Evidence map›Paper›PMID 33400401›Full record

ArticleMolecular oncology2021

Multiomics integrative analysis reveals antagonistic roles of CBX2 and CBX7 in metabolic reprogramming of breast cancer.

Mohammad Askandar Iqbal, Shumaila Siddiqui, Asad Ur Rehman, Farid Ahmad Siddiqui, Prithvi Singh, Bhupender Kumar, Daman Saluja

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. CBX6 induces CD8Cell biology and toxicology · 2025
    Article
  4. Article
  5. Review
  6. DNMT1-Induced Downregulation of CBX7 Inhibits ERK Phosphorylation and Promotes Pancreatic Ductal Adenocarcinoma Progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Review
  8. Article
  9. CBX2 suppresses interferon signaling to diminish tumor immunogenicity via a noncanonical corepressor complex.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

7 authors at 3 institutions in 2 countries.

Mohammad Askandar IqbalDepartment of Biotechnology, Faculty of Natural Sciences, Jamia Millia Islamia (A Central University), New Delhi, India.ORCID 0000-0003-3485-3530
Shumaila SiddiquiDepartment of Biotechnology, Faculty of Natural Sciences, Jamia Millia Islamia (A Central University), New Delhi, India.
Asad Ur RehmanDr. B. R. Ambedkar Center for Biomedical Research, University of Delhi, India.
Farid Ahmad SiddiquiDepartment of Biotechnology, Faculty of Natural Sciences, Jamia Millia Islamia (A Central University), New Delhi, India.
Prithvi SinghDepartment of Biotechnology, Faculty of Natural Sciences, Jamia Millia Islamia (A Central University), New Delhi, India.
Bhupender KumarDepartment of Biochemistry, Institute of Home Economics, University of Delhi, India.
Daman SalujaDr. B. R. Ambedkar Center for Biomedical Research, University of Delhi, India.
Department of Biotechnology · INUniversity of Delhi · INÅbo Akademi University · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Striking similarity exists between metabolic changes associated with embryogenesis and tumorigenesis. Chromobox proteins-CBX2/4/6/7/8, core components of canonical polycomb repressor complex 1, play essential roles in embryonic development and aberrantly expressed in breast cancer. Understanding how altered CBX expression relates to metabolic reprogramming in breast cancer may reveal vulnerabilities of therapeutic pertinence. Using transcriptomic and metabolomic data from breast cancer patients (N > 3000 combined), we performed pathway-based analysis and identified outstanding roles of CBX2 and CBX7 in positive and negative regulation of glucose metabolism, respectively. Genetic ablation experiments validated the contrasting roles of two isoforms in cancer metabolism and cell growth. Furthermore, we provide evidence for the role of mammalian target of rapamycin complex 1 signaling in mediating contrary effects of CBX2 and CBX7 on breast cancer metabolism. Underpinning the biological significance of metabolic roles, CBX2 and CBX7 were found to be the most up- and downregulated isoforms, respectively, in breast tumors compared with normal tissues. Moreover, CBX2 and CBX7 expression (not other isoforms) correlated strongly, but oppositely, with breast tumor subtype aggressiveness and the proliferation markers. Consistently, genomic data also showed higher amplification frequency of CBX2, not CBX7, in breast tumors. Highlighting the clinical significance of findings, disease-specific survival and drug sensitivity analysis revealed that CBX2 and CBX7 predicted patient outcome and sensitivity to FDA-approved/investigational drugs. In summary, this work identifies novel cross talk between CBX2/7 and breast tumor metabolism, and the results presented may have implications in strategies targeting breast cancer.

Indexed as

Breast NeoplasmsWarburg Effect, OncologicCarcinogenesisDrug Resistance, NeoplasmEnergy MetabolismFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksGenomicsGlycolysisHumansMCF-7 CellsMetabolismMetabolomicsPolycomb Repressive Complex 1CBX2 protein, humanCBX7 protein, humanPolycomb Repressive Complex 1breast cancerCBX2CBX7glycolysismetabolic reprogrammingWarburg effect

Identifiers

PMID33400401
PMCPMC8096797
OpenAlexW3119234364

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.