Evidence map›Paper›PMID 32773006›Full record

ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2020

[Down-regulation of HOTAIR Reverses the Resistance of Gefitinib in HCC827 Cells by Increasing the Expression of PTEN].

Yang Zhai, Qian Chen, Yuzhen Wang, Xu Li, Lina Li

Open access · greenAbstract read
In one paragraph

Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
–field-weighted citation impact, top 91% of its field
1 · What the graph read from it

What it found

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 1 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Yang ZhaiDepartment of Oncology, Tumor hospital of Shaanxi Province, Xi'an 710061, China.
Qian ChenDepartment of Reproductive Medicine, The First Affiliated Hospital of Xian Jiaotong University, Xi'an 710061, China.
Yuzhen WangDepartment of Oncology, Tumor hospital of Shaanxi Province, Xi'an 710061, China.
Xu LiDepartment of Oncology, Tumor hospital of Shaanxi Province, Xi'an 710061, China.
Lina LiDepartment of Oncology, Tumor hospital of Shaanxi Province, Xi'an 710061, China.
Jilin Province Tumor Hospital · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer is the most common cancer worldwide with the highest morbidity and mortality, in which the non-small cell lung cancer accounts for 80% of all cases. The expression of (HOX transcript antisense RNA) HOTAIR were abnormal in a variety of tumor tissues and is involved in the regulation of the occurrence and development of lung cancer. The purpose of this study is to investigate the effect and mechanism of down-regulation of HOTAIR on gefitinib resistance of lung adenocarcinoma HCC827 cells by targeting PTEN.

methodsThe HOTAIR downstream target gene was predicted by bioinformatics database. The small interfering RNAs (siRNA) which is corresponding to HOTAIR was transfected using Lipofectamine™ 2000. Quantitative real-time PCR (RT-qPCR) and Western blot were used to detect the expression of HOTAIR, PTEN, PI3K and AKT in HCC827 and HCC827GR cells. MTT assay was used to detect the changes in drug resistance of HCC827GR cells. Flow cytometry analysis were used to test the cell proliferation and the rate of apoptosis.

resultsThe expression of HOTAIR increased in HCC827GR and the serum of NSCLC patients with gefitinib resistance (P<0.05). Transfection of HOTAIR siRNA decreased the expression of HOTAIR (P<0.05), and increased the expressions of PTEN (P<0.05), while the expression of PI3K and AKT were decreased (P<0.05). Compared with the blank control group, down-regulation of HOTAIR increased the sensitivity of HCC827GR cells to gefitinib. The cell proliferation ability was decreased and the apoptosis was promoted apparently (P<0.05).

conclusionsDown-regulation of HOTAIR can suppress the cell growth and promote the apoptosis, and it can reverse the resistance of HCC827GR cells to gefitinib. Its potential mechanism may be related with the targeting of PTEN/PI3K/AKT pathway.

Indexed as

Down-RegulationAgedApoptosisCell Cycle CheckpointsCell Line, TumorDrug Resistance, NeoplasmFemaleGefitinibGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMalePTEN PhosphohydrolaseRNA, Long NoncodingGefitinibHOTAIR long untranslated RNA, humanPTEN PhosphohydrolaseRNA, Long NoncodingDrug resistanceGefitinbHCC827HOTAIRPTEN

Identifiers

PMID32773006
PMCPMC7519959
OpenAlexW3049436141

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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.