Evidence map›Paper›PMID 28655885›Full record

ArticleScientific reports2017

miR-15a/miR-16 down-regulates BMI1, impacting Ub-H2A mediated DNA repair and breast cancer cell sensitivity to doxorubicin.

Nibedita Patel, Koteswara Rao Garikapati, Raj K Pandita, Dharmendra Kumar Singh, Tej K Pandita, Utpal Bhadra, Manika Pal Bhadra

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-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, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. The Role of MiRNA in Cancer: Pathogenesis, Diagnosis, and Treatment.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  11. Study on effects of miR-141-3p in proliferation, migration, invasion and apoptosis of colon cancer cells by inhibiting Bcl2.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Cell Cycle Regulation of Stem Cells by MicroRNAs.Stem cell reviews and reports · 2018
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Nibedita PatelCentre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Tarnaka, Hyderabad, Telangana State, 500007, India.
Koteswara Rao GarikapatiCentre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Tarnaka, Hyderabad, Telangana State, 500007, India.
Raj K PanditaDepartment of Radiation Oncology, Weill Cornell Medical College, The Methodist Hospital Research Institute, Houston, TX, 77030, USA.
Dharmendra Kumar SinghDepartment of Radiation Oncology, Weill Cornell Medical College, The Methodist Hospital Research Institute, Houston, TX, 77030, USA.
Tej K PanditaDepartment of Radiation Oncology, Weill Cornell Medical College, The Methodist Hospital Research Institute, Houston, TX, 77030, USA.ORCID 0000-0002-1399-808X
Utpal BhadraGene Silencing Group, Centre for Cellular and Molecular Biology, Hyderabad, Telangana State, 500007, India.
Manika Pal BhadraCentre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Tarnaka, Hyderabad, Telangana State, 500007, India. manikapb@gmail.com.
Cornell University · USIndian Institute of Chemical Technology · INCentre for Cellular and Molecular Biology · IN

Funding

CHROMATIN MODIFYING FACTORS CONTROL RADIATION RESPONSE AND GENOMIC STABILITYR01CA129537 · NCI · WASHINGTON UNIVERSITY · PI PANDITA, TEJ K · 2008 to 2018
$3.3M
Role of Heterochromatin protein 1 Beta in Genome Maintenance and OncogenesisR01GM109768 · NIGMS · METHODIST HOSPITAL RESEARCH INSTITUTE · PI PANDITA, TEJ K · 2014 to 2017
$1.2M
NCI NIH HHS R01 CA129537NIGMS NIH HHS R01 GM109768
6 · The paper itself

Abstract

The B-lymphoma Moloney murine leukemia virus insertion region-1 protein (BMI1) acts as an oncogene in various cancers, including breast cancer. Recent evidence suggests that BMI1 is rapidly recruited to sites of DNA double strand breaks where it facilitates histone H2A ubiquitination and DNA double strand break repair by homologous recombination. Here we show that miR-15a and miR-16 expression is decreased during the initial period after DNA damage where it would otherwise down-regulate BMI1, impairing DNA repair. Elevated miR-15a and miR-16 levels down-regulated BMI1 and other polycomb group proteins like RING1A, RING1B, EZH2 and also altered the expression of proteins associated with the BMI1 dependent ubiquitination pathway. Antagonizing the expression of miR-15a and miR-16, enhanced BMI1 protein levels and increased DNA repair. Further, overexpression of miR-15a and miR-16 sensitized breast cancer cells to DNA damage induced by the chemotherapeutic drug doxorubicin. Our results suggest that miR-15a and miR-16 mediate the down-regulation of BMI1, which impedes DNA repair while elevated levels can sensitize breast cancer cells to doxorubicin leading to apoptotic cell death. This data identifies a new target for manipulating DNA damage response that could impact the development of improved therapeutics for breast cancer.

Identifiers

PMID28655885
PMCPMC5487337
OpenAlexW2687743292

What OpenQuestion holds

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LicenceCC BY
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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.