Evidence map›Paper›PMID 32524576›Full record

ArticleHistology and histopathology2020

Silence of FOXD2-AS1 inhibited the proliferation and invasion of esophagus cells by regulating miR-145-5p/CDK6 axis.

Woda Shi, Zhengya Gao, Jianxiang Song, Wencai Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Histology and histopathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 32% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. FOXD2-AS1 acts an oncogene in esophageal squamous cell carcinoma through sponging miR-204-3p.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. mMolecular therapy oncolytics · 2021
    Article
  11. Article
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

4 authors at 1 institution in 1 country.

Woda Shi *Department of Cardio-Thoracic Surgery, Yancheng Third People's Hospital, Yancheng, Jiangsu, China.
Zhengya Gao *Department of Cardio-Thoracic Surgery, Yancheng Third People's Hospital, Yancheng, Jiangsu, China.
Jianxiang SongDepartment of Cardio-Thoracic Surgery, Yancheng Third People's Hospital, Yancheng, Jiangsu, China.
Wencai WangDepartment of Cardio-Thoracic Surgery, Yancheng Third People's Hospital, Yancheng, Jiangsu, China. wangwencai00001@126.com.
Yancheng Third People's Hospital · CN

Funding

- -
6 · The paper itself

Abstract

This study aimed to investigate the function of long non-coding RNA FOXD2 adjacent opposite strand RNA 1 (lncRNA FOXD2-AS1) during the progression of esophagus cancer (EC) and explore its underlying molecular mechanisms. The level of FOXD2-AS1 in EC tissues and paracancerous tissues was detected by using RT-qPCR; ROC curve was used to evaluate the diagnostic value of FOXD2-AS1 for EC. In addition, CCK8 assay and immunofluorescence staining assay were used to detect the proliferation of Eca-109 and TE-1 cells. To investigate the function of FOXD2-AS1 on cell apoptosis and cell cycle, flow cytometry was performed. To detect the invasion ability of EC cells, transwell invasion assay was performed. Starbase3.0 and Targetscan were used to predict the target genes of FOXD2-AS1 and miR-145-5p, and protein expressions were detected with western blot. We found FOXD2-AS1 was significantly upregulated in EC tissues compared with adjacent normal tissues, which was positively correlated with clinicopathological parameters of patients with EC. Downregulation of FOXD2-AS1 inhibited the proliferation and invasion by inducing apoptosis of EC cells. Moreover, FOXD2-AS1 may regulate the expression of CDK6 by targeting miR-145-3p. Meanwhile, silencing of FOXD2-AS1 caused G1 phase arrest of EC cells by reducing the expression of CDK6. In conclusion, silening FOXD2-AS1 significantly inhibited the proliferation and invasion of EC cells by regulating the miR-145-5p/CDK6 axis. Therefore, FOXD2-AS1 might be used as diagnostic biomarker and therapeutic target for EC.

Indexed as

Gene Expression Regulation, NeoplasticAdultApoptosisCell Line, TumorCell MovementCell ProliferationCyclin-Dependent Kinase 6Esophageal NeoplasmsEsophagusGene SilencingHumansMicroRNAsMiddle AgedRNA, Long NoncodingSignal TransductionCDK6 protein, humanCyclin-Dependent Kinase 6long non-coding RNA FOXD2-AS1, humanMicroRNAsMIRN145 microRNA, humanRNA, Long Noncoding

Identifiers

PMID32524576
OpenAlexW3033204307

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.