Evidence map›Paper›PMID 32396871›Full record

ArticleAging2020

STAT1-induced upregulation of lncRNA KTN1-AS1 predicts poor prognosis and facilitates non-small cell lung cancer progression via miR-23b/DEPDC1 axis.

Changmin Liu, Xiaoming Li, Yanzhang Hao, Feng Wang, Zhiwen Cheng, Haitao Geng, Dianzhong Geng

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  6. Article
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  9. A novel immunogenomic classification for prognosis in non-small cell lung cancer.Journal of cancer research and clinical oncology · 2023
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Pan-cancer analysis ofAnnals of translational medicine · 2022
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  16. Spermine synthase (Annals of translational medicine · 2022
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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

7 authors at 3 institutions in 1 country.

Changmin LiuDepartment of Oncology, Binzhou Medical University Hospital, Binzhou, Shandong, China.
Xiaoming LiDepartment of Hepatobiliary Surgery, Shandong Provincial ENT Hospital, Shandong Provincial ENT Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Yanzhang HaoDepartment of Oncology, Binzhou Medical University Hospital, Binzhou, Shandong, China.
Feng WangDepartment of Oncology, Binzhou Medical University Hospital, Binzhou, Shandong, China.
Zhiwen ChengDepartment of Oncology, Binzhou Medical University Hospital, Binzhou, Shandong, China.
Haitao GengDepartment of Oncology, Binzhou Medical University Hospital, Binzhou, Shandong, China.
Dianzhong GengDepartment of Oncology, Binzhou Medical University Hospital, Binzhou, Shandong, China.
Binzhou Medical University · CNBinzhou University · CNShandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several of the thousands of long noncoding RNAs (lncRNAs) have been functionally characterized in various tumors. In this study, we aimed to explore the function and possible molecular mechanism of lncRNA KTN1 antisense RNA 1 (KTN1-AS1) involved in non-small cell lung cancer (NSCLC). We identified a novel NSCLC-related lncRNA, KTN1 antisense RNA 1 (KTN1-AS1) which was demonstrated to be distinctly highly expressed in NSCLC. KTN1-AS1 upregulation was induced by STAT1. Clinical study also suggested that higher levels of KTN1-AS1 were associated with advanced clinical progression and a shorter five-year overall survival. Functionally, loss-of-function assays with in vitro and in vivo experiments revealed that KTN1-AS1 promoted the proliferation, migration, invasion and EMT progress of NSCLC cells, and suppressed apoptosis. Mechanistic studies indicated that miR-23b was a direct target of KTN1-AS1, which functioned as a ceRNA to subsequently facilitate miR-23b's target gene DEPDC1 expression in NSCLC cells. Rescue experiments confirmed that KTN1-AS1 overexpression could increase the colony formation and migration ability suppressed by miR-23b upregulation in NSCLC cells. Overall, our findings imply that STAT1-induced upregulation of KTN1-AS1 display tumor-promotive roles in NSCLC progression via regulating miR-23b/DEPDC1 axis, suggesting that KTN1-AS1 may be a novel biomarker and therapeutic target for NSCLC patients.

Indexed as

A549 CellsAnimalsApoptosisCarcinoma, Non-Small-Cell LungCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticGTPase-Activating ProteinsHumansLung NeoplasmsMaleMembrane ProteinsMiceMice, Inbred BALB CDEPDC1 protein, humanGTPase-Activating ProteinsKTN1 protein, humanMembrane ProteinsMicroRNAsMIRN23b microRNA, humanNeoplasm ProteinsRNA, Long NoncodingSTAT1 protein, humanSTAT1 Transcription FactorDEPDC1lncRNA KTN1-AS1metastasismiR-23bNSCLC

Identifiers

PMID32396871
PMCPMC7244022
OpenAlexW3024335614

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.