Evidence map›Paper›PMID 34264003›Full record

ArticleCancer medicine2021

Identification of a competing endogenous RNA axis "SVIL-AS1/miR-103a/ICE1" associated with chemoresistance in lung adenocarcinoma by comprehensive bioinformatics analysis.

Lili Guo, Lina Ding, Junfang Tang

Open access · goldAbstract read
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Article in Cancer medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Lili GuoDepartment of Medical Oncology, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing Chest Hospital, Capital Medical University, Beijing, China.
Lina DingKey Laboratory of Henan Province for Drug Quality and Evaluation, School of Pharmaceutical Sciences, Ministry of Education of China, Zhengzhou University, Zhengzhou, P.R. China.
Junfang TangDepartment of Medical Oncology, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing Chest Hospital, Capital Medical University, Beijing, China.ORCID 0000-0002-8836-6036
Capital Medical University · CNZhengzhou University · CN

Funding

The Beijing CSCO-Hengrui Oncology Research Foundation Y-HR2018-119
6 · The paper itself

Abstract

backgroundChemotherapy is an important treatment for lung cancer. The molecular mechanism of lung adenocarcinoma (LUAD) chemoresistance is not completely understood.

methodsWeighted gene co-expression network analysis (WGCNA) was applied to screen the modules related to chemosensitivity using the data of LUAD patients receiving chemotherapy in The Cancer Genome Atlas database. GDCRNATools package was used to establish competing endogenous RNA (ceRNA) network based on the key chemotherapy-related module. Kaplan-Meier and risk models were used to analyze the influence of genes in the ceRNA network on the prognosis of LUAD patients receiving chemotherapy. Cell counting kit-8, reverse transcription-quantitative PCR, and dual-luciferase reporter assay were used to detect the effects of abnormal expression of genes in the ceRNA network on the proliferation and IC50 of cisplatin (DDP)-resistant LUAD cells, and the targeting relationship of genes in the ceRNA network. The signaling pathways and functions of ICE1 in LUAD were analyzed by LinkOmics and CancerSEA databases, and validated by Western blot.

resultsMidnightblue module was the only WGCNA module positively correlated with chemosensitivity, in which the function of genes was related to cancer progression. SVIL-AS1/miR-103a/ICE1 was constructed based on midnightblue module. High expression of SVIl-AS1 and ICE1 corresponded to a favorable prognosis. High expression of miR-103a corresponded to a dismal prognosis. SVIl-AS1 was downregulated in DDP-resistant LUAD cells. SVIL-AS1 overexpression retarded the proliferation and DDP resistance of DDP-resistant LUAD cell. miR-103a was sponged by SVIL-AS1 and directly targeted ICE1. miR-103a overexpression and ICE1 knockdown overturned the suppressive effect of SVIL-AS1 overexpression on cell proliferation and DDP resistance. Further bioinformatics analysis and experimental verification showed that SVIL-AS1/miR-103a-3p/ICE1 axis can enhance DNA damage caused by chemotherapeutic agents.

conclusionsSVIL-AS1 inhibited chemoresistance by acting as a sponge for miR-103a and upregulating ICE1 expression, which may be a potential therapeutic target for chemotherapy in LUAD.

Indexed as

Adenocarcinoma of LungComputational BiologyDrug Resistance, NeoplasmHumansPrognosisRNASurvival AnalysisTransfectionRNAchemoresistancecompeting endogenous RNAlung adenocarcinomaprognosisweighted gene co-expression network analysis

Identifiers

PMID34264003
PMCPMC8419767
OpenAlexW3181155417

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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.