Evidence map›Paper›PMID 35188072›Full record

ArticleBioengineered2022

CircRNA SOD2 motivates non-small cell lungs cancer advancement with EMT via acting as microRNA-2355-5p's competing endogenous RNA to mediate calmodulin regulated spectrin associated proteins-2.

Changsheng Lv, Yiying Hu, Xin Zhou, Yuntao Zhu, Jin Wang, Fachen Zhou

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Microtubule Minus-End Binding Proteins in Cancer: Advances.Diagnostics (Basel, Switzerland) · 2025
    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

6 authors at 2 institutions in 1 country.

Changsheng LvDepartment of Thoracic Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian City, Liaoning Province, China.
Yiying HuDepartment of Neuroelectrophysiology, The First Affiliated Hospital of Dalian Medical University, Dalian City, Liaoning Province, China.
Xin ZhouDepartment of Histology and Embryology, Dalian Medical University, Dalian City, Liaoning Province, China.
Yuntao ZhuDepartment of Thoracic Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian City, Liaoning Province, China.
Jin WangDepartment of Thoracic Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian City, Liaoning Province, China.
Fachen ZhouDepartment of Thoracic Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian City, Liaoning Province, China.
Dalian Medical University · CNFirst Affiliated Hospital of Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circular RNAs (circRNAs) are closely linked with human cancer development such as non-small-cell lung cancer (NSCLC). However, the characteristics and specific functions of most circRNAs in NSCLC remained unknown. Previous studies have suggested that circRNA SOD2 (CircSOD2) expression was upregulated in a number of cancers. This study aimed to explore the functions of circSOD2 in NSCLC advancement with epithelial-mesenchymal transition (EMT). Expression profile analysis of circSOD2, miR-2355-5p, and calmodulin-regulated spectrin-associated protein 2 (CAMSAP2) was detected by real-time quantitative PCR (RT-qPCR). Transwell assay, cell migration assay, CCK8, ELISA, RIP assay, RNA pull-down assay, and Western blot analysis were performed to evaluate the functions of circSOD2, miR-2355-5p, and CAMSAP2. We found elevated expression of circSOD2 and CAMSAP2 while reduced expression of miR-2355-5p in NSCLC tumor tissues. Silencing or overexpression of CircSOD2 resulted in increased or decreased expression of miR-2355-5p, respectively. Mechanically, we showed that silencing of CircSOD2 and overexpression of miR-2355-5p resulted in the reduced rate of NSCLC cell proliferation. Inhibition of miR-2355-5p reversed the changes induced via silencing of CircSOD2. MiR-2355-5p binds to the CircSOD2 promoter and triggered its stimulation, which further activated circSOD2 expression. CircSOD2 suppression impaired lung cancer cell growth, cell migration, prohibited cell cycle progression, and in vivo tumor growth by targeting miR-2355-5p expression in NSCLC tissues. Meanwhile, increased expression of CAMSAP2 reversed the changes stimulated by the elevated level of miR-2355-5p in NSCLC progression. This innovative signaling axis CircSOD2/miR-2355-5p/CAMSAP2 illustrated the new horizon to investigate NSCLC tumorigenesis and provided new prognosis and treatment of NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsMicroRNAsCalmodulinCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansLungMicrotubule-Associated ProteinsRNA, CircularSpectrinCalmodulinCAMSAP2 protein, humanMicroRNAsMicrotubule-Associated ProteinsRNA, CircularSpectrinCAMSAP2Circular RNA SOD2epithelial-mesenchymal transitioninvasion and migrationMicroRNA-2355-5pnon-small cell lung cancer

Identifiers

PMID35188072
PMCPMC8974208
OpenAlexW4212802508

What OpenQuestion holds

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LicenceCC BY
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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.