Evidence map›Paper›PMID 30837325›Full record

ArticleBioscience reports2019

Increased expression of miR-27 predicts poor prognosis and promotes tumorigenesis in human multiple myeloma.

Feifei Che, Chunqian Wan, Jingying Dai, Jiao Chen

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 22% 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, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Multiple Myeloma: Genetic and Epigenetic Biomarkers with Clinical Potential.International journal of molecular sciences · 2024
    Article
  3. The crucial relationship between miRNA-27 and CSE/HInternational journal of medical sciences · 2024
    Article
  4. Review
  5. Review
  6. Article
  7. Autophagy Regulation by Crosstalk between miRNAs and Ubiquitination System.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Identification of MicroRNAs WithCancer genomics & proteomics
    Review
  15. Review
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

4 authors at 1 institution in 1 country.

Feifei CheDepartment of Hematology, Sichuan Academy of Medical Science and Sichuan People's Hospital, Chengdu 610072, China.
Chunqian WanDepartment of Hematology, Sichuan Academy of Medical Science and Sichuan People's Hospital, Chengdu 610072, China.
Jingying DaiDepartment of Hematology, Sichuan Academy of Medical Science and Sichuan People's Hospital, Chengdu 610072, China.
Jiao ChenDepartment of Hematology, Sichuan Academy of Medical Science and Sichuan People's Hospital, Chengdu 610072, China jchen1125@163.com.ORCID 0000-0002-4068-9290
Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is an incurable hematological malignancy characterized by abnormal infiltration of plasma cells in the bone marrow. MicroRNAs (miRNAs) have emerged as crucial regulators in human tumorigenesis and tumor progression. miR-27, a novel cancer-related miRNA, has been confirmed to be implicated in multiple types of human tumors; however, its biological role in MM remains largely unknown. The present study aimed to characterize the biological role of miR-27 in MM and elucidate the potential molecular mechanisms. Here we found that miR-27 was significantly up-regulated in MM samples compared with normal bone marrow samples from healthy donors. Moreover, the log-rank test and Kaplan-Meier survival analysis displayed that MM patients with high miR-27 expression experienced a significantly shorter overall survival than those with low miR-27 expression. In the current study, we transfected MM cells with miR-27 mimics or miR-27 inhibitor to manipulate its expression. Functional studies demonstrated that miR-27 overexpression promoted MM cell proliferation, facilitated cell cycle progression, and expedited cell migration and invasion; whereas miR-27 knockdown inhibited cell proliferation, induced cell cycle arrest, and slowed down cell motility. Mechanistic studies revealed that Sprouty homolog 2 (SPRY2) was a direct target of miR-27 and that rescuing SPRY2 expression reversed the promoting effects of miR-27 on MM cell proliferation, migration, and invasion. Besides, miR-27 ablation suppressed tumorigenecity of MM cells in mouse xenograft models. Collectively, our data indicate that miR-27 exerts its oncogenic functions in MM by targetting SPRY2 and that miR-27 may be used as a promising candidate target in MM treatment.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinogenesisCell MovementCell ProliferationFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMice, Inbred BALB CMice, NudeMicroRNAsMiddle AgedMultiple MyelomaPrognosisIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicroRNAsMIRN27 microRNA, humanSPRY2 protein, humancell invasionmiR-27multiple myelomapoor prognosisSPRY2

Identifiers

PMID30837325
PMCPMC6454019
OpenAlexW2919865509

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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.