Evidence map›Paper›PMID 36846943›Full record

ArticleCancer science2023

ELF1 suppresses autophagy to reduce cisplatin resistance via the miR-152-3p/NCAM1/ERK axis in lung cancer cells.

Lifeng Zhao, Xiangsheng Wu, Zhiwen Zhang, Lini Fang, Bo Yang, Yepeng Li

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.7field-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

20 citing papers in PubMed, 28 citations in OpenAlex.

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  16. World journal of gastrointestinal oncology · 2024
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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

6 authors at 1 institution in 1 country.

Lifeng ZhaoDepartments of Oncology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China.
Xiangsheng WuSchool of Clinical Medicine, Graduate School of Youjiang Medical University for Nationalities, Baise, China.
Zhiwen ZhangSchool of Clinical Medicine, Graduate School of Youjiang Medical University for Nationalities, Baise, China.
Lini FangDepartments of Oncology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China.
Bo YangDepartments of Oncology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China.
Yepeng LiDepartments of Oncology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China.ORCID https://orcid.org/0000-0002-8380-2839
Affiliated Hospital of Youjiang Medical University for Nationalities · CN

Funding

the Science and Technology Department of Guangxi Zhuang Autonomous Region 2019JJA140044the Science and Technology Department of Guangxi Zhuang Autonomous Region 2019JJA140084
6 · The paper itself

Abstract

Resistance to chemotherapeutic drugs limits the efficacy of chemotherapy in non-small cell lung cancer (NSCLC). Autophagy is an essential mechanism which involves in drug resistance. Our previous research has revealed that miR-152-3p represses NSCLC progression. However, the mechanism of miR-152-3p in autophagy-mediated chemoresistance in NSCLC remains unclear. Cisplatin-resistant cell lines (A549/DDP and H446/DDP) were transfected with related vectors and subjected to cisplatin, autophagy inhibitor, activator, or extracellular signal-regulated kinase (ERK) activator. Flow cytometry, CCK8 and colony formation assays were performed for testing apoptosis and cell viability. The related RNAs or proteins were detected by qRT-PCR or Western blot. Chromatin immunoprecipitation, luciferase reporter assay or RNA immunoprecipitation were used for validating the interaction between miR-152-3p and ELF1 or NCAM1. Co-IP verified the binding between NCAM1 and ERK. The role of miR-152-3p in cisplatin resistance of NSCLC was also validated in vivo. The results showed that miR-152-3p and ELF1 were decreased in NSCLC tissues. miR-152-3p reversed cisplatin resistance by inhibiting autophagy through NCAM1. NCAM1 promoted autophagy through the ERK pathway and facilitated cisplatin resistance. ELF1 positively regulated miR-152-3p level by directly interacting with miR-152-3p promoter. miR-152-3p targeted NCAM1 to regulate NCAM1 level and then affected the binding of NCAM1 to ERK1/2. ELF1 inhibited autophagy and reversed cisplatin resistance through miR-152-3p/NCAM1. miR-152-3p inhibited autophagy and cisplatin resistance of xenograft tumor in mice. In conclusion, our study revealed that ELF1 inhibited autophagy to attenuate cisplatin resistance through the miR-152-3p/NCAM1/ERK pathway in H446/DDP and A549/DDP cells, suggesting a potential novel treatment strategy for NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsMicroRNAsAnimalsAutophagyCD56 AntigenCell Line, TumorCell ProliferationCisplatinDrug Resistance, NeoplasmExtracellular Signal-Regulated MAP KinasesHumansMiceNuclear ProteinsTranscription FactorsCD56 AntigenCisplatinELF1 protein, humanExtracellular Signal-Regulated MAP KinasesMicroRNAsMIRN152 microRNA, humanNCAM1 protein, humanNcam1 protein, mouseNuclear ProteinsTranscription FactorsautophagychemoresistanceELF1miR-152-3pNCAM1non-small cell lung cancer

Identifiers

PMID36846943
PMCPMC10236622
OpenAlexW4322495147

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.