Evidence map›Paper›PMID 28182004›Full record

ArticleCell death & disease2017

Tenovin-6 impairs autophagy by inhibiting autophagic flux.

Hongfeng Yuan, Brandon Tan, Shou-Jiang Gao

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  8. The Roles of Histone Deacetylases and Their Inhibitors in Cancer Therapy.Frontiers in cell and developmental biology · 2020
    Review
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  10. Article
  11. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Hongfeng YuanDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Brandon TanDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Shou-Jiang GaoDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
University of Southern California · US

Funding

Cell Model for KSHV Infection and Genetic ManipulationR01CA096512 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Shou-Jiang Gao · 2003 to 2026
$7.4M
Roles of the K3 and K5 in KSHV Persistence and PathogenesisP01CA180779 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JUNG, JAE U · 2013 to 2017
$7.3M
Regulation of KSHV replication by N6-methyladenosine (m6A) - Diversity SupplementR01CA124332 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GAO, SHOU-JIANG · 2007 to 2025
$5.0M
Mechanism of KSHV-induced angiogenesisR01CA132637 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GAO, SHOU-JIANG · 2008 to 2020
$3.6M
HISTONE MODIFIERS IN ORAL KSHV INFECTION AND MALIGNANCIESR01DE025465 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GAO, SHOU-JIANG · 2015 to 2019
$2.0M
Targeting KSHV malignancies and persistent infectionR01CA197153 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GAO, SHOU-JIANG · 2015 to 2019
$1.9M
KSHV microRNAs in tumor invasion and angiogenesisR01CA213275 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GAO, SHOU-JIANG · 2017 to 2021
$959k
NCI NIH HHS P01 CA180779NCI NIH HHS R01 CA096512NCI NIH HHS R01 CA124332NCI NIH HHS R01 CA132637NCI NIH HHS R01 CA197153NCI NIH HHS R01 CA213275NIDCR NIH HHS R01 DE025465
6 · The paper itself

Abstract

Tenovin-6 has attracted significant interest because it activates p53 and inhibits sirtuins. It has anti-neoplastic effects on multiple hematopoietic malignancies and solid tumors in both in vitro and in vivo studies. Tenovin-6 was recently shown to impair the autophagy pathway in chronic lymphocytic leukemia cells and pediatric soft tissue sarcoma cells. However, whether tenovin-6 has a general inhibitory effect on autophagy and whether there is any involvement with SIRT1 and p53, both of which are regulators of the autophagy pathway, remain unclear. In this study, we have demonstrated that tenovin-6 increases microtubule-associated protein 1 light chain 3 (LC3-II) level in diverse cell types in a time- and dose-dependent manner. Mechanistically, the increase of LC3-II by tenovin-6 is caused by inhibition of the classical autophagy pathway via impairing lysosomal function without affecting the fusion between autophagosomes and lysosomes. Furthermore, we have revealed that tenovin-6 activation of p53 is cell type dependent, and tenovin-6 inhibition of autophagy is not dependent on its regulatory functions on p53 and SIRT1. Our results have shown that tenovin-6 is a potent autophagy inhibitor, and raised the precaution in interpreting results where tenovin-6 is used as an inhibitor of SIRT1.

Indexed as

A549 CellsAutophagosomesAutophagyBenzamidesCell LineCell Line, TumorHEK293 CellsHumansLeukemia, Lymphocytic, Chronic, B-CellLysosomesMicrotubule-Associated ProteinsSirtuin 1Tumor Suppressor Protein p53BenzamidesMicrotubule-Associated ProteinsSirtuin 1tenovin-6Tumor Suppressor Protein p53

Identifiers

PMID28182004
PMCPMC5386474
OpenAlexW2586808754

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.