Evidence map›Paper›PMID 32249461›Full record

ArticleJournal of clinical laboratory analysis2020

Analysis of lncRNA UCA1-related downstream pathways and molecules of cisplatin resistance in lung adenocarcinoma.

Huixin Zhou, Qiang Shen, Jiali Fu, Feng Jiang, Liangxing Wang, Yumin Wang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of clinical laboratory analysis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 39% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 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

6 authors at 1 institution in 1 country.

Huixin ZhouDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Qiang ShenDepartment of Respiratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Jiali FuDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Feng JiangDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Liangxing WangDepartment of Respiratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Yumin WangDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0001-8243-3659
Wenzhou Medical University · CN

Funding

The National Natural Science Foundation of China 81672088Wenzhou Municipal Science and Technology Bureau of China Y20190461Zhejiang Provincial Health Planning Commission 2018KY514Zhejiang Provincial Natural Science Foundation LY19H200002
6 · The paper itself

Abstract

backgroundTo analyze the lncRNA UCA1-related downstream pathways and molecules of cisplatin resistance in lung adenocarcinoma.

methodsWe constructed overexpression and siRNA vectors targeting UCA1 and TXNIP and then used next-generation sequencing to compare the UCA1 overexpression and negative control from A549 cell.

resultsIt shown that 647 upregulated mRNAs and 633 downregulated differentially expressed mRNAs-related UCA1, and the top ten upregulated mRNAs were CPD, AC007192.1, TGOLN2, LGR4, TFPI, CYP1B1, TOMM6, HLA-B, SLC35F6, and TOP2A, and top ten downregulated mRNAs were TXNIP, SESN2, STC2, HSPA1A, MMP10, CHAC1, DNAJB1, AC004922.1, ATF3, and GABARAPL1. We found TXNIP mRNA expression level was the most significantly downexpressed mRNA. TXNIP mRNA expression level of LAD tissues was clearly lower than the adjacent tissues. UCA1 expression level of cisplatin insensitive group was markedly higher than that of cisplatin-sensitive group, while TXNIP mRNA expression level of cisplatin insensitive group was clearly lower than that of cisplatin-sensitive group. Compared to the BEAS-2B, TXNIP mRNA expression level cut down in A549 and A549/DDP cell and that of A549/DDP cell was lower than A549 cell. After UCA1 overexpression, TXNIP mRNA obviously decreased, while proliferation ability and IC50 of A549 heightened. After knocking down UCA1, TXNIP mRNA was significantly increased, while proliferation ability and IC50 of A549/DDP lowered. PPI analysis result showed that TXNIP could interact with multiple proteins such as TXN, DDIT4, and NLRP3.

conclusionUCA1 promoted cisplatin resistance by downregulating TXNIP expression in LAD, and TXNIP could interact with multiple proteins. So, UCA1/TXNIP axis might affect cisplatin resistance in LAD.

Indexed as

Adenocarcinoma of LungDrug Resistance, NeoplasmLung NeoplasmsRNA, Long NoncodingA549 CellsAntineoplastic AgentsCarrier ProteinsCisplatinGene Expression Regulation, NeoplasticHumansLungSignal TransductionAntineoplastic AgentsCarrier ProteinsCisplatinRNA, Long NoncodingTXNIP protein, humanUCA1 RNA, humanlung adenocarcinomasignaling pathwayTXNIPUCA1

Identifiers

PMID32249461
PMCPMC7439354
OpenAlexW3014162570

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.