Evidence map›Paper›PMID 35567340›Full record

ArticleThoracic cancer2022

Circ_0001273 downregulation inhibits the growth, migration and glutamine metabolism of esophageal cancer cells via targeting the miR-622/SLC1A5 signaling axis.

Bomeng Wu, Ying Chen, Ying Chen, Xihao Xie, Hanping Liang, Fengyuan Peng, Weibi Che

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Targeting glutamine metabolism as a potential target for cancer treatment.Journal of experimental & clinical cancer research : CR · 2025
    Review
  3. Article
  4. Review
  5. Circular RNAs and Cancers.Advances in experimental medicine and biology · 2025
    Review
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  7. Review
  8. Review
  9. Article
  10. Review
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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 1 institution in 1 country.

Bomeng WuDepartment of Thoracic Surgery, Gaozhou People's Hospital, Gaozhou City, Guangdong Province, China.
Ying ChenDepartment of Thoracic Surgery, Gaozhou People's Hospital, Gaozhou City, Guangdong Province, China.ORCID 0000-0002-5367-3132
Ying ChenDepartment of Thoracic Surgery, Gaozhou People's Hospital, Gaozhou City, Guangdong Province, China.
Xihao XieDepartment of Thoracic Surgery, Gaozhou People's Hospital, Gaozhou City, Guangdong Province, China.
Hanping LiangDepartment of Thoracic Surgery, Gaozhou People's Hospital, Gaozhou City, Guangdong Province, China.
Fengyuan PengDepartment of Thoracic Surgery, Gaozhou People's Hospital, Gaozhou City, Guangdong Province, China.
Weibi CheDepartment of Thoracic Surgery, Gaozhou People's Hospital, Gaozhou City, Guangdong Province, China.
Gaozhou People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEsophageal cancer is a relatively rare cancer. However, its death rate is not to be taken lightly. Accumulating evidence indicates circular RNA (circRNA) is implicated in cancer development. The objective of this study was to unveil the role of circ_0001273 in esophageal cancer (EC).

methodsFor expression analysis of circ_0001273, miR-622 and solute carrier family 1 member 5 (SLC1A5), quantitative real-time PCR (qPCR) and Western blot were conducted. Cell proliferation was evaluated by cell counting kit-8 (CCK-8), EdU and colony formation assays. Cell apoptosis and cell migration were investigated using flow cytometry assay and wound healing assay. Glutamine metabolism was assessed by glutamine consumption and glutamate production using matched kits. The predicted binding relationship between miR-622 and circ_0001273 or SLC1A5 was validated by dual-luciferase reporter assay. An in vivo xenograft model was established to determine the role of circ_0001273 on tumor growth.

resultsCirc_0001273 was upregulated in EC tumor tissues and cells. Knockdown of circ_0001273 repressed EC cell proliferation, migration, epithelial-mesenchymal transition (EMT) and glutamine metabolism. Circ_0001273 knockdown also blocked tumor development in animal models. MiR-622 was targeted by circ_0001273, and its inhibition reversed the functional effects of circ_0001273 knockdown. SLC1A5 was a target gene of miR-622, and circ_0001273 targeted miR-622 to positively regulate SLC1A5 expression. The inhibitory effects of miR-622 enrichment on EC cell proliferation, migration, EMT and glutamine metabolism were recovered by SLC1A5 overexpression.

conclusionCirc_0001273 high expression contributed to EC progression via modulating the miR-622/SLC1A5 signaling axis.

Indexed as

Esophageal NeoplasmsMicroRNAsAmino Acid Transport System ASCAnimalsCell Line, TumorCell ProliferationDown-RegulationGene Expression Regulation, NeoplasticGlutamineHumansMinor Histocompatibility AntigensRNA, CircularAmino Acid Transport System ASCGlutamineMicroRNAsMinor Histocompatibility AntigensMIRN622 microRNA, humanRNA, CircularSLC1A5 protein, humancirc_0001273esophageal cancermiR-622SLC1A5

Identifiers

PMID35567340
PMCPMC9200876
OpenAlexW4280506388

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.