Evidence map›Paper›PMID 28429085›Full record

ReviewHuman genetics2017

The role of RNA alternative splicing in regulating cancer metabolism.

Itamar Kozlovski, Zahava Siegfried, Adi Amar-Schwartz, Rotem Karni

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
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  7. Article
  8. Review
  9. Article
  10. Mucin Expression and Splicing Determine Novel Subtypes and Patient Mortality in Pancreatic Ductal Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Metabolic reprogramming in epithelial ovarian cancer.American journal of translational research · 2021
    Review
  19. Article
  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

4 authors at 1 institution in 1 country.

Itamar KozlovskiDepartment of Biochemistry and Molecular Biology, IMRIC, Hebrew University-Hadassah Medical School, Ein Karem, 91120, Jerusalem, Israel.
Zahava SiegfriedDepartment of Biochemistry and Molecular Biology, IMRIC, Hebrew University-Hadassah Medical School, Ein Karem, 91120, Jerusalem, Israel.
Adi Amar-SchwartzDepartment of Biochemistry and Molecular Biology, IMRIC, Hebrew University-Hadassah Medical School, Ein Karem, 91120, Jerusalem, Israel.
Rotem KarniDepartment of Biochemistry and Molecular Biology, IMRIC, Hebrew University-Hadassah Medical School, Ein Karem, 91120, Jerusalem, Israel. rotemka@ekmd.huji.ac.il.ORCID 0000-0002-7552-9617
Hebrew University of Jerusalem · IL

Funding

Israel Cancer Research Fund Len & Susan Mark Initiative for Ovarian and Uterine/MMMT Cancers AwardIsrael Science Foundation 1290/12Melanoma Research Alliance 307699
6 · The paper itself

Abstract

Tumor cells alter their metabolism by a wide array of mechanisms to promote growth and proliferation. Dysregulated expression and/or somatic mutations of key components of the glycolytic pathway/TCA cycle as well as other metabolic pathways allow tumor cells to improve their ability to survive harsh conditions such as hypoxia and the presence of reactive oxygen species, as well as the ability to obtain nutrients to increase lipids, protein, and nucleic acids biogenesis. Approximately 95% of the human protein encoding genes undergo alternative splicing (AS), a regulated process of gene expression that greatly diversifies the proteome by creating multiple proteins from a single gene. In recent years, a growing body of evidence suggests that unbalanced AS, the formation of certain pro-tumorigenic isoforms and the reduction of anti-tumorigenic isoforms, is implicated in a variety of cancers. It is becoming increasingly clear that cancer-associated AS contributes to increased growth and proliferation, partially due to effects on metabolic reprogramming. Here, we summarize the known roles of AS in regulating cancer metabolism. We present evidence supporting the idea that AS, in many types of cancer, acts as a molecular switch that alters metabolism to drive tumorigenesis. We propose that the elucidation of misregulated AS and its downstream effects on cancer metabolism emphasizes the need for new therapeutic approaches aiming to modulate the splicing machinery to selectively target cancer cells.

Indexed as

Alternative SplicingNeoplasmsRNA, NeoplasmAnimalsCitric Acid CycleGlycolysisHumansRNA, NeoplasmAerobic GlycolysisAlternative PolyadenylationAlternative SpliceSplice EventSplice Factor

Identifiers

PMID28429085
OpenAlexW2606183535

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.