Evidence map›Paper›PMID 38052858›Full record

ArticleCancer gene therapy2024

Cancer-associated fibroblast exosome LINC00355 promotes epithelial-mesenchymal transition and chemoresistance in colorectal cancer through the miR-34b-5p/CRKL axis.

Jun-Hong Hu, Hong-Na Tang, Yu-Hang Wang

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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  5. Cytoskeleton governs exosome-mediated drug resistance under mechanical stress.Extracellular vesicles and circulating nucleic acids · 2026
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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

3 authors at 2 institutions in 1 country.

Jun-Hong HuDepartment of Colorectal Anal Surgery, The First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, Henan Province, China. hujunhong@zzu.edu.cn.ORCID 0000-0002-9725-3789
Hong-Na TangDepartment of Colorectal Anal Surgery, Huaihe Hospital of Henan University, Kaifeng, Henan Province, China.
Yu-Hang WangDepartment of Colorectal Anal Surgery, The First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, Henan Province, China.
First Affiliated Hospital of Zhengzhou University · CNHenan University Huaihe Hospital and Huaihe Clinical Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was designed to investigate the role and mechanism of cancer-associated fibroblasts (CAFs)-derived exosomes (CAFs-exo) in metastatic and chemoresistant colorectal cancer (CRC). First, CAFs and normal fibroblasts (NFs) were isolated from CRC tissues and histologically normal adjacent tissues. Then, CAFs-exo and NFs-exo were separated with the help of ultracentrifugation. Next, the morphology, diameter and marker expression of exos were evaluated by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA) and western blot, respectively. Besides, real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression levels of LINC00355, miR-34b-5p, and CRKL in clinical tissue samples, CRC cells, fibroblasts and exos; MTT assay and cell colony formation assay to assess the chemoresistance and colony formation ability of CRC cells, respectively. Subsequently, the targeting relationship among LINC00355, miR-34b-5p, and CRKL (a target gene of miR-34b-5p) was verified by Luciferase reporter assay; and the binding relationship between LINC00355 and miR-34b-5p was assessed by a pull-down assay. Finally, the expression of epithelial-mesenchymal transition (EMT)-related proteins, and CRKL in cells or exos were detected using western blot. After a series of treatments, CAFs and NFs, CAFs-exo and NFs-exo were successfully isolated and identified. It could be observed that CAFs-exo promoted EMT, colony formation and multidrug resistance in CRC cells by secreting LINC00355. Further studies demonstrated that CAFs-exo-secreted LINC00355 increased the expression of CRKL via inhibiting the expression of miR-34b-5p, thereby enhancing chemoresistance and promoting EMT progression in CRC cells. Collectively, CAFs-exo-derived LINC00355 promotes EMT and chemoresistance in CRC by regulating the miR-34b-5p/CRKL axis.

Indexed as

Cancer-Associated FibroblastsColorectal NeoplasmsExosomesMicroRNAsAdaptor Proteins, Signal TransducingCell Line, TumorCell ProliferationDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansAdaptor Proteins, Signal TransducingCRKL proteinMicroRNAsMIRN34 microRNA, human

Identifiers

PMID38052858
OpenAlexW4389339072

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.