Evidence map›Paper›PMID 34746118›Full record

ArticleFrontiers in cell and developmental biology2021

NR2F1-AS1/miR-190a/PHLDB2 Induces the Epithelial-Mesenchymal Transformation Process in Gastric Cancer by Promoting Phosphorylation of AKT3.

Jinqi Lv, Simeng Zhang, Yang Liu, Ce Li, Tianshu Guo, Shuairan Zhang, Zenan Li, Zihan Jiao, Haina Sun, Ye Zhang and 1 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  10. Canadian journal of gastroenterology & hepatology · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Jinqi LvDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
Simeng ZhangDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
Yang LiuDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
Ce LiDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
Tianshu GuoDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
Shuairan ZhangDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
Zenan LiDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
Zihan JiaoDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
Haina SunDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
Ye ZhangThe First Laboratory of Cancer Institute, The First Hospital of China Medical University, Shenyang, China.
Ling XuDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.
China Medical University · CNMinistry of Education of the People's Republic of China · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The median survival time of patients with advanced gastric cancer (GC) who received radiotherapy and chemotherapy was <1 year. Epithelial-mesenchymal transformation (EMT) gives GC cells the ability to invade, which is an essential biological mechanism in the progression of GC. The long non-coding RNA (lncRNA)-based competitive endogenous RNA (ceRNA) system has been shown to play a key role in the GC-related EMT process. Although the AKT pathway is essential for EMT in GC, the relationship between AKT3 subtypes and EMT in GC is unclear. Here, we evaluated the underlying mechanism of ceRNA involving NR2F1-AS1/miR-190a/PHLDB2 in inducing EMT by promoting the expression and phosphorylation of AKT3. The results of bioinformatics analysis showed that the expression of NR2F1-AS1/miR-190a/PHLDB2 in GC was positively associated with the pathological features, staging, poor prognosis, and EMT process. We performed cell transfection, qRT-PCR, western blot, cell viability assay, TUNEL assay, Transwell assay, cell morphology observation, and double luciferase assay to confirm the regulation of NR2F1-AS1/miR-190a/PHLDB2 and its effect on EMT transformation. Finally, GSEA and GO/KEGG enrichment analysis identified that PI3K/AKT pathway was positively correlated to NR2F1-AS1/miR-190a/PHLDB2 expression. AKT3 knockout cells were co-transfected with PHLDB2-OE, and the findings revealed that AKT3 expression and phosphorylation were essential for the PHLDB2-mediated EMT process. Thus, our results showed that NR2F1-AS1/miR-190a/PHLDB2 promoted the phosphorylation of AKT3 to induce EMT in GC cells. This study provides a comprehensive understanding of the underlying mechanism involved in the EMT process as well as the identification of new EMT markers.

Indexed as

AKT3EMTmiR-190aNR2F1-AS1PHLDB2

Identifiers

PMID34746118
PMCPMC8569557
OpenAlexW3209937574

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.