Evidence map›Paper›PMID 34895039›Full record

ArticleBioengineered2021

The long noncoding RNA noncoding RNA activated by DNA damage (NORAD)-microRNA-496-Interleukin-33 axis affects carcinoma-associated fibroblasts-mediated gastric cancer development.

Chaoqun Huang, Jiuyang Liu, Liang He, Fubing Wang, Bin Xiong, Yan Li, Xiaojun Yang

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

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  11. Effect of tumor-stromal fibroblasts on the biological behavior of salivary gland pleomorphic adenoma cellsHua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2023
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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

7 authors at 4 institutions in 1 country.

Chaoqun HuangDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Jiuyang LiuHubei Cancer Clinical Study Center & Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, Hubei, China.
Liang HeDepartment of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Fubing WangDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Bin XiongDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Yan LiDepartment of Peritoneal Cancer Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Xiaojun YangDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Zhongnan Hospital of Wuhan University · CNHubei Cancer Hospital · CNCapital Medical University · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carcinoma-associated fibroblasts (CAFs) are one of the crucial parts of in the tumor microenvironment and contribute to tumor progression. Interleukin-33 (IL-33), a tissue-derived nuclear cytokine from the IL-1 family, has been found abnormally expressed in tumor cells and Fibroblast. However, the role and mechanism of IL-33 in the interaction between gastric cancer (GC) cells and CAFs need investigation. Presently, we inquire into the function of lncRNA NORAD-miR-496 axis-mediated IL-33 in modulating the GC-CAFs interaction. Real-time reverse transcription-polymerase chain reaction (RT-PCR) was adopted to gauge the expression of NORAD, miR-496, and IL-33 in GC tissues and cells, and gain- or loss-of-function assays were conducted to investigate the role of them in GC. A GC cell-CAFs co-culture model was established to explore the interaction between CAFs and GCs. As exhibited, NORAD was up-regulated in GC tissues and cells, while miR-496 was remarkably down-regulated. Overexpressing NORAD substantially promoted the proliferation, migration, invasion, and EMT of GC cells and repressed cell death, while overexpressing miR-496 had the opposite effects. Additionally, NORAD enhanced the IL-33 expression and the release of IL-33 from GC cells. The dual-luciferase reporter assay confirmed that miR-496 was a target of NORAD and targeted IL-33. CAFs aggravated the malignant behaviors of GC cells as indicated by both experiments. However, NORAD knockdown in CAFs reversed CAFs-mediated promotive effects on GC cells. In conclusion, NORAD enhanced the promotive effect of CAFs in GC cells by up-regulating IL-33 and targeting miR-496, which provided new insights into the microenvironment of GC cells and CAFs.

Indexed as

Base SequenceCancer-Associated FibroblastsCarcinogenesisCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansInterleukin-33MaleMicroRNAsMiddle AgedModels, BiologicalNeoplasm InvasivenessRNA, Long NoncodingStomach NeoplasmsInterleukin-33MicroRNAsMIRN496 microRNA, humanNORAD long non-coding RNA, humanRNA, Long Noncodingcarcinoma-associated fibroblastsgastric cancerIL-33Lncrna NORADmiR-496

Identifiers

PMID34895039
PMCPMC8810175
OpenAlexW4200342543

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.