Evidence map›Paper›PMID 36322827›Full record

ArticleBlood advances2023

miR-148a-3p and DDX6 functional link promotes survival of myeloid leukemia cells.

Maryam Ghashghaei, Cong Truc Le, Haya Shaalan, Leo Escano, Marty Yue, Aaremish Arsalan, Arefeh Rouhi, Tuan Anh Nguyen, Ly P Vu

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Effects ofNanomaterials (Basel, Switzerland) · 2024
    Article
  7. Article
  8. 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

9 authors at 3 institutions in 2 countries.

Maryam GhashghaeiFaculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, Canada.
Cong Truc LeDivision of Life Science, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.ORCID 0000-0002-8261-2718
Haya ShaalanTerry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.
Leo EscanoTerry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.
Marty YueTerry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.
Aaremish ArsalanTerry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.
Arefeh RouhiTerry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.
Tuan Anh NguyenDivision of Life Science, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.ORCID 0000-0001-7793-2699
Ly P VuFaculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, Canada.ORCID 0000-0002-1682-7702
Terry Fox Research Institute · CAHong Kong University of Science and Technology · HKUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulation of gene expression at the RNA level is an important regulatory mechanism in cancer. However, posttranscriptional molecular pathways underlying tumorigenesis remain largely unexplored. In this study, we uncovered a functional axis consisting of microRNA (miR)-148a-3p, RNA helicase DDX6, and its downstream target thioredoxin-interacting protein (TXNIP) in acute myeloid leukemia (AML). Using a DROSHA-knockout cell system to evaluate miR-mediated gene expression control, we comprehensively profiled putative transcripts regulated by miR-148a-3p and identified DDX6 as a direct target of miR-148a-3p in AML cells. DDX6 depletion induced cell cycle arrest, apoptosis, and differentiation, although delaying leukemia development in vivo. Genome-wide assessment of DDX6-binding transcripts and gene expression profiling of DDX6-depleted cells revealed TXNIP, a tumor suppressor, as the functional downstream target of DDX6. Overall, our study identified DDX6 as a posttranscriptional regulator that is required for AML survival. We proposed the regulatory link between miR-148a-3p and DDX6 as a potential therapeutic target in leukemia.

Indexed as

Leukemia, Myeloid, AcuteMicroRNAsCell DifferentiationDEAD-box RNA HelicasesGenes, Tumor SuppressorHumansProto-Oncogene ProteinsDDX6 protein, humanDEAD-box RNA HelicasesMicroRNAsProto-Oncogene Proteins

Identifiers

PMID36322827
PMCPMC10393768
OpenAlexW4308061192

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.