognoses for astrocytoma patients. The results reported herein show that PRDM16 was inhibited by miR-101 directly and also through epigenetic regulation. PRDM16 was confirmed as a new target of miR-101 and shown to be directly inhibited by miR-101. miR-101 also decreased the expression of PRDM16 by altering the methylation status of the PRDM16 promoter. miR-101 was associated with a decrease in the methylation-related histones H3K4me2 and H3K27me3 and an increase in H3K9me3 and H4K20me3 on the PRDM16 promoter. In addition, EZH2, EED and DNMT3A were identified as direct targets of miR-101, and miR-101 suppressed PRDM16 expression by targeting DNMT3A which decreases histone H3K27me3 and H3K4me2 at the PRDM16 core promoter. The results reported here demonstrate that miR-101 disrupted cellular mitochondrial function and induced cellular apoptosis via the mitochondrial pathway; for example, MMP and ATP levels decreased, while there was an increase in ADP/ATP ratios and ROS levels, levels of cleaved Caspase-9 and cleaved-PARP, the Bax/Bcl-2 ratios, and Smac release from the mitochondria to the cytoplasm. Knockdown of PRDM16 reversed the anti-apoptotic effect of miR-101 inhibition. In summary, miR-101 reversed the hypomethylation of the PRDM16 promoter which suppressed the expression of PRDM16, disrupted cellular mitochondrial function, and induced cellular apoptosis.

Indexed as

DNA MethylationAdolescentAdultAgedAstrocytomaBlotting, WesternDNA-Binding ProteinsEpigenesis, GeneticFemaleHumansImmunoenzyme TechniquesMaleMembrane Potential, MitochondrialMicroRNAsMiddle AgedMitochondriaDNA-Binding ProteinsMicroRNAsMIRN101 microRNA, humanPRDM16 protein, humanReactive Oxygen SpeciesRNA, MessengerTranscription FactorshypomethylationmiR-101mitochondriaPRDM16ROS

Identifiers

PMID26701852
PMCPMC4826261
OpenAlexW2219658062

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.