Evidence map›Paper›PMID 32583631›Full record

ArticleJournal of cellular and molecular medicine2020

LncRNA FAM83H-AS1 promotes oesophageal squamous cell carcinoma progression via miR-10a-5p/Girdin axis.

Bo Feng, Gaoyan Wang, Xiaoliang Liang, Zheng Wu, Xinchen Wang, Zhiming Dong, Yanli Guo, Supeng Shen, Jia Liang, Wei Guo

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

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  7. LncRNA NR_003508 SuppressesInternational journal of molecular sciences · 2023
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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

10 authors at 1 institution in 1 country.

Bo FengLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Gaoyan WangLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Xiaoliang LiangLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Zheng WuLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Xinchen WangLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Zhiming DongLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Yanli GuoLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Supeng ShenLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Jia LiangLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Wei GuoLaboratory of Pathology, Hebei Cancer Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.ORCID 0000-0001-9690-161X
Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) have been well demonstrated to emerge as crucial regulators in cancer progression, and they can function as regulatory network based on their interactions. Although the biological functions of FAM83H-AS1 have been confirmed in various tumour progressions, the underlying molecular mechanisms of FAM83H-AS1 in oesophageal squamous cell carcinoma (ESCC) remained poorly understood. To address this, we treated human oesophageal cancer cell line Eca109 cells with TGF-β and found FAM83H-AS1 was notably overexpressed. In the present study, FAM83H-AS1 was observed to be significantly up-regulated in ESCC tissues and was associated with TNM stage, pathological differentiation and lymph node metastasis. FAM83H-AS1 reinforced oesophageal cancer cell proliferation, migration and invasion, and participated in epithelial-to-mesenchymal transition (EMT) process at mRNA and protein levels. In addition, a concordant regulation between FAM83H-AS1 and its sense strand FAM83H was detected at the transcriptional and translational levels. Furthermore, FAM83H-AS1 could act as competing endogenous RNA to affect the expression of Girdin by sponging miR-10a-5p verified by RIP and luciferase reporter assays. Consequently, the study provided a unique perspective of FAM83H-AS1 in ESCC progression, which may be considered as potential biomarker and therapeutic target for ESCC therapy.

Indexed as

Cell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionEsophageal Squamous Cell CarcinomaGene Expression Regulation, NeoplasticHumansLymphatic MetastasisMicrofilament ProteinsMicroRNAsNeoplasm InvasivenessProteinsRNA, MessengerUp-RegulationVesicular Transport ProteinsCCDC88A protein, humanFAM83H protein, humanMicrofilament ProteinsMicroRNAsMIRN10 microRNA, humanProteinsRNA, MessengerVesicular Transport ProteinsceRNAFAM83H-AS1long non-coding RNAoesophageal squamous cell carcinoma

Identifiers

PMID32583631
PMCPMC7417701
OpenAlexW3037555209

What OpenQuestion holds

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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.