Evidence map›Paper›PMID 32345326›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

CPI-613 rewires lipid metabolism to enhance pancreatic cancer apoptosis via the AMPK-ACC signaling.

Lixia Gao, Zhigang Xu, Zheng Huang, Yan Tang, Donglin Yang, Jiuhong Huang, Leilei He, Manran Liu, Zhongzhu Chen, Yong Teng

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

77 citing papers in PubMed, 135 citations in OpenAlex.

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  17. PANoptosis: potential new targets and therapeutic prospects in digestive diseases.Apoptosis : an international journal on programmed cell death · 2025
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17 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 2 countries.

Lixia GaoNational & Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, College of Pharmacy, Chongqing University of Arts and Sciences, Chongqing, 402160, People's Republic of China.
Zhigang XuNational & Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, College of Pharmacy, Chongqing University of Arts and Sciences, Chongqing, 402160, People's Republic of China.
Zheng HuangNational & Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, College of Pharmacy, Chongqing University of Arts and Sciences, Chongqing, 402160, People's Republic of China.
Yan TangNational & Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, College of Pharmacy, Chongqing University of Arts and Sciences, Chongqing, 402160, People's Republic of China.
Donglin YangNational & Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, College of Pharmacy, Chongqing University of Arts and Sciences, Chongqing, 402160, People's Republic of China.
Jiuhong HuangNational & Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, College of Pharmacy, Chongqing University of Arts and Sciences, Chongqing, 402160, People's Republic of China.
Leilei HeDepartment of Oral Biology and Diagnostic Sciences, Dental College of Georgia, Augusta University, 1120 15th Street, Augusta, GA, 30912, USA.
Manran LiuKey Laboratory of Laboratory Medical Diagnostics Designated By Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China.
Zhongzhu ChenNational & Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, College of Pharmacy, Chongqing University of Arts and Sciences, Chongqing, 402160, People's Republic of China.
Yong TengDepartment of Oral Biology and Diagnostic Sciences, Dental College of Georgia, Augusta University, 1120 15th Street, Augusta, GA, 30912, USA. yteng@augusta.edu.ORCID http://orcid.org/0000-0002-1856-7289
Chongqing University of Arts and Sciences · CNAugusta University · USChongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic cancer remains one of the most rapidly progressive and deadly malignancies worldwide. Current treatment regimens only result in small improvements in overall survival for patients with this cancer type. CPI-613 (Devimistat), a novel lipoate analog inhibiting mitochondrial metabolism, shows the new hope for pancreatic cancer treatment as an efficient and well-tolerated therapeutic option treated alone or in combination with chemotherapy.

methodsPancreatic cancer cells growing in planar 2D cultures and 3D scaffold were used as research platforms. Cell viability was measured by MTT and alamarBlue, and apoptosis was assessed by JC-1 staining and flow cytometry with Annexin V-FITC/PI staining. The mechanism behind CPI-613 action was analyzed by western blot, transmission electron microscopy, and lipolysis assay kits, in the presence or absence of additional signaling pathway inhibitors or gene modifications.

resultsCPI-613 exhibits anticancer activity in pancreatic cancer cells by triggering ROS-associated apoptosis, which is accompanied by increased autophagy and repressed lipid metabolism through activating the AMPK signaling. Intriguingly, ACC, the key enzyme modulating lipid metabolism, is identified as a vital target of CPI-613, which is inactivated in an AMPK-dependent manner and influences apoptotic process upon CPI-613. Blockade or enhancement of autophagic process does not increase or blunt apoptosis to CPI-613, but inhibition of the AMPK-ACC signaling significantly attenuates apoptosis induced by CPI-613, suggesting CPI-613-mediated lipid metabolism reduction contributes to its cytotoxicity in pancreatic cancer cells.

conclusionsThese findings explore the critical role of lipid metabolism in apoptosis, providing new insights into the AMPK-ACC signaling axis in crosstalk between lipid metabolism and apoptosis in CPI-613 treatment.

Indexed as

Acetyl-CoA CarboxylaseAMP-Activated Protein KinasesApoptosisCaprylatesCell Line, TumorHumansLipid MetabolismMitochondriaPancreatic NeoplasmsReactive Oxygen SpeciesSignal TransductionSulfidesAcetyl-CoA CarboxylaseAMP-Activated Protein KinasesCaprylatesdevimistatReactive Oxygen SpeciesSulfidesApoptosisCPI-613Lipid metabolismPancreatic cancerThe AMPK-ACC signaling

Identifiers

PMID32345326
PMCPMC7187515
OpenAlexW3017886823

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.