Evidence map›Paper›PMID 31578585›Full record

ArticleOncology reports2019

Apurinic endonuclease 1 promotes the cisplatin resistance of lung cancer cells by inducing Parkin‑mediated mitophagy.

Zheng Li, Yongqiang Wang, Linbo Wu, Yalu Dong, Jing Zhang, Fan Chen, Wei Xie, Jianguo Huang, Ning Lu

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.9field-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

19 citing papers in PubMed, 34 citations in OpenAlex.

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  9. METTL3 promotes chemoresistance in small cell lung cancer by inducing mitophagy.Journal of experimental & clinical cancer research : CR · 2023
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  10. Review
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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.

Zheng LiCancer Center, Xinjiang Military Area General Hospital, Urumchi, Xinjiang Uygur Autonomous Region 830000, P.R. China.
Yongqiang WangCancer Center, Xinjiang Military Area General Hospital, Urumchi, Xinjiang Uygur Autonomous Region 830000, P.R. China.
Linbo WuCancer Center, Xinjiang Military Area General Hospital, Urumchi, Xinjiang Uygur Autonomous Region 830000, P.R. China.
Yalu DongCancer Center, Xinjiang Military Area General Hospital, Urumchi, Xinjiang Uygur Autonomous Region 830000, P.R. China.
Jing ZhangCancer Center, Xinjiang Military Area General Hospital, Urumchi, Xinjiang Uygur Autonomous Region 830000, P.R. China.
Fan ChenCancer Center, Xinjiang Military Area General Hospital, Urumchi, Xinjiang Uygur Autonomous Region 830000, P.R. China.
Wei XieCancer Center, Xinjiang Military Area General Hospital, Urumchi, Xinjiang Uygur Autonomous Region 830000, P.R. China.
Jianguo HuangCancer Center, Xinjiang Military Area General Hospital, Urumchi, Xinjiang Uygur Autonomous Region 830000, P.R. China.
Ning LuCancer Center, Xinjiang Military Area General Hospital, Urumchi, Xinjiang Uygur Autonomous Region 830000, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platinum‑containing doublet chemotherapy is the cornerstone of lung cancer treatment; however, cisplatin resistance is a major obstacle in the treatment of lung cancer. However, the mechanism underlying this resistance has not been fully elucidated. Previous studies have shown that serum apurinic/apyrimidinic endonuclease 1 (APE1) levels in patients with NSCLC are inversely associated with progression‑free survival after platinum‑containing doublet chemotherapy, and can serve as a biomarker for predicting disease prognosis and treatment efficacy. The present study was designed to investigate the role played by APE1 in the resistance of lung cancer to cisplatin. The levels of mitochondrial apurinic endonuclease 1 (m‑APE1) and total APE1 (t‑APE1) protein in a cisplatin‑resistant A549 cell line (A549/DDP) and cisplatin‑sensitive A549 cells were analyzed by western blotting. Mitochondrial membrane potential was detected by using the JC‑1 staining method. The cisplatin‑resistance of APE1‑overexpressing A549 cells and APE1‑silenced A549/DDP cells was assessed by cell apoptosis and colony formation assays. The results revealed that cisplatin‑resistant A549 cells contained high levels of APE1, and exhibited elevated levels of autophagy. The levels of m‑APE1 and t‑APE1 protein were increased in the A549/DDP cells when compared with these levels in the A549 cells. Overexpression of APE1 and Mia40 enhanced the cisplatin resistance and autophagy of the A549 cells. APE1 knockdown restored the cisplatin sensitivity and reduced the levels of LC3II and Parkin in the A549/DDP cells, but promoted the release of cytochrome c. Furthermore, Parkin silencing or treatment with 3‑methyladenine (3‑MA, an autophagy inhibitor) promoted the apoptosis of APE1‑overexpressing A549 cells, indicating that Parkin‑mediated mitophagy plays an important role in the APE1‑induced cisplatin resistance of A549 cells. In conclusion, APE1 promotes the cisplatin resistance of lung cancer cells by inducing Parkin‑mediated mitophagy.

Indexed as

AutophagyDrug Resistance, NeoplasmMitophagyA549 CellsAntineoplastic AgentsApoptosisCell ProliferationCisplatinDNA-(Apurinic or Apyrimidinic Site) LyaseHumansLung NeoplasmsMembrane Potential, MitochondrialTumor Cells, CulturedUbiquitin-Protein LigasesAntineoplastic AgentsAPEX1 protein, humanCisplatinDNA-(Apurinic or Apyrimidinic Site) Lyaseparkin proteinUbiquitin-Protein Ligases

Identifiers

PMID31578585
PMCPMC6826301
OpenAlexW2994421311

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.