Evidence map›Paper›PMID 25474301›Full record

ReviewCell proliferation2015

Key autophagic targets and relevant small-molecule compounds in cancer therapy.

X-P Tong, Y Chen, S-Y Zhang, T Xie, M Tian, M-R Guo, R Kasimu, L Ouyang, J-H Wang

Abstract readReview
In one paragraph

Review in Cell proliferation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. The role of autophagy in cardiac hypertrophy.Acta biochimica et biophysica Sinica · 2016
    Review
  13. Article
  14. Article
  15. Review
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

9 authors at 3 institutions in 1 country.

X-P TongState Key Laboratory of Biotherapy & Collaborative Innovation Center of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China; School of Pharmacy, China Pharmaceutical University, Nanjing, 211198, China.
Y Chen
S-Y Zhang
T Xie
M Tian
M-R Guo
R Kasimu
L Ouyang
J-H Wang
Sichuan University · CNState Key Laboratory of BiotherapyXinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a highly conserved lysosomal degradation process which can recycle unnecessary or dysfunctional cell organelles and proteins, thereby playing a crucial regulatory role in cell survival and maintenance. It has been widely accepted that autophagy regulates various pathological processes, among which cancer attracts much attention. Autophagy may either promote cancer cell survival by providing energy during unfavourable metabolic circumstance or can induce individual cancer cell death by preventing necrosis and increasing genetic instability. Thus, dual roles of autophagy may determine the destiny of cancer cells and make it an attractive target for small-molecule drug discovery. Collectively, key autophagy-related elements as potential targets, oncogenes mTORC1, class I PI3K and AKT, as well as tumour suppressor class III PI3K, Beclin-1 and p53, have been discussed. In addition, some small molecule drugs, such as rapamycin and its derivatives, rottlerin, PP242 and AZD8055 (targeting PI3K/AKT/mTORC1), spautin-1, and tamoxifen, as well as oridonin and metformin (targeting p53), can modulate autophagic pathways in different types of cancer. All these data will shed new light on targeting the autophagic process for cancer therapy, using small-molecule compounds, to fight cancer in the near future.

Indexed as

AutophagyAnimalsApoptosis Regulatory ProteinsBeclin-1HumansMembrane ProteinsNeoplasmsSignal TransductionSmall Molecule LibrariesTumor Suppressor Protein p53Apoptosis Regulatory ProteinsBeclin-1BECN1 protein, humanMembrane ProteinsSmall Molecule LibrariesTumor Suppressor Protein p53

Identifiers

PMID25474301
PMCPMC6496147
OpenAlexW2000805947

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.