Evidence map›Paper›PMID 31574980›Full record

ArticleCancers2019

CNOT2 Is Critically Involved in Atorvastatin Induced Apoptotic and Autophagic Cell Death in Non-Small Cell Lung Cancers.

Jihyun Lee, Ji Hoon Jung, Jisung Hwang, Ji Eon Park, Ju-Ha Kim, Woon Yi Park, Jin Young Suh, Sung-Hoon Kim

Open access · goldAbstract read
In one paragraph

Article in Cancers, 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
2.1field-weighted citation impact, top 13% 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, 26 citations in OpenAlex.

  1. Article
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  3. Elucidating the Role ofCurrent issues in molecular biology · 2025
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  7. Review
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  10. Gene regulatory Networks Reveal Sex Difference in Lung Adenocarcinoma.bioRxiv : the preprint server for biology · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Design and Characterization of Atorvastatin Dry Powder Formulation as a potential Lung Cancer Treatment.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

8 authors at 1 institution in 1 country.

Jihyun LeeCollege of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. jhlee096@naver.com.
Ji Hoon JungCollege of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. johnsperfume@gmail.com.ORCID 0000-0002-5644-5960
Jisung HwangCollege of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. hjsung0103@naver.com.
Ji Eon ParkCollege of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. wdnk77@naver.com.
Ju-Ha KimCollege of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. 964juha@daum.net.
Woon Yi ParkCollege of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. wy1319@naver.com.
Jin Young SuhCollege of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. jysuh3670@gmail.com.
Sung-Hoon KimCollege of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. sungkim7@khu.ac.kr.ORCID 0000-0003-2423-1973
Kyung Hee University · KR

Funding

National Research Foundation of Korea 2017R1A2A1A17069297
6 · The paper itself

Abstract

Though Atorvastatin has been used as a hypolipidemic agent, its anticancer mechanisms for repurposing are not fully understood so far. Thus, in the current study, its apoptotic and autophagic mechanisms were investigated in non-small cell lung cancers (NSCLCs). Atorvastatin increased cytotoxicity, sub G1 population, the number of apoptotic bodies, cleaved poly (ADP-ribose) polymerase (PARP) and caspase 3 and activated p53 in H1299, H596, and H460 cells. Notably, Atorvastatin inhibited the expression of c-Myc and induced ribosomal protein L5 and L11, but depletion of L5 reduced PARP cleavages induced by Atorvastatin rather than L11 in H1299 cells. Also, Atorvastatin increased autophagy microtubule-associated protein 1A/1B-light chain 3II (LC3 II) conversion, p62/sequestosome 1 (SQSTM1) accumulation with increased number of LC3II puncta in H1299 cells. However, late stage autophagy inhibitor chloroquine (CQ) increased cytotoxicity in Atorvastatin treated H1299 cells compared to early stage autophagy inhibitor 3-methyladenine (3-MA). Furthermore, autophagic flux assay using RFP-GFP-LC3 constructs and Lysotracker Red or acridine orange-staining demonstrated that autophagosome-lysosome fusion is blocked by Atorvastatin treatment in H1299 cells. Conversely, overexpression of CCR4-NOT transcription complex subunit 2(CNOT2) weakly reversed the ability of Atorvastatin to increase cytotoxicity, sub G1 population, cleavages of PARP and caspase 3, LC3II conversion and p62/SQSTM1 accumulation in H1299 cells. In contrast, CNOT2 depletion enhanced cleavages of PARP and caspase 3, LC3 conversion and p62/SQSTM1 accumulation in Atorvastatin treated H1299 cells. Overall, these findings suggest that CNOT2 signaling is critically involved in Atorvastatin induced apoptotic and autophagic cell death in NSCLCs.

Indexed as

apoptosisatorvastatinautophagyCNOT2non-small lung cancer cells

Identifiers

PMID31574980
PMCPMC6826547
OpenAlexW2975655478

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.