Evidence map›Paper›PMID 27186394›Full record

ArticleAmerican journal of cancer research2016

MiR-326 regulates cell proliferation and migration in lung cancer by targeting phox2a and is regulated by HOTAIR.

Rong Wang, Xiaofeng Chen, Tongpeng Xu, Rui Xia, Liang Han, Wenming Chen, Wei De, Yongqian Shu

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 95 citations in OpenAlex.

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  12. miRNA-Seq Tissue Diagnostic Signature: A Novel Model for NSCLC Subtyping.International journal of molecular sciences · 2023
    Article
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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

8 authors at 1 institution in 1 country.

Rong WangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital Nanjing 210029, People's Republic of China.
Xiaofeng ChenDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital Nanjing 210029, People's Republic of China.
Tongpeng XuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital Nanjing 210029, People's Republic of China.
Rui XiaDepartment of Biochemistry and Molecular Biology, Nanjing Medical University Nanjing 210029, People's Republic of China.
Liang HanDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital Nanjing 210029, People's Republic of China.
Wenming ChenDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital Nanjing 210029, People's Republic of China.
Wei DeDepartment of Biochemistry and Molecular Biology, Nanjing Medical University Nanjing 210029, People's Republic of China.
Yongqian ShuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital Nanjing 210029, People's Republic of China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent findings indicate that microRNAs (miRNAs) play a crucial role in lung cancer development, progression and regression. In our previous study, we identified miR-326 is down-regulated in lung cancer. However, the role of miR-326 hasn't been revealed yet. The aim of the current study is to investigate the function and regulation mechanism of miR-326 in lung cancer. MTT assays, Transwell migration assays and xenograft model in nude mice were carried to detect the effects of miR-326 on cell proliferation, migration and tumor growth in nude mice. Flow cytometry was used to analyze the effects of miR-326 on cell cycle and apoptosis. By using siRNAs and luciferase assays, we also demonstrated that Phox2a is a functional target of miR-326, and that miR-326 is regulated by long non-coding RNA HOTAIR through silencing HOTAIR. Enforced expression of miR-326 inhibited cell proliferation and migration in vitro and tumor growth in nude mice, decreased proportion of cells in S phase and increased cell apoptosis in both A549 and H838 cells. In addition, we found miR-326 bound to 3'UTR of Phox2a but not KLF3, and enforced expression of miR-326 decreased accumulation of Phox2a in both A549 and H838. Moreover, exogenous expression of Phox2a compromised inhibitory effects of miR-326 on cell proliferation and migration. We also found silencing of HOTAIR caused increased expression of miR-326. miR-326 regulates cell proliferation and migration in lung cancer by targeting Phox2a and is regulated by HOTAIR.

Indexed as

cell proliferationHOTAIRlung cancermigrationmiR-326Phox2a

Identifiers

PMID27186394
PMCPMC4859651
OpenAlexW2419326786

What OpenQuestion holds

Textmetadata
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.