Evidence map›Paper›PMID 29512746›Full record

ArticleMolecular medicine reports2018

MicroRNA‑4284 promotes gastric cancer tumorigenicity by targeting ten-eleven translocation 1.

Yansen Li, Zhanlong Shen, Hongpeng Jiang, Zhiyong Lai, Zhu Wang, Kewei Jiang, Yingjiang Ye, Shan Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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  4. Regulation of Cell-Signaling Pathways by Berbamine in Different Cancers.International journal of molecular sciences · 2022
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  14. Article
  15. MiR-183-5p promotes renal cell carcinoma metastasis by targeting TET1.International journal of immunopathology and pharmacology
    Article
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

8 authors at 2 institutions in 1 country.

Yansen LiDepartment of Gastroenterological Surgery, Peking University People's Hospital, Beijing 100044, P.R. China.
Zhanlong ShenDepartment of Gastroenterological Surgery, Peking University People's Hospital, Beijing 100044, P.R. China.
Hongpeng JiangLaboratory of Surgical Oncology, Peking University People's Hospital, Beijing 100044, P.R. China.
Zhiyong LaiDepartment of Gastroenterological Surgery, Peking University People's Hospital, Beijing 100044, P.R. China.
Zhu WangBeijing Key Laboratory of Colorectal Cancer Diagnosis and Treatment Research, Peking University People's Hospital, Beijing 100044, P.R. China.
Kewei JiangDepartment of Gastroenterological Surgery, Peking University People's Hospital, Beijing 100044, P.R. China.
Yingjiang YeDepartment of Gastroenterological Surgery, Peking University People's Hospital, Beijing 100044, P.R. China.
Shan WangDepartment of Gastroenterological Surgery, Peking University People's Hospital, Beijing 100044, P.R. China.
Peking University · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence has shown that abnormal expression of miR-4284 participates in the progression of several types of cancer. However, the expression and the role of miR‑4284 in gastric cancer remain largely unknown. Therefore, in the present study the miR‑4284 expression levels in gastric cancer tissues and cell lines, was examined using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and found that miR‑4284 was significantly upregulated in 40 pairs of gastric cancer tissues and five gastric cancer cell lines compared to the corresponding normal tissues and GES‑1 cell line. In addition, increased miR‑4284 expression was positively associated with TNM stage (P=0.035), distal metastasis (P=0.022) and poor prognosis in gastric cancer patients. Furthermore, the overexpression of miR‑4284 expression was shown to promote cell proliferation, clone formation, invasion and migration, while the suppression of miR‑4284 expression induced opposite effects. Additionally, luciferase reporter assay was conducted and showed that ten-eleven translocation 1 (TET1), a tumor suppressor gene that regulating cell survival and metastasis, was a direct target of miR‑4284. Upregulated miR‑4284 decreased the mRNA and protein levels of TET1 in SGC‑7901 cells and downregulated miR‑4284 increased the mRNA and protein levels of TET1 in AGS cells. In addition, miR‑4284 expression was negatively correlated with the TET1 expression in gastric cancer tissues. Moreover, inhibition of TET1 suppressed the effect of miR‑4284 inhibitors on cell proliferation in AGS cells. Therefore, data demonstrated that miR‑4284 could promote tumor cell growth, migration and invasion by directly targeting TET1 in gastric cancer, which may provide a potential therapeutic target for gastric cancer treatment.

Indexed as

Cell MovementGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticCell Line, TumorCell SurvivalFemaleHumansMaleMicroRNAsMixed Function OxygenasesNeoplasm InvasivenessNeoplasm MetastasisProto-Oncogene ProteinsRNA, NeoplasmStomach NeoplasmsMicroRNAsMIRN4284 microRNA, humanMixed Function OxygenasesProto-Oncogene ProteinsRNA, NeoplasmTET1 protein, humancell migrationgastric cancermiR-4284prognosisTET1

Identifiers

PMID29512746
PMCPMC5928641
OpenAlexW2792486919

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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.