Evidence map›Paper›PMID 36592158›Full record

ArticleEMBO reports2023

MYB sustains hypoxic survival of pancreatic cancer cells by facilitating metabolic reprogramming.

Shashi Anand, Mohammad Aslam Khan, Haseeb Zubair, Sarabjeet Kour Sudan, Kunwar Somesh Vikramdeo, Sachin Kumar Deshmukh, Shafquat Azim, Sanjeev Kumar Srivastava, Seema Singh, Ajay Pratap Singh

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Proteomics in pancreatic cancer.Biomarker research · 2025
    Review
  6. Review
  7. Article
  8. Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Article
  11. Article
  12. Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

10 authors at 1 institution in 1 country.

Shashi AnandDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA.
Mohammad Aslam KhanDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA.
Haseeb ZubairDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA.ORCID 0000-0002-2340-592X
Sarabjeet Kour SudanDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA.
Kunwar Somesh VikramdeoDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA.
Sachin Kumar DeshmukhDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA.
Shafquat AzimDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA.
Sanjeev Kumar SrivastavaDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA.
Seema SinghDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA.
Ajay Pratap SinghDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, AL, USA.ORCID 0000-0003-3492-6330
USA Mitchell Cancer Institute · US

Funding

A novel molecular cross-talk driving pancreatic cancer progressionR01CA224306 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SINGH, AJAY PRATAP · 2018 to 2022
$1.7M
NCI NIH HHS R01 CA224306NCI NIH HHS R01CA224306
6 · The paper itself

Abstract

Extensive desmoplasia and poor vasculature renders pancreatic tumors severely hypoxic, contributing to their aggressiveness and therapy resistance. Here, we identify the HuR/MYB/HIF1α axis as a critical regulator of the metabolic plasticity and hypoxic survival of pancreatic cancer cells. HuR undergoes nuclear-to-cytoplasmic translocation under hypoxia and stabilizes MYB transcripts, while MYB transcriptionally upregulates HIF1α. Upon MYB silencing, pancreatic cancer cells fail to survive and adapt metabolically under hypoxia, despite forced overexpression of HIF1α. MYB induces the transcription of several HIF1α-regulated glycolytic genes by directly binding to their promoters, thus enhancing the recruitment of HIF1α to hypoxia-responsive elements through its interaction with p300-dependent histone acetylation. MYB-depleted pancreatic cancer cells exhibit a dramatic reduction in tumorigenic ability, glucose-uptake and metabolism in orthotopic mouse model, even after HIF1α restoration. Together, our findings reveal an essential role of MYB in metabolic reprogramming that supports pancreatic cancer cell survival under hypoxia.

Indexed as

Pancreatic NeoplasmsAnimalsCell HypoxiaCell Line, TumorHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMicePromoter Regions, GeneticHypoxia-Inducible Factor 1, alpha SubunitHIF1αhypoxiametabolic reprogrammingMYBpancreatic cancer

Identifiers

PMID36592158
PMCPMC9986821
OpenAlexW4313424415

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.