Evidence map›Paper›PMID 34403532›Full record

ArticleJournal of clinical laboratory analysis2021

AC016405.3 functions as an oncogenic long non-coding RNA by regulating ERBB3 via sponging miR-22-3p in breast cancer.

Min Wei, Jie Wang, Qi He, Lei Liu, Zhiwei Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 43% 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

6 citing papers in PubMed, 7 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

5 authors at 2 institutions in 1 country.

Min WeiDepartment of Breast, School of Medicine, The International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University, Shanghai, China.
Jie WangDepartment of Breast, School of Medicine, The International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University, Shanghai, China.
Qi HeDepartment of Breast, School of Medicine, The International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University, Shanghai, China.
Lei LiuDepartment of Surgery, The Affiliated Tumor Hospital of Nantong University, Nantong, China.
Zhiwei WangDepartment of Breast, School of Medicine, The International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0001-8728-1543
Shanghai Jiao Tong University · CNNantong University · CN

Funding

Ministry of Education of China 20110073120089Natural Science Foundation of China 81101847Shanghai Committee of Science and Technology, ChinaShanghai Committee of Science and Technology, China 124119a4801
6 · The paper itself

Abstract

backgroundIncreasing studies reported that long non-coding RNAs are involved in regulating breast cancer (BRCA) progression. However, the specific roles and mechanisms of lncRNAs in BRCA remain largely unknown. Here, we sought to explore the functions and mechanisms of AC016405.3 in BRCA progression.

methodsBioinformatic analysis for AC016405.3, miR-22-3p, and ERBB3 were performed on starBase. The expressions of AC016405.3, miR-22-3p, and ERBB3 were examined by RT-qPCR. The functions of AC016405.3 on the proliferation, migration, and invasion of cells were evaluated by conducting CCK-8, colony formation, wound-healing, and Transwell assays. The subcellular distribution of AC016405.3 in BRCA cells was identified by performing fluorescence in situ hybridization (FISH) and subcellular fractionation techniques. Dual-luciferase assay was applied to validate the interactions of miR-22-3p with AC016405.3 or ERBB3. The interaction between ERBB3 and miR-22-3p was also tested by Anti-Ago2 RNA immunoprecipitation (RIP) assay.

resultsThe results showed that AC016405.3 is highly expressed in BRCA tissues as well as cells and positively correlated with poor prognosis in BRCA patients. Silencing AC016405.3 obviously repressed the malignant behaviors of BRCA cells. Mechanistically, AC016405.3 functioned as a competing endogenous RNA (ceRNA) for miR-22-3p in the cytoplasm and sponged miR-22-3p to release its suppression of ERBB3. Rescue experiments revealed that the suppression role induced by AC016405.3 depletion on malignant behaviors of BRCA cells could be obviously counter by inhibiting miR-22-3p or overexpressing ERBB3.

conclusionAC016405.3 promotes BRCA progression by the derepression of ERBB3 via sponging miR-22-3p, which may represent a potential target for BRCA treatment.

Indexed as

Breast NeoplasmsFemaleHumansAC016405.3breast cancercompeting endogenous RNA networkERBB3miR-22-3p

Identifiers

PMID34403532
PMCPMC8418490
OpenAlexW3195236807

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.