Evidence map›Paper›PMID 37041291›Full record

ArticleCell death and differentiation2023

Long non-coding RNA HIF1A-As2 and MYC form a double-positive feedback loop to promote cell proliferation and metastasis in KRAS-driven non-small cell lung cancer.

Kaixin Yang, Wenyang Zhang, Linghui Zhong, Yinan Xiao, Sudhakar Sahoo, Matteo Fassan, Kang Zeng, Peter Magee, Michela Garofalo, Lei Shi

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

Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
14.1field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 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 3 institutions in 3 countries.

Kaixin Yang *RNA Oncology Group, School of Public Health, Lanzhou University, 730000, Lanzhou, People's Republic of China.
Wenyang Zhang *RNA Oncology Group, School of Public Health, Lanzhou University, 730000, Lanzhou, People's Republic of China.
Linghui Zhong *RNA Oncology Group, School of Public Health, Lanzhou University, 730000, Lanzhou, People's Republic of China.
Yinan Xiao *RNA Oncology Group, School of Public Health, Lanzhou University, 730000, Lanzhou, People's Republic of China.
Sudhakar SahooComputational Biology Support, Cancer Research UK Manchester Institute, University of Manchester, Alderley Park, Manchester, SK10 4TG, UK.
Matteo FassanDepartment of Medicine, Surgical Pathology & Cytopathology Unit, University of Padua, Padua, 35100, Italy.
Kang ZengImaging & Cytometry Facility, Cancer Research UK Manchester Institute, University of Manchester, Alderley Park, Manchester, SK10 4TG, UK.
Peter MageeTranscriptional Networks in Lung Cancer Group, Cancer Research UK Manchester Institute, University of Manchester, Alderley Park, Manchester, SK10 4TG, UK.
Michela GarofaloTranscriptional Networks in Lung Cancer Group, Cancer Research UK Manchester Institute, University of Manchester, Alderley Park, Manchester, SK10 4TG, UK.
Lei ShiRNA Oncology Group, School of Public Health, Lanzhou University, 730000, Lanzhou, People's Republic of China. leishi@lzu.edu.cn.ORCID 0000-0003-4027-2396
University of Manchester · GBLanzhou University · CNUniversity of Padua · IT

Funding

Cancer Research UK MICR_CORE_COMPU _2324
6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer-related deaths worldwide. KRAS is the main oncogenic driver in lung cancer that can be activated by gene mutation or amplification, but whether long non-coding RNAs (lncRNAs) regulate its activation remains unknown. Through gain and loss of function approaches, we identified that lncRNA HIF1A-As2, a KRAS-induced lncRNA, is required for cell proliferation, epithelial-mesenchymal transition (EMT) and tumor propagation in non-small cell lung cancer (NSCLC) in vitro and in vivo. Integrative analysis of HIF1A-As2 transcriptomic profiling reveals that HIF1A-As2 modulates gene expression in trans, particularly regulating transcriptional factor genes including MYC. Mechanistically, HIF1A-As2 epigenetically activates MYC by recruiting DHX9 on MYC promoter, consequently stimulating the transcription of MYC and its target genes. In addition, KRAS promotes HIF1A-As2 expression via the induction of MYC, suggesting HIF1A-As2 and MYC form a double-regulatory loop to strengthen cell proliferation and tumor metastasis in lung cancer. Inhibition of HIF1A-As2 by LNA GapmeR antisense oligonucleotides (ASO) significantly improves sensitization to 10058-F4 (a MYC-specific inhibitor) and cisplatin treatment in PDX and KRAS

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsMicroRNAsRNA, Long NoncodingCell Line, TumorCell ProliferationFeedbackGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitProto-Oncogene Proteins p21(ras)HIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitKRAS protein, humanMicroRNAsProto-Oncogene Proteins p21(ras)RNA, Long Noncoding

Identifiers

PMID37041291
PMCPMC10089381
OpenAlexW4364356802

What OpenQuestion holds

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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.