Evidence map›Paper›PMID 33621425›Full record

ArticleJournal of cellular and molecular medicine2021

Cancer-associated fibroblast-derived exosomal microRNA-24-3p enhances colon cancer cell resistance to MTX by down-regulating CDX2/HEPH axis.

Hong-Wei Zhang, Yi Shi, Ji-Bin Liu, Hui-Min Wang, Pei-Yao Wang, Zhi-Jun Wu, Liu Li, Li-Peng Gu, Ping-Sheng Cao, Gao-Ren Wang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 3 pooled it
4.7field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 3 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Iron metabolism in colorectal cancer: a balancing act.Cellular oncology (Dordrecht, Netherlands) · 2023
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. The biology of mammalian multi-copper ferroxidases.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023
    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

12 authors at 3 institutions in 1 country.

Hong-Wei ZhangCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Yi ShiCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Ji-Bin LiuCancer Institute, Nantong Tumor Hospital, Nantong, China.
Hui-Min WangCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Pei-Yao WangCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Zhi-Jun WuDepartment of Oncology, Nantong Second People's Hospital, Nantong, China.
Liu LiCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Li-Peng GuCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Ping-Sheng CaoCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Gao-Ren WangDepartment of Radiotherapy, Nantong Tumor Hospital, Nantong, China.ORCID 0000-0001-5749-8493
Yu-Shui MaCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Da FuCentral Laboratory for Medical Research, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.ORCID 0000-0002-0878-2575
Tongji University · CNNantong Tumor Hospital · CNNantong University · CN

Funding

Construction of Clinical Medical Center for Tumor Biological Samples in Nantong HS2016004Jiangsu 333 Program BRA2017205Nantong Medical Key Talents Training Plan Key 43Nantong Science and Technology Project yyz15026Shanghai Municipal Commission of Health and Family Planning 201540228Shanghai Natural Science Foundation 12ZR1436000the National Natural Science Foundation of China 81201535the National Natural Science Foundation of China 81302065the National Natural Science Foundation of China 81472202the National Natural Science Foundation of China 81772932the National Natural Science Foundation of China 81972214The Peak of Six Personnel Foundation in Jiangsu Province WSW-009Wu Jieping Medical Foundation 320.6750.14326
6 · The paper itself

Abstract

MicroRNA-24-3p (miR-24-3p) has been implicated as a key promoter of chemotherapy resistance in numerous cancers. Meanwhile, cancer-associated fibroblasts (CAFs) can secret exosomes to transfer miRNAs, which mediate tumour development. However, little is known regarding the molecular mechanism of CAF-derived exosomal miR-24-3p in colon cancer (CC). Hence, this study intended to characterize the functional relevance of CAF-derived exosomal miR-24-3p in CC cell resistance to methotrexate (MTX). We identified differentially expressed HEPH, CDX2 and miR-24-3p in CC through bioinformatics analyses, and validated their expression in CC tissues and cells. The relationship among HEPH, CDX2 and miR-24-3p was verified using ChIP and dual-luciferase reporter gene assays. Exosomes were isolated from miR-24-3p inhibitor-treated CAFs (CAFs-exo/miR-24-3p inhibitor), which were used in combination with gain-of-function and loss-of-function experiments and MTX treatment. CCK-8, flow cytometry and colony formation assays were conducted to determine cell viability, apoptosis and colony formation, respectively. Based on the findings, CC tissues and cells presented with high expression of miR-24-3p and low expression of HEPH and CDX2. CDX2 was a target gene of miR-24-3p and could up-regulate HEPH. Under MTX treatment, overexpressed CDX2 or HEPH and down-regulated miR-24-3p reduced cell viability and colony formation and elevated cell apoptosis. Furthermore, miR-24-3p was transferred into CC cells via CAF-derived exosomes. CAF-derived exosomal miR-24-3p inhibitor diminished cell viability and colony formation and increased cell apoptosis in vitro and inhibited tumour growth in vivo under MTX treatment. Altogether, CAF-derived exosomal miR-24-3p accelerated resistance of CC cells to MTX by down-regulating CDX2/HEPH axis.

Indexed as

Drug Resistance, NeoplasmAgedAnimalsAntimetabolites, AntineoplasticApoptosisBiomarkers, TumorCancer-Associated FibroblastsCDX2 Transcription FactorCell ProliferationColonic NeoplasmsExosomesFemaleGene Expression Regulation, NeoplasticHumansMaleMembrane ProteinsAntimetabolites, AntineoplasticBiomarkers, TumorCDX2 protein, humanCDX2 Transcription FactorHEPH protein, humanMembrane ProteinsMethotrexateMicroRNAsMIRN24 microRNA, humancancer-associated fibroblastscaudal-related homeobox 2chemoresistancecolon cancerhephaestinmethotrexatemicroRNA-24-3p

Identifiers

PMID33621425
PMCPMC8051723
OpenAlexW3132646778

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.