Evidence map›Paper›PMID 40251609›Full record

ArticleCancer cell international2025

Molecular and phenotypic characterization of 5-FU resistant colorectal cancer cells: toward enrichment of cancer stem cells.

Amirhesam Babajnai, Saeed Rahmani, Mohammad Jamal Asadi, Elmira Gheytanchi, Glavizh Adibhesami, Faezeh Vakhshiteh, Zahra Madjd

Erratum issuedAbstract read
In one paragraph

Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  4. METTL3-YTHDF1-driven mMolecular and cellular biochemistry · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Amirhesam Babajnai *Oncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Saeed Rahmani *Oncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Mohammad Jamal AsadiDepartment of Computer Engineering, Sharif University of Technology, Tehran, Iran.
Elmira GheytanchiOncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Glavizh AdibhesamiOncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Faezeh VakhshitehOncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran. f.vakhshiteh@gmail.com.
Zahra MadjdOncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran. Zahra.madjd@yahoo.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells (CSCs) as a subgroup of cells within a tumor capable of self-renewal, thereby driving tumor initiation and spread. Addressing treatment failures in cancer, linked to CSCs and their resistance mechanisms, requires effective preclinical models for testing targeted therapies. Caco2- and HT-29-resistant cells were generated by repeated treatment of cells with growing concentrations of 5-fluorouracil (5-FU) anticancer drug for an extended time. The sensitivity of 5-FU-resistant cells was evaluated by cytotoxicity assay. Stemness, epithelial-mesenchymal transition (EMT), migration and drug resistance characteristics were assessed through gene expression investigation by real-time PCR. The expression of CD44, CD133, and CD66 were evaluated by flow cytometry. To end, the bioinformatic analysis estimated the molecular function and biological pathways considering the differential expression of selected genes and proteins. 5-FU-exposed cells displayed increased resistance to 5-FU. The gene expression analysis showed an upregulation of stemness genes (KLF4, SOX2, OCT4, C-MYC), enhanced scavenging system, and elevated expression of CSC surface markers (CD44 and CD133) compared to parental cells. Additionally, pro-EMT genes (TWIST1, SNAIL1, ZEB1, Vimentin, and N-cadherin) were significantly upregulated compared to parental cells, with the downregulation of E-cadherin as an EMT suppressor gene reflected in increased migration capacity. Moreover, increased expression of ABC transporter genes (ABCB1, ABCC1) was observed, correlating with enhanced drug resistance. The bioinformatic analysis highlighted pathways related to microRNAs in cancer, cells pluripotency, and proteoglycans. Methods of drug exposure take priority over spheroid formation, particularly due to their enhanced efficacy in stemness, EMT, and surface markers. This positions them as a promising protocol for establishing experimental models of CSCs.

Indexed as

5-FU, EMTABC, Drug resistanceCancer stem cellColorectal cancer

Identifiers

PMID40251609
PMCPMC12008981

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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.