Evidence map›Paper›PMID 36807391›Full record

ArticleCancer gene therapy2023

Suppression of fatty acid oxidation supports pancreatic cancer growth and survival under hypoxic conditions through autophagy induction.

Byungjoo Kim, Jihye Gwak, Minjoong Kim, Seungyeon Yang, Sunsook Hwang, Seungmin Shin, Ji Hye Kim, Jaekyoung Son, Seung Min Jeong

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

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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 2 institutions in 1 country.

Byungjoo KimDepartment of Biochemistry, Institute for Aging and Metabolic Diseases, Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul, 06591, South Korea.
Jihye GwakDepartment of Biochemistry, Institute for Aging and Metabolic Diseases, Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul, 06591, South Korea.
Minjoong KimDepartment of Biochemistry, Institute for Aging and Metabolic Diseases, Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul, 06591, South Korea.ORCID 0000-0003-1065-7914
Seungyeon YangDepartment of Biochemistry, Institute for Aging and Metabolic Diseases, Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul, 06591, South Korea.
Sunsook HwangDepartment of Biochemistry, Institute for Aging and Metabolic Diseases, Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul, 06591, South Korea.
Seungmin ShinDepartment of Biochemistry, Institute for Aging and Metabolic Diseases, Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul, 06591, South Korea.
Ji Hye KimDepartment of Biomedical Sciences, Asan Medical Center, AMIST, University of Ulsan College of Medicine, Seoul, 05505, South Korea.
Jaekyoung SonDepartment of Biomedical Sciences, Asan Medical Center, AMIST, University of Ulsan College of Medicine, Seoul, 05505, South Korea.
Seung Min JeongDepartment of Biochemistry, Institute for Aging and Metabolic Diseases, Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul, 06591, South Korea. smjeong@catholic.ac.kr.ORCID 0000-0002-9787-2539
Catholic University of Korea · KRUlsan College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia, one of the key features of solid tumors, induces autophagy, which acts as an important adaptive mechanism for tumor progression under hypoxic environment. Cellular metabolic reprogramming has been correlated with hypoxia, but the molecular connection to the induction of autophagy remains obscure. Here, we show that suppression of fatty acid oxidation (FAO) by hypoxia induces autophagy in human pancreatic ductal adenocarcinoma (PDAC) cells that is required for their growth and survival. Reduced cellular acetyl-CoA levels caused by FAO inhibition decreases LC3 acetylation, resulting in autophagosome formation. Importantly, PDAC cells are significantly dependent on this metabolic reprogramming, as improving FAO leads to a reduction in hypoxia-induced autophagy and an increase in cell death after chemotherapy. Thus, our study supports that suppression of FAO is an important metabolic response to hypoxia and indicates that targeting this pathway in PDAC may be an effective therapeutic approach.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsAutophagyCell Line, TumorCell ProliferationFatty AcidsHumansHypoxiaFatty Acids

Identifiers

PMID36807391
OpenAlexW4321212702

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.