Evidence map›Paper›PMID 32883024›Full record

ArticleCells2020

Targeting Oxidative Phosphorylation Reverses Drug Resistance in Cancer Cells by Blocking Autophagy Recycling.

Jae-Seon Lee, Ho Lee, Hyonchol Jang, Sang Myung Woo, Jong Bae Park, Seon-Hyeong Lee, Joon Hee Kang, Hee Yeon Kim, Jaewhan Song, Soo-Youl Kim

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Mapping cross-domain drivers of Alzheimer's disease risk through integrated network analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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

10 authors at 2 institutions in 1 country.

Jae-Seon LeeDivision of Cancer Biology, Research Institute, National Cancer Center, Goyang, Gyeonggi-do 10408, Korea.
Ho LeeDepartment of System Cancer Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Gyeonggi-do 10408, Korea.
Hyonchol JangDivision of Cancer Biology, Research Institute, National Cancer Center, Goyang, Gyeonggi-do 10408, Korea.ORCID 0000-0003-1436-457X
Sang Myung WooCenter for Liver and Pancreatobiliary Cancer, National Cancer Center, Goyang, Gyeonggi-do 10408, Korea.ORCID 0000-0003-3786-4403
Jong Bae ParkDepartment of System Cancer Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Gyeonggi-do 10408, Korea.
Seon-Hyeong LeeDivision of Cancer Biology, Research Institute, National Cancer Center, Goyang, Gyeonggi-do 10408, Korea.
Joon Hee KangDivision of Cancer Biology, Research Institute, National Cancer Center, Goyang, Gyeonggi-do 10408, Korea.
Hee Yeon KimDivision of Cancer Biology, Research Institute, National Cancer Center, Goyang, Gyeonggi-do 10408, Korea.
Jaewhan SongDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Korea.
Soo-Youl KimDivision of Cancer Biology, Research Institute, National Cancer Center, Goyang, Gyeonggi-do 10408, Korea.
National Cancer Center · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The greatest challenge in cancer therapy is posed by drug-resistant recurrence following treatment. Anticancer chemotherapy is largely focused on targeting the rapid proliferation and biosynthesis of cancer cells. This strategy has the potential to trigger autophagy, enabling cancer cell survival through the recycling of molecules and energy essential for biosynthesis, leading to drug resistance. Autophagy recycling contributes amino acids and ATP to restore mTOR complex 1 (mTORC1) activity, which leads to cell survival. However, autophagy with mTORC1 activation can be stalled by reducing the ATP level. We have previously shown that cytosolic NADH production supported by aldehyde dehydrogenase (ALDH) is critical for supplying ATP through oxidative phosphorylation (OxPhos) in cancer cell mitochondria. Inhibitors of the mitochondrial complex I of the OxPhos electron transfer chain and ALDH significantly reduce the ATP level selectively in cancer cells, terminating autophagy triggered by anticancer drug treatment. With the aim of overcoming drug resistance, we investigated combining the inhibition of mitochondrial complex I, using phenformin, and ALDH, using gossypol, with anticancer drug treatment. Here, we show that OxPhos targeting combined with anticancer drugs acts synergistically to enhance the anticancer effect in mouse xenograft models of various cancers, which suggests a potential therapeutic approach for drug-resistant cancer.

Indexed as

Aldehyde DehydrogenaseAnimalsAntineoplastic AgentsAutophagyDrug Resistance, NeoplasmDrug SynergismElectron Transport Complex IGossypolHT29 CellsHumansMiceMice, Inbred BALB CMice, NudeMitochondriaNeoplasmsOxidative PhosphorylationAldehyde DehydrogenaseAntineoplastic AgentsElectron Transport Complex IGossypolPhenforminaldehyde dehydrogenaseATP productioncancer metabolismenergy metabolismoxidative phosphorylation (OxPhos)

Identifiers

PMID32883024
PMCPMC7565066
OpenAlexW3081729395

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.