Evidence map›Paper›PMID 30200804›Full record

ArticleCell cycle (Georgetown, Tex.)2018

LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway.

Li Zhang, Wenquan Kang, Xiaolan Lu, Shiyang Ma, Lei Dong, Baicang Zou

RetractedOpen access · bronzeAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
5.6field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 143 citations in OpenAlex.

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  17. Artificial intelligence-guided discovery of gastric cancer continuum.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023
    Article
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  19. Review
  20. Article

36 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Li Zhanga Department of Gastroenterology , the Second Affiliated Hospital of Xi'an Jiaotong University , Xi'an , China.
Wenquan Kangb Department of Gastroenterology, Shenzhen Sixth People's Hospital (Nanshan Hospital) , Huazhong University of Science and Technology Union Shenzhen Hospital , Shenzhen , China.
Xiaolan Lua Department of Gastroenterology , the Second Affiliated Hospital of Xi'an Jiaotong University , Xi'an , China.
Shiyang Maa Department of Gastroenterology , the Second Affiliated Hospital of Xi'an Jiaotong University , Xi'an , China.
Lei Donga Department of Gastroenterology , the Second Affiliated Hospital of Xi'an Jiaotong University , Xi'an , China.
Baicang Zoua Department of Gastroenterology , the Second Affiliated Hospital of Xi'an Jiaotong University , Xi'an , China.
Second Affiliated Hospital of Xi'an Jiaotong University · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we aimed to investigate the effects of lncRNA CASC11 on gastric cancer (GC) cell progression through regulating miR-340-5p and cell cycle pathway. Expressions of lncRNA CASC11 in gastric cancer tissues and cell lines were determined by qRT-PCR. Differentially expressed lncRNAs, mRNAs and miRNAs were screened through microarray analysis. The relationship among CASC11, CDK1 and miR-340-5p was predicted by TargetScan and validated through dual luciferase reporter assay. Western blot assay examined the protein level of CDK1 and several cell cycle regulatory proteins. GO functional analysis and KEGG pathway analysis were used to predict the association between functions and related pathways. Cell proliferation was determined by CCK-8 assays. Cell apoptosis and cell cycle were detected by flow cytometry assay. CASC11 was highly expressed in GC tissues and cell lines. Knockdown of CASC11 inhibited GC cell proliferation, promoted cell apoptosis and blocked cell cycle. KEGG further indicated an enriched cell cycle pathway involving CDK1. QRT-PCR showed that miR-340-5p was down-regulated in GC cells tissues, while CDK1 was up-regulated. Furthermore, CASC11 acted as a sponge of miR-340-5p which directly targeted CDK1. Meanwhile, miR-340-5p overexpression promoted GC cell apoptosis and induced cell cycle arrest, while CDK1 overexpression inhibited cell apoptosis and accelerated cell cycle. Our study revealed the mechanism of CASC11/miR-340-5p/CDK1 network in GC cell line, and suggested that CASC11 was a novel facilitator that exerted a biological effect by activating the cell cycle signaling pathway. This finding provides a potential therapeutic target for GC.

Indexed as

Cell CycleApoptosisBiomarkers, TumorCDC2 Protein KinaseCell Line, TumorCell MovementCell ProliferationDisease ProgressionHumansMicroarray AnalysisNeoplasm InvasivenessRNA, Long NoncodingRNA, NeoplasmSignal TransductionStomach NeoplasmsBiomarkers, TumorCDC2 Protein KinaseCDK1 protein, humanlong noncoding RNA CASC11, humanRNA, Long NoncodingRNA, NeoplasmCDK1cell cycleGastric cancerLncRNA CASC11miR-340-5p

Identifiers

PMID30200804
PMCPMC6152531
OpenAlexW2889677605

What OpenQuestion holds

Textmetadata
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.