Evidence map›Paper›PMID 36697993›Full record

ArticleMolecular biotechnology2023

CYTOR Promotes Proliferation of Lung Cancer Cell by Targeting miR-103a-3p to Upregulate HMGB1.

Xinxin Xu, Yi Chen, Yan Zhang, Hua Cai, Pei Shen, Jingjing Peng, Hongli Liu, Xiang Chen, Fuying Chu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. lncRNAlyzr: Enrichment Analysis for lncRNA Sets.Journal of molecular biology · 2025
    Article
  3. 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

9 authors at 3 institutions in 1 country.

Xinxin Xu *Department of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Yi Chen *Department of Clinical Laboratory Shanghai East Hospital, Tongji University, Shanghai, 200123, China.
Yan ZhangDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Hua CaiDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Pei ShenDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Jingjing PengDepartment of Laboratory Medicine, Nantong First People's Hospital, Nantong, 226001, China.
Hongli LiuDepartment of Laboratory Medicine, Nantong Tumor Hospital, Nantong, 226001, China.
Xiang ChenDepartment of Laboratory Medicine, Nantong First People's Hospital, Nantong, 226001, China.
Fuying ChuDepartment of Laboratory Medicine, Nantong First People's Hospital, Nantong, 226001, China. fychu19870817@163.com.ORCID http://orcid.org/0000-0001-8400-396X
Nantong University · CNNantong Tumor Hospital · CNShanghai East Hospital · CN

Funding

Nantong Science and Technology Project JC2020070Science and Technology Project of Nantong City MS220211001
6 · The paper itself

Abstract

Lung cancer is one of the most dangerous malignant tumors to human health in the world. Previous researches have shown that cytoskeleton regulator RNA (CYTOR), a long noncoding RNA was involved in the occurrence and development of various types of cancer. The aim of this study is to investigate the clinical significance and biological function of CYTOR in lung cancer. Real-time quantitative PCR was applied to detect the expression of CYTOR. The proliferation of A549 and H1299 cells was analyzed by CCK8 assay. The luciferase reporter assay and RNA pull-down assay were used to reveal the interactions between CYTOR and its downstream targets. Western blot was used to detect the expression of high-mobility group protein B1 (HMGB1). Here we found CYTOR was upregulated in lung cancer tissues and cell lines. The proliferation of A549 and H1299 cells was inhibited after CYTOR silencing. In addition, CYTOR could directly interact with and negatively regulate miR-103a-3p, and miR-103a-3p inhibited cell proliferation by targeting HMGB1. The CYTOR/miR-103a-3p/HMGB1 axis promoted lung cancer cell proliferation. CYTOR sponges miR-103a-3p to promote the proliferation of lung cancer cells through HMGB1. The CYTOR/miR-103a-3p/HMGB1 axis plays a critical role in the progression of lung cancer.

Indexed as

HMGB1 ProteinLung NeoplasmsMicroRNAsCell LineCell Line, TumorCell ProliferationHumansHMGB1 ProteinMicroRNAsCYTORHMGB1Lung cancermiR-103a-3pProliferation

Identifiers

PMID36697993
OpenAlexW4317989822

What Socratic 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 Socratic graph.