Evidence map›Paper›PMID 36539799›Full record

ArticleJournal of experimental & clinical cancer research : CR2022

LINC00629 protects osteosarcoma cell from ER stress-induced apoptosis and facilitates tumour progression by elevating KLF4 stability.

Yuan Wang, Shuo Zheng, Jian Han, Na Li, Renchen Ji, Xiaodong Li, Chuanchun Han, Wenzhi Zhao, Lu Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. KLF transcription factors in bone diseases.Journal of cellular and molecular medicine · 2024
    Review
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  8. Article
  9. 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

9 authors at 2 institutions in 1 country.

Yuan Wang *The Second Affiliated Hospital & Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China.
Shuo Zheng *The Second Affiliated Hospital & Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China.
Jian Han *Department of Orthopedics, The Third People's Hospital of Dalian, Dalian Medical University, Dalian, Liaoning, 116033, People's Republic of China.
Na Li *National-Local Joint Engineering Research Center for Drug-Research and Development (R&D) of Neurodegenerative Diseases, Dalian Medical University, Dalian, 116044, People's Republic of China.
Renchen JiThe Second Affiliated Hospital & Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China.
Xiaodong LiThe Second Affiliated Hospital & Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China. xd_li201212@dmu.edu.cn.
Chuanchun HanThe Second Affiliated Hospital & Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China. hanchuanchun@163.com.
Wenzhi ZhaoThe Second Affiliated Hospital & Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China. drzwz@163.com.
Lu ZhangThe Second Affiliated Hospital & Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China. zhanglu_dalian@163.com.
Dalian Medical University · CNSecond Affiliated Hospital of Dalian Medical University · CN

Funding

National Natural Science Foundation of China 81874136National Natural Science Foundation of China 81902743National Nature Science Foundation of China 81972518Natural Science Foundation of Liaoning Province 2015020670 and LJKZ0837Natural Science Foundation of Liaoning Province 2019-BS-074Natural Science Foundation of Liaoning Province 2021-MS-291
6 · The paper itself

Abstract

backgroundEscaping from ER stress-induced apoptosis plays an important role in the progression of many tumours. However, its molecular mechanism in osteosarcoma remains incompletely understood.

methodsThe molecular mechanism was investigated using RNA sequencing, qRT-PCR and Western blot assays. The relationship between LINC00629 and KLF4 was investigated using RNA pulldown and ubiquitylation assays. The transcriptional regulation of laminin subunit alpha 4 (LAMA4) by KLF4 was identified using bioinformatic analysis, a luciferase assay, and a chromatin immunoprecipitation assay.

resultsHere, we demonstrated that LINC00629 was increased under ER stress treatment. Elevated LINC00629 inhibited ER stress-induced osteosarcoma cell apoptosis and promoted clonogenicity and migration in vitro and in vivo. Further mechanistic studies indicated that LINC00629 interacted with KLF4 and suppressed its degradation, which led to a KLF4 increase in osteosarcoma. In addition, we also found that KLF4 upregulated LAMA4 expression by directly binding to its promoter and that LINC00629 inhibited ER stress-induced apoptosis and facilitated osteosarcoma cell clonogenicity and metastasis by activating the KLF4-LAMA4 pathway.

conclusionCollectively, our data indicate that LINC00629 is a critical long noncoding RNA (lncRNA) induced by ER stress and plays an oncogenic role in osteosarcoma cell by activating the KLF4-LAMA4 axis.

Indexed as

Bone NeoplasmsMicroRNAsOsteosarcomaRNA, Long NoncodingApoptosisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMicroRNAsRNA, Long NoncodingKLF4LAMA4LINC00629Osteosarcoma

Identifiers

PMID36539799
PMCPMC9764730
OpenAlexW4312114351

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.