Evidence map›Paper›PMID 34378314›Full record

ArticleJournal of cellular and molecular medicine2021

Overexpression of lncRNA SLC26A4-AS1 inhibits papillary thyroid carcinoma progression through recruiting ETS1 to promote ITPR1-mediated autophagy.

Dong Peng, Wenfa Li, Bojuan Zhang, Xuefen Liu

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  8. The role of LncRNA-mediated autophagy in cancer progression.Frontiers in cell and developmental biology · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Non-Apoptotic Programmed Cell Death in Thyroid Diseases.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Dong PengDepartment of Nuclear Medicine, Chongqing Rongchang People's Hospital, Chongqing, China.
Wenfa LiDepartment of Cardiac Macrovascular Surgery, Chongqing University, Three Gorges Hospital/Chongqing Three Gorges Central Hospital, Chongqing, China.
Bojuan ZhangDepartment of Oncology, Chongqing University, Three Gorges Hospital/Chongqing Three Gorges Central Hospital, Chongqing, China.
Xuefen LiuDepartment of Oncology, Chongqing Rongchang People's Hospital, Chongqing, China.ORCID 0000-0002-3462-196X
Chongqing University · CNRongcheng City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Papillary thyroid carcinoma (PTC), accounting for approximately 85% cases of thyroid cancer, is a common endocrine tumour with a relatively low mortality but an alarmingly high rate of recurrence or persistence. Long non-coding RNAs (lncRNAs) is emerging as a critical player modulating diverse cellular mechanisms correlated with the progression of various cancers, including PTC. Herein, we aimed to investigate the role of lncRNA SLC26A4-AS1 in regulating autophagy and tumour growth during PTC progression. Initially, ITPR1 was identified by bioinformatics analysis as a differentially expressed gene. Then, Western blot and RT-qPCR were conducted to determine the expression of ITPR1 and SLC26A4-AS1 in PTC tissues and cells, both of which were found to be poorly expressed in PTC tissues and cells. Then, we constructed ITPR1-overexpressing cells and revealed that ITPR1 overexpression could trigger the autophagy of PTC cells. Further, we performed a series of gain- and loss-of function experiments. The results suggested that silencing of SLC26A4-AS1 led to declined ITPR1 level, up-regulation of ETS1 promoted ITPR1 expression, and either ETS1 knockdown or autophagy inhibitor Bafilomycin A1 could mitigate the promoting effects of SLC26A4-AS1 overexpression on PTC cell autophagy. In vivo experiments also revealed that SLC26A4-AS1 overexpression suppressed PTC tumour growth. In conclusion, our study elucidated that SLC26A4-AS1 overexpression promoted ITPR1 expression through recruiting ETS1 and thereby promotes autophagy, alleviating PTC progression. These finding provides insight into novel target therapy for the clinical treatment of PTC.

Indexed as

AnimalsAutophagyCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansInositol 1,4,5-Trisphosphate ReceptorsMaleMiceMice, Inbred BALB CPrimary Cell CultureProto-Oncogene Protein c-ets-1RNA, Long NoncodingSulfate TransportersThyroid Cancer, PapillaryETS1 protein, humanInositol 1,4,5-Trisphosphate ReceptorsITPR1 protein, humanProto-Oncogene Protein c-ets-1RNA, Long NoncodingSLC26A4 protein, humanSulfate TransportersautophagyITPR1Long non-coding RNApapillary thyroid carcinomaSLC26A4-AS1transcription factor

Identifiers

PMID34378314
PMCPMC8419164
OpenAlexW3190237182

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.