Evidence map›Paper›PMID 34353342›Full record

ArticleCancer cell international2021

Blocking circ-SCMH1 (hsa_circ_0011946) suppresses acquired DDP resistance of oral squamous cell carcinoma (OSCC) cells both in vitro and in vivo by sponging miR-338-3p and regulating LIN28B.

Feng Qiu, Bin Qiao, Nan Zhang, Zheng Fang, Lu Feng, Shanfeng Zhang, Weiliu Qiu

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cancer cell international, 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 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
2.2field-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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Feng Qiu *Department of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Bin Qiao *Department of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Nan Zhang *School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China.
Zheng FangDepartment of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Lu FengDepartment of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Shanfeng ZhangExperimental Center for Basic Medicine, Biochemistry and Molecular Biology, Zhengzhou University, Zhengzhou, 450000, Henan, China. zsf@zzu.edu.cn.ORCID http://orcid.org/0000-0003-3736-7781
Weiliu QiuDepartment of Oral and Maxillofacial Surgery, School of Medicine, Ninth People's Hospital, Shanghai Jiao Tong University, No. 639, Manufacturing Bureau Road, Shanghai, 200011, China. qiuwl@cae.cn.
First Affiliated Hospital of Zhengzhou University · CNZhengzhou University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCircular RNAs (circRNAs) could participate in cis-dichlorodiammineplatinum (DDP) resistance of human cancers. However, circRNAs role in DDP resistance of oral squamous cell carcinoma (OSCC) progression remains largely undeveloped. Here, we attempted to explore the role of circ-SCMH1 (ID hsa_circ_0011946) in acquired DDP resistance.

methodsExpression of circ-SCMH1, microRNA (miR)-338-3p and Lin-28 homolog B (LIN28B) was detected by real-time quantitative PCR and western blotting, and their interactions were confirmed by dual-luciferase reporter assay, RNA immunoprecipitation and RNA pull-down assay. DDP resistance was assessed by MTT assay, colony formation assay, flow cytometry, transwell assays, western blotting, and xenograft experiment. Transmission electron microscopic analysis, nanoparticle tracking analysis and western blotting confirmed the characterizations of extracellular vesicles (EVs).

resultsCirc-SCMH1 was upregulated in DDP-resistant OSCC tissues and cells (SCC-15/DDP and CAL-27/DDP). Circ-SCMH1 knockdown suppressed the half-maximal inhibitory concentration of DDP, colony formation, and migration/invasion in SCC-15/DDP and CAL-27/DDP cells, but promoted apoptosis rate and apoptotic proteins (Bax and cleaved-caspase-3) expression. However, silencing miR-338-3p abrogated above effects, and overexpressing miR-338-3p mimicked that. Similarly, miR-338-3p overexpression role could be counteracted by restoring LIN28B. Moreover, interfering circ-SCMH1 retarded tumor growth of SCC-15/DDP cells in vivo with DDP treatment or not. Mechanistically, circ-SCMH1 directly sponged miR-338-3p in regulating LIN28B, a target gene for miR-338-3p. Notably, circ-SCMH1 was an EVs cargo, and DDP-resistant OSCC cells-derived EVs could provoke circ-SCMH1 upregulation in parental cells.

conclusionCirc-SCMH1 contributes to chemoresistance of DDP-resistant OSCC cells partially via EVs secretion and circ-SCMH1/miR-338-3p/LIN28B axis.

Indexed as

Circ-SCMH1DDP resistanceLIN28BmiR-338-3pOSCC

Identifiers

PMID34353342
PMCPMC8340538
OpenAlexW3192784334

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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.