Evidence map›Paper›PMID 37946265›Full record

ArticleJournal of experimental & clinical cancer research : CR2023

Lnc AC016727.1/BACH1/HIF-1 α signal loop promotes the progression of non-small cell lung cancer.

Li Zhang, Jingtian Liang, Hao Qin, Yin Lv, Xiucheng Liu, Zhuoqun Li, Zhixiang Chao, Caili Jia, Xichun Qin, Hao Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

9 citing papers in PubMed, 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

10 authors at 1 institution in 1 country.

Li Zhang *Thoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, China.
Jingtian Liang *Thoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, China.
Hao QinThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, China.
Yin LvThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, China.
Xiucheng LiuThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, China.
Zhuoqun LiThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, China.
Zhixiang ChaoThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, China.
Caili JiaThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, China.
Xichun QinThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, China.
Hao ZhangThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, 221006, Jiangsu Province, China. zhanghao@xzhmu.edu.cn.ORCID http://orcid.org/0000-0002-2926-737X
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong noncoding RNAs (lncRNAs) have been reported to play vital roles in the development and progression of cancer. However, their biological significance and functional mechanisms in non-small cell lung cancer (NSCLC) are mostly unclear.

methodsWe performed RNA-sequencing to predict the differential expression of lncRNAs in clinical NSCLC and paired paracancerous lung tissues. To identify lncRNA expression, quantitative polymerase chain reaction (qPCR) was used. Using both cell and mouse models, We studied lncRNA AC016727.1's function in NSCLC growth and metastasis. Western blot assays, dual luciferase reporter assays, and chromatin immunoprecipitation were used to analyze the functional mechanism of lncRNA AC016727.1.

resultsOur larger NSCLC cohorts validated that the lncRNA AC016727.1 was upregulated in 94 paired NSCLC tissues and correlated with poor survival. Functionally, lncRNA AC016727.1 downregulation inhibited NSCLC cell proliferation, aerobic glycolysis, EMT, and migration, inducing apoptosis. Conversely, upregulated lncRNA AC016727.1 expression exhibited the opposite effect, promoting NSCLC cell survival. Importantly, lncRNA AC016727.1 knockdown inhibited lung cancer growth and slowed the progression of lung metastasis in nude mouse models. Mechanistically, lncRNA AC016727.1 upregulated BACH1 target gene expression by acting as a sponge for miR-98-5p, thereby functioning as a competing endogenous RNA. The function of lncRNA AC016727.1 is mediated by the miR-98-5p/BACH1 axis in NSCLC cells. Meanwhile, the transcription factor HIF-1α can bind to the promoter and activate lncRNA AC016727.1 transcription. lncRNA AC016727.1 regulates HIF-1α expression via BACH1 in NSCLC and forms the lncRNA AC016727.1/BACH1/HIF-1α signaling loop under hypoxic conditions.

conclusionOur study reveals a novel lncRNA AC016727.1/BACH1/HIF-1α signaling loop in the progression of NSCLC under hypoxic conditions, suggesting that lncRNA AC016727.1 could act as a useful biomarker for NSCLC and a new therapeutic target.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsMicroRNAsRNA, Long NoncodingAnimalsBasic-Leucine Zipper Transcription FactorsCell ProliferationGene Expression Regulation, NeoplasticHumansMiceBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsMicroRNAsMIRN98 microRNA, humanRNA, Long NoncodingAerobic glycolysisBTB and CNC homolog 1HypoxialncRNA AC016727.1miR-98-5pNon-small cell lung cancer

Identifiers

PMID37946265
PMCPMC10636976
OpenAlexW4388550928

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.