Evidence map›Paper›PMID 31532704›Full record

ArticleRNA biology2020

Targeting of stromal versican by miR-144/199 inhibits multiple myeloma by downregulating FAK/STAT3 signalling.

Nidhi Gupta, Raman Kumar, Tulika Seth, Bhavuk Garg, Alpana Sharma

Open access · bronzeAbstract read
In one paragraph

Article in RNA biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. VCAN Is Essential for ERK5-Driven Tumorigenesis in Soft Tissue Sarcoma.International journal of biological sciences · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. [Over-expression of miR-144 inhibits invasion of liver cancer SMMC-7721 cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
    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

5 authors at 1 institution in 1 country.

Nidhi GuptaDepartment of Biochemistry, All India Institute of Medical Sciences (AIIMS), New Delhi, India.
Raman KumarDepartment of Biochemistry, All India Institute of Medical Sciences (AIIMS), New Delhi, India.
Tulika SethDepartment of Hematology, All India Institute of Medical Sciences (AIIMS), New Delhi, India.
Bhavuk GargDepartment of Orthopedics, All India Institute of Medical Sciences (AIIMS), New Delhi, India.
Alpana SharmaDepartment of Biochemistry, All India Institute of Medical Sciences (AIIMS), New Delhi, India.
All India Institute of Medical Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The abnormal growth of malignant plasma cells in Multiple Myeloma (MM) requires bone marrow (BM) niche consisting of proteoglycans, cytokines, etc. Versican (VCAN), a chondroitin sulphate proteoglycan promotes progression in solid tumours but there is dearth of literature in MM. Hence, we studied the involvement of VCAN in MM and its regulation by microRNAs as a therapeutic approach. Thirty MM patients and 20 controls were recruited and BM stromal cells (BMSCs) were isolated by primary culture. Molecular levels of VCAN, miR-144, miR-199 & miR-203 were determined in study subjects and cell lines. The involvement of VCAN in myeloma pathogenesis was studied using BMSCs-conditioned medium (BMSCs-CM) and VCAN-neutralizing antibody or microRNA mimics. Elevated expression of VCAN was observed in patients especially in BM stroma while microRNA expression was significantly lower and showed negative correlation with VCAN. Moreover, BMSCs-CM showed the presence of VCAN which upon supplementing to MM cells alter parameters in favour of myeloma progression, however, this effect was neutralized by VCAN antibody or miR (miR-144 and miR-199) mimics. The downstream signalling of VCAN was found to activate FAK and STAT3 which subsides by using VCAN antibody or miR mimics. The neutralization of oncogenic effect of BMSCs-CM by VCAN blockage affirms its plausible role in progression of MM. VCAN was observed as a paracrine mediator in the cross-talk of BMSCs and myeloma cells in BM microenvironment. Therefore, these findings suggest exploring VCAN as novel therapeutic target and utilization of microRNAs as a therapy to regulate VCAN for better management of MM.

Indexed as

BiopsyDisease SusceptibilityFocal Adhesion Kinase 1Gene Expression Regulation, NeoplasticHumansMesenchymal Stem CellsMicroRNAsMultiple MyelomaNeoplasm StagingRNA InterferenceSignal TransductionSTAT3 Transcription FactorStromal CellsTumor MicroenvironmentVersicansFocal Adhesion Kinase 1MicroRNAsMIRN144 microRNA, humanmirn199 microRNA, humanPTK2 protein, humanSTAT3 protein, humanSTAT3 Transcription FactorVersicansbone marrow microenvironmentmicroRNAsMultiple myelomatherapeuticsversican

Identifiers

PMID31532704
PMCPMC6948970
OpenAlexW2973268621

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.