Evidence map›Paper›PMID 26983466›Full record

ArticleAutophagy2016

A role for ABCG2 beyond drug transport: Regulation of autophagy.

Rui Ding, Shengkan Jin, Kirk Pabon, Kathleen W Scotto

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Biomedicines · 2024
    Article
  6. Article
  7. Cannabis Pharmacogenomics: A Path to Personalized Medicine.Current issues in molecular biology · 2023
    Review
  8. Review
  9. Two Important Anticancer Mechanisms of Natural and Synthetic Chalcones.International journal of molecular sciences · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020
    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.

Rui Dinga Cancer Institute of New Jersey and Robert Wood Johnson Medical School, Rutgers, State University of New Jersey , New Brunswick , NJ , USA.
Shengkan Jina Cancer Institute of New Jersey and Robert Wood Johnson Medical School, Rutgers, State University of New Jersey , New Brunswick , NJ , USA.
Kirk Pabona Cancer Institute of New Jersey and Robert Wood Johnson Medical School, Rutgers, State University of New Jersey , New Brunswick , NJ , USA.
Kathleen W Scottoa Cancer Institute of New Jersey and Robert Wood Johnson Medical School, Rutgers, State University of New Jersey , New Brunswick , NJ , USA.
Rutgers, The State University of New Jersey · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
NCI NIH HHS P30 CA072720
6 · The paper itself

Abstract

The ABC drug transporters, including ABCG2, are well known for their ability to efflux a wide spectrum of chemotherapeutic agents, thereby conferring a multidrug-resistant phenotype. However, studies over the past several years suggest that the ABC transporters may play additional role(s) in cell survival in the face of stress inducers that are not ABCG2 substrates (i.e., nutrient deprivation, ionizing radiation, rapamycin). The mechanism by which this occurs is largely unknown. In the present study, using several cancer cell lines and their ABCG2-overexpressing sublines, we show that cells overexpressing ABCG2 were more resistant to these stressors. This resistance was associated with an elevated level of autophagy flux, as measured by a higher rate of SQSTM1/p62 degradation and greater accumulation of LC3-II when compared to parental cells. Knockdown of ABCG2 reduced autophagic activity in resistant cells to a level similar to that observed in parental cells, confirming that the enhanced autophagy was ABCG2-dependent. Moreover, using cell viability, apoptosis, and clonogenic assays, we demonstrated that the ABCG2-expressing cells were more resistant to amino acid starvation and radiation-induced cell death. Importantly, knockdown of the critical autophagy factors ATG5 and ATG7 greatly reduced cell survival, verifying that enhanced autophagy was critical for this effect. Taken together, these data indicate that autophagy induced by various stressors is enhanced/accelerated in the presence of ABCG2, resulting in delayed cell death and enhanced cell survival. This defines a new role for this transporter, one with potential clinical significance.

Indexed as

Antineoplastic AgentsApoptosisATP Binding Cassette Transporter, Subfamily G, Member 2AutophagyCell Line, TumorCell SurvivalHumansMicrotubule-Associated ProteinsNeoplasm ProteinsRNA, Small InterferingABCG2 protein, humanAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily G, Member 2Microtubule-Associated ProteinsNeoplasm ProteinsRNA, Small InterferingABCG2ABC transportersamino acid starvationautophagyBCRPdrug transportersmultidrug resistanceradiationtumor cell survival

Identifiers

PMID26983466
PMCPMC4854550
OpenAlexW2300423472

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.