Evidence map›Paper›PMID 24905352›Full record

ArticleAutophagy2014

Autophagy promotes resistance to photodynamic therapy-induced apoptosis selectively in colorectal cancer stem-like cells.

Ming-Feng Wei, Min-Wei Chen, Ke-Cheng Chen, Pei-Jen Lou, Susan Yun-Fan Lin, Shih-Chieh Hung, Michael Hsiao, Cheng-Jung Yao, Ming-Jium Shieh

Open access · hybridAbstract read
In one paragraph

Article in Autophagy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
12.4field-weighted citation impact, top 1% 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

103 citing papers in PubMed, 196 citations in OpenAlex.

  1. Article
  2. Photodynamic effect of carbon dots and aluminum chloride phthalocyanine against skin cancer: modulation by an autophagy inducer.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
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43 more citing papers are in PubMed but not listed here.

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 5 institutions in 3 countries.

Ming-Feng WeiInstitute of Biomedical Engineering; National Taiwan University; Taipei, Taiwan.
Min-Wei ChenDepartment of Oncology; National Taiwan University Hospital; Taipei, Taiwan.
Ke-Cheng ChenInstitute of Biomedical Engineering; National Taiwan University; Taipei, Taiwan; Department of Surgery; National Taiwan University Hospital; Taipei, Taiwan.
Pei-Jen LouDepartment of Otolaryngology; National Taiwan University Hospital; Taipei, Taiwan.
Susan Yun-Fan LinInstitute of Biomedical Engineering; National Taiwan University; Taipei, Taiwan.
Shih-Chieh HungInstitute of Clinical Medicine; National Yang-Ming University; Taipei, Taiwan.
Michael HsiaoGenomics Research Center; Academia Sinica; Taipei, Taiwan.
Cheng-Jung YaoGastroenterology; Taipei Medical University-Municipal Wan Fang Hospital; Taipei, Taiwan.
Ming-Jium ShiehInstitute of Biomedical Engineering; National Taiwan University; Taipei, Taiwan; Department of Oncology; National Taiwan University Hospital; Taipei, Taiwan.
National Taiwan University · TWNational Taiwan University Hospital · TWGenomics Research Center, Academia Sinica · TWNational Yang Ming Chiao Tung University · TWUniversity Gastroenterology · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have indicated that cancer stem-like cells (CSCs) exhibit a high resistance to current therapeutic strategies, including photodynamic therapy (PDT), leading to the recurrence and progression of colorectal cancer (CRC). In cancer, autophagy acts as both a tumor suppressor and a tumor promoter. However, the role of autophagy in the resistance of CSCs to PDT has not been reported. In this study, CSCs were isolated from colorectal cancer cells using PROM1/CD133 (prominin 1) expression, which is a surface marker commonly found on stem cells of various tissues. We demonstrated that PpIX-mediated PDT induced the formation of autophagosomes in PROM1/CD133(+) cells, accompanied by the upregulation of autophagy-related proteins ATG3, ATG5, ATG7, and ATG12. The inhibition of PDT-induced autophagy by pharmacological inhibitors and silencing of the ATG5 gene substantially triggered apoptosis of PROM1/CD133(+) cells and decreased the ability of colonosphere formation in vitro and tumorigenicity in vivo. In conclusion, our results revealed a protective role played by autophagy against PDT in CSCs and indicated that targeting autophagy could be used to elevate the PDT sensitivity of CSCs. These findings would aid in the development of novel therapeutic approaches for CSC treatment.

Indexed as

ApoptosisAutophagyDrug Resistance, NeoplasmPhotochemotherapyAC133 AntigenAnimalsAntigens, CDCarcinogenesisChloroquineColorectal NeoplasmsCytoprotectionGene SilencingGlycoproteinsHumansMice, Inbred NODMice, SCIDAC133 AntigenAntigens, CDChloroquineGlycoproteinsPeptidesPROM1 protein, humanProm1 protein, mouseprotoporphyrin IXProtoporphyrinsRNA, Small Interferingapoptosisautophagyautophagy-related proteinscancer stem-like cellscolonospherecolorectal cancerphotodynamic therapyprominin 1 (PROM1)/CD133tumorigenicity

Identifiers

PMID24905352
PMCPMC4203546
OpenAlexW2034050926

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.