Evidence map›Paper›PMID 27682875›Full record

ArticleOncotarget2016

Targeting cancer initiating cells by promoting cell differentiation and restoring chemosensitivity via dual inactivation of STAT3 and src activity using an active component of antrodia cinnamomea mycelia.

Ching-Wen Chang, Yu-Syuan Chen, Chien-Chih Chen, Ik-On Chan, Chin-Chu Chen, Sen-Je Sheu, Ting-Wei Lin, Shiu-Huey Chou, Chung-Ji Liu, Te-Chang Lee and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Patient-Derived Tumor Chemosensitization of GKB202, anMolecules (Basel, Switzerland) · 2021
    Article
  5. Article
  6. Protective Effect ofInternational journal of molecular sciences · 2019
    Article
  7. Effects ofMycology · 2018
    Article
  8. Article
  9. Article
  10. Antcin-H Isolated fromEvidence-based complementary and alternative medicine : eCAM · 2017
    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

11 authors at 7 institutions in 1 country.

Ching-Wen ChangInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
Yu-Syuan ChenInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
Chien-Chih ChenDepartment of Biotechnology, Hungkuang University, Taichung, Taiwan.
Ik-On ChanInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
Chin-Chu ChenGrape King Inc., Taoyuan County, Taiwan.
Sen-Je SheuGrape King Inc., Taoyuan County, Taiwan.
Ting-Wei LinGrape King Inc., Taoyuan County, Taiwan.
Shiu-Huey ChouDepartment of Life Science, Fu-Jen University, Taipei, Taiwan.
Chung-Ji LiuDepartment of Oral and Maxillofacial Surgery, Mackay Memorial Hospital, Taipei, Taiwan.
Te-Chang LeeInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Jeng-Fan LoInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
National Yang Ming Chiao Tung University · TWGrape King (Taiwan) · TWHungkuang University · TWChina Medical University · TWFu Jen Catholic University · TWInstitute of Biomedical Sciences, Academia Sinica · TWMackay Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer initiating cells (CICs) represent a subpopulation of cancer cells, which are responsible for tumor growth and resistance to chemotherapy. Herein, we first used a cell-based aldehyde dehydrogenase (ALDH) activity assay to identify that YMGKI-2 (also named as Ergone), an active component purified from Antrodia cinnamomea Mycelia extract (ACME), effectively abrogated the ALDH activity and abolished the CICs in head and neck squamous cell carcinoma cells (HNSCCs). Consequently, YMGKI-2 treatment suppressed self-renewal ability and expression of stemness signature genes (Oct-4 and Nanog) of sphere cells with enriched CICs. Moreover, YMGKI-2 treated sphere cells displayed reduction of CICs properties and promotion of cell differentiation, but not significant cytotoxicity. YMGKI-2 treatment also attenuated the tumorigenicity of HNSCC cells in vivo. Mechanistically, treatment of YMGKI-2 resulted in inactivation of STAT3 and Src. Lastly, combinatorial treatments with YMGKI-2 and standard chemotherapeutic drugs (cisplatin or Fluorouracil) restored the chemosensivity on sphere cells and cisplatin-resistant HNSCC cells. Together, we demonstrate that YMGKI-2 treatment effectively induces differentiation and reduces tumorigenicity of CICs. Further, combined treatment of YMGKI-2 and conventional chemotherapy can overcome chemoresistance. These results suggest that YMGKI-2 treatment may be used to improve future clinical responses in head and neck cancer treatment through targeting CICs.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsAscomycotaCell DifferentiationCell Line, TumorCell MovementCell Self RenewalCell SurvivalCholestenonesCisplatinDisease Models, AnimalDrug SynergismHumansMiceModels, BiologicalAntineoplastic AgentsCholestenonesCisplatinergosta-4,6,8(14),22-tetraen-3-onesrc-Family KinasesSTAT3 Transcription Factorcancer initiating cellsDifferentiationergonesrcSTAT3

Identifiers

PMID27682875
PMCPMC5341960
OpenAlexW2522588126

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.