Evidence map›Paper›PMID 36472478›Full record

ArticleAutophagy2023

Autophagy inhibition signals through senescence to promote tumor suppression.

Nanfang Peng, Helen H Kang, Yan Feng, Alexander M Minikes, Xuejun Jiang

Open access · greenAbstract read
In one paragraph

Article in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  6. mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  13. Therapy-Induced Senescence: Novel Approaches for Markers Identification.International journal of molecular sciences · 2024
    Review
  14. Article
  15. Review
  16. 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

5 authors at 2 institutions in 1 country.

Nanfang PengCell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Helen H KangCell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Yan FengCell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Alexander M MinikesCell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Xuejun JiangCell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Memorial Sloan Kettering Cancer Center · USCornell University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Ferroptosis, Cellular Metabolism, and CancerR01CA204232 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI JIANG, XUEJUN · 2017 to 2025
$4.1M
Mechanisms and Function of Autophagy in CancerR01CA166413 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI JIANG, XUEJUN · 2013 to 2023
$3.9M
Ferroptosis and Cancer Cell SignalingR01CA258622 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Xuejun Jiang · 2022 to 2026
$2.2M
Morphine versus Methadone as First Line Strong Opioid for Cancer PainR01CA124481 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BRUERA, EDUARDO · 2007 to 2009
$1.2M
Cell adhesion and ferroptosis: investigating a potential vulnerability in cancer cellsF31CA247112 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MINIKES, ALEXANDER MICHAEL · 2020 to 2021
$92k
NCI NIH HHS F31 CA247112NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA124481NCI NIH HHS R01 CA166413NCI NIH HHS R01 CA204232NCI NIH HHS R01 CA258622
6 · The paper itself

Abstract

Macroautophagy/autophagy, a stress-responsive cellular survival mechanism, plays important and context-dependent roles in cancer, and its inhibition has been implicated as a promising cancer therapeutic approach. The detailed mechanisms underlying the function of autophagy in cancer have not been fully understood. In this study, we show that autophagy inhibition promotes both the efficacy of chemotherapy for the treatment of glioblastoma (GBM) and therapy-induced senescence of GBM cells. As a specific cell fate characterized by permanent cell cycle arrest, senescence is also associated with the expression of a panel of specific secreted protein factors known as senescence-associated secretory phenotype (SASP). Intriguingly, we found that autophagy inhibition not only quantitatively enhanced GBM cell senescence but also qualitatively altered the spectrum of SASP. The altered SASP had increased potent activity to induce paracrine senescence of neighboring GBM cells, to skew macrophage polarization toward the anti-tumor M1 state, and to block the recruitment of pro-tumor neutrophils to GBM tumor tissues. Taken together, this study reveals novel functional communication between autophagy and senescence and suggests cancer therapeutic approaches harnessing autophagy blockage in inducing senescence-mediated antitumor immunity.

Indexed as

AutophagyGlioblastomaCellular SenescenceHumansantitumor immunityAutophagyglioblastoma multiformSASPsenescence

Identifiers

PMID36472478
PMCPMC10262760
OpenAlexW4311588711

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.