Evidence map›Paper›PMID 28633434›Full record

ArticleCarcinogenesis2017

PSIP1/p75 promotes tumorigenicity in breast cancer cells by promoting the transcription of cell cycle genes.

Deepak K Singh, Omid Gholamalamdari, Mahdieh Jadaliha, Xiao Ling Li, Yo-Chuen Lin, Yang Zhang, Shuomeng Guang, Seyedsasan Hashemikhabir, Saumya Tiwari, Yuelin J Zhu and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. PSIP1 promotes gefitinib resistance in lung adenocarcinoma by inducing the expression of WASF3 and its downstream ITGB3/AKT signaling.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. LEDGF/p75 Is Required for an Efficient DNA Damage Response.International journal of molecular sciences · 2021
    Article
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

21 authors at 7 institutions in 1 country.

Deepak K SinghDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Omid GholamalamdariDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Mahdieh JadalihaDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Xiao Ling LiDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Yo-Chuen LinDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Yang ZhangDepartment of Bioengineering, Beckman Institute of Advanced Science and Technology, UIUC, Urbana, IL 61801, USA.
Shuomeng GuangDepartment of Bioengineering, Beckman Institute of Advanced Science and Technology, UIUC, Urbana, IL 61801, USA.
Seyedsasan HashemikhabirDepartment of Biohealth Informatics, School of Informatics and Computing, Indiana University Purdue University Indianapolis, Indianapolis, IN 46202,USA.
Saumya TiwariDepartment of Bioengineering, Beckman Institute of Advanced Science and Technology, UIUC, Urbana, IL 61801, USA.
Yuelin J ZhuDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Abid KhanDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Anu Thomas
Arindam ChakrabortyDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Virgilia MaciasDepartment of Pathology, College of Medicine, University of Illinois at Chicago,Chicago, IL 60612, USA.
Andre K BallaDepartment of Pathology, College of Medicine, University of Illinois at Chicago,Chicago, IL 60612, USA.
Rohit BhargavaDepartment of Bioengineering, Beckman Institute of Advanced Science and Technology, UIUC, Urbana, IL 61801, USA.
Sarath Chandra JangaDepartment of Biohealth Informatics, School of Informatics and Computing, Indiana University Purdue University Indianapolis, Indianapolis, IN 46202,USA.
Jian MaDepartment of Bioengineering, Beckman Institute of Advanced Science and Technology, UIUC, Urbana, IL 61801, USA.
Supriya G PrasanthDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Ashish LalDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Kannanganattu V PrasanthDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL 61801,USA, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Center for Cancer Research · USUrbana University · USUniversity of Illinois Urbana-Champaign · USIndiana University – Purdue University Indianapolis · USUniversity of Illinois Chicago · USNational Cancer Institute · USThe University of Texas Southwestern Medical Center · US

Funding

Computational Methods for Next-Generation Comparative GenomicsR01HG007352 · NHGRI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI MA, JIAN · 2014 to 2023
$2.8M
Mapping RNA protein interaction networks in the human genomeR01GM123314 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI JANGA, SARATH CHANDRA · 2017 to 2021
$1.7M
Characterization of nuclear retained RNA-mediated gene regulatory mechanismR01GM088252 · NIGMS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI KANNANGANATTU, PRASANTH KUMAR VIJAYAN · 2011 to 2015
$1.4M
Role of ORCA in DNA replicationR01GM099669 · NIGMS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI PRASANTH, SUPRIYA G · 2012 to 2016
$1.3M
NHGRI NIH HHS R01 HG007352NIGMS NIH HHS R01 GM088252NIGMS NIH HHS R01 GM099669NIGMS NIH HHS R01 GM123314
6 · The paper itself

Abstract

Breast cancer (BC) is a highly heterogeneous disease, both at the pathological and molecular level, and several chromatin-associated proteins play crucial roles in BC initiation and progression. Here, we demonstrate the role of PSIP1 (PC4 and SF2 interacting protein)/p75 (LEDGF) in BC progression. PSIP1/p75, previously identified as a chromatin-adaptor protein, is found to be upregulated in basal-like/triple negative breast cancer (TNBC) patient samples and cell lines. Immunohistochemistry in tissue arrays showed elevated levels of PSIP1 in metastatic invasive ductal carcinoma. Survival data analyses revealed that the levels of PSIP1 showed a negative association with TNBC patient survival. Depletion of PSIP1/p75 significantly reduced the tumorigenicity and metastatic properties of TNBC cell lines while its over-expression promoted tumorigenicity. Further, gene expression studies revealed that PSIP1 regulates the expression of genes controlling cell-cycle progression, cell migration and invasion. Finally, by interacting with RNA polymerase II, PSIP1/p75 facilitates the association of RNA pol II to the promoter of cell cycle genes and thereby regulates their transcription. Our findings demonstrate an important role of PSIP1/p75 in TNBC tumorigenicity by promoting the expression of genes that control the cell cycle and tumor metastasis.

Indexed as

Adaptor Proteins, Signal TransducingBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationChromatinFemaleGene Expression Regulation, NeoplasticHumansOncogenesPromoter Regions, GeneticRNA Polymerase IITissue Array AnalysisTranscription FactorsTriple Negative Breast NeoplasmsAdaptor Proteins, Signal TransducingChromatinPSIP1 protein, humanRNA Polymerase IITranscription Factors

Identifiers

PMID28633434
PMCPMC6410955
OpenAlexW2626514904

What OpenQuestion holds

Textmetadata
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.