Evidence map›Paper›PMID 28409693›Full record

ArticleAutophagy2017

TPT1 (tumor protein, translationally-controlled 1) negatively regulates autophagy through the BECN1 interactome and an MTORC1-mediated pathway.

Seong-Yeon Bae, Sanguine Byun, Soo Han Bae, Do Sik Min, Hyun Ae Woo, Kyunglim Lee

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  14. When autophagy meets placenta development and pregnancy complications.Frontiers in cell and developmental biology · 2024
    Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Autophagy · 2021
    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

6 authors at 4 institutions in 1 country.

Seong-Yeon Baea Graduate School of Pharmaceutical Sciences , College of Pharmacy, Ewha Womans University , Seoul , Korea.
Sanguine Byunb Division of Bioengineering , College of Life and Sciences and Bioengineering, Incheon National University , Incheon , Korea.
Soo Han Baec Severance Biomedical Science Institute, Yonsei Biomedical Research Institute, Yonsei University College of Medicine , Seoul , Korea.
Do Sik Mind Department of Molecular Biology , College of Natural Sciences, Pusan National University , Busan , Korea.
Hyun Ae Wooa Graduate School of Pharmaceutical Sciences , College of Pharmacy, Ewha Womans University , Seoul , Korea.
Kyunglim Leea Graduate School of Pharmaceutical Sciences , College of Pharmacy, Ewha Womans University , Seoul , Korea.
Ewha Womans University · KRIncheon National University · KRPusan National University · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TPT1/TCTP (tumor protein, translationally-controlled 1) is highly expressed in tumor cells, known to participate in various cellular activities including protein synthesis, growth and cell survival. In addition, TPT1 was identified as a direct target of the tumor suppressor TP53/p53 although little is known about the mechanism underlying the anti-survival function of TPT1. Here, we describe a role of TPT1 in the regulation of the MTORC1 pathway through modulating the molecular machinery of macroautophagy/autophagy. TPT1 inhibition induced cellular autophagy via the MTORC1 and AMPK pathways, which are inhibited and activated, respectively, during treatment with the MTOR inhibitor rapamycin. We also found that the depletion of TPT1 potentiated rapamycin-induced autophagy by synergizing with MTORC1 inhibition. We further demonstrated that TPT1 knockdown altered the BECN1 interactome, a representative MTOR-independent pathway, to stimulate autophagosome formation, via downregulating BCL2 expression through activating MAPK8/JNK1, and thereby enhancing BECN1-phosphatidylinositol 3-kinase (PtdIns3K)-UVRAG complex formation. Furthermore, reduced TPT1 promoted autophagic flux by modulating not only early steps of autophagy but also autophagosome maturation. Consistent with in vitro findings, in vivo organ analysis using Tpt1 heterozygote knockout mice showed that autophagy is enhanced because of haploinsufficient TPT1 expression. Overall, our study demonstrated the novel role of TPT1 as a negative regulator of autophagy that may have potential use in manipulating various diseases associated with autophagic dysfunction.

Indexed as

AnimalsAutophagyBeclin-1Biomarkers, TumorGene Knockdown TechniquesHumansMechanistic Target of Rapamycin Complex 1MiceNeoplasm ProteinsPhosphatidylinositol 3-KinasesProtein Processing, Post-TranslationalSignal TransductionTumor Protein, Translationally-Controlled 1Beclin-1BECN1 protein, humanBecn1 protein, mouseBiomarkers, TumorMechanistic Target of Rapamycin Complex 1Neoplasm ProteinsPhosphatidylinositol 3-KinasesTPT1 protein, humanTpt1 protein, mouseTumor Protein, Translationally-Controlled 1autophagyBCL2BECN1MTORC1TP53 target geneTPT1/TCTP

Identifiers

PMID28409693
PMCPMC5446065
OpenAlexW2588981667

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.