Evidence map›Paper›PMID 27629140›Full record

ReviewTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Emerging tale of UPR and cancer: an essentiality for malignancy.

Younis Mohammad Hazari, Arif Bashir, Ehtisham Ul Haq, Khalid Majid Fazili

Abstract readReview
PubMed Publisher
In one paragraph

Review in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.4field-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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
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  6. Article
  7. Article
  8. Type I interferons and endoplasmic reticulum stress in health and disease.International review of cell and molecular biology · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Ethyl Acetate Extract ofInternational journal of molecular sciences · 2018
    Article
  13. O-GlcNAc in cancer: An Oncometabolism-fueled vicious cycle.Journal of bioenergetics and biomembranes · 2018
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
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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.

Younis Mohammad HazariDepartment of Biotechnology, University of Kashmir, Srinagar, Jammu and Kashmir, 190006, India.
Arif BashirDepartment of Biotechnology, University of Kashmir, Srinagar, Jammu and Kashmir, 190006, India.
Ehtisham Ul HaqDepartment of Biotechnology, University of Kashmir, Srinagar, Jammu and Kashmir, 190006, India.
Khalid Majid FaziliDepartment of Biotechnology, University of Kashmir, Srinagar, Jammu and Kashmir, 190006, India. fazili@kashmiruniversity.ac.in.
University of Kashmir · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A set of cellular response to counter any alteration in homeostasis of a cell originating at endoplasmic reticulum is collectively termed as unfolded protein response (UPR). It initially is adaptive in nature as to restore cellular normalcy failing in course often activates pro-apoptotic signaling pathway resulting in cell death. UPR has emerged as an essential adaptation mechanism that cross talk with various cellular processes for cancer pathogenesis. Interestingly, it plays diverse role in plethora of signaling pathways instrumental in transformation, cell invasion, cell migration, metastasis, neovascularization, proliferation, and maintenance of energy metabolism of cancerous cells. In cancerous cells, it is triggered by change in microenvironment of a cell usually driven by hypoxia, acidosis, and nutrient deprivation, which often leads to positive selection pressure involving the reprogramming of energy metabolism which promotes channelization of limited metabolites into the hexosamine biosynthetic pathway (HBP). Substantial evidences suggest the role of UPR in oncogene (Myc, mTOR, RAS, HER2) driven cancer transformation and progression. In this review, we have comprehensively underlined the role played by UPR in adaptation, transformation, proliferation, invasion, and metastasis of cancerous cells.

Indexed as

Cell ProliferationCell Transformation, NeoplasticEndoplasmic ReticulumEndoplasmic Reticulum StressHumansNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsSignal TransductionTumor MicroenvironmentUnfolded Protein ResponseAcidosisAngiogenesisCancer metabolismER stressHexosamine biosynthesis pathwayHypoxiaNutrient deprivationTumor microenvironmentUnfolded protein response

Identifiers

PMID27629140
OpenAlexW2520532243

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.