Evidence map›Paper›PMID 30959809›Full record

ArticleInternational journal of molecular sciences2019

PGC-1α Controls Mitochondrial Biogenesis in Drug-Resistant Colorectal Cancer Cells by Regulating Endoplasmic Reticulum Stress.

Chul Won Yun, Yong-Seok Han, Sang Hun Lee

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

30 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Mitochondrial function and gastrointestinal diseases.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Mitochondrial Control in Inflammatory Gastrointestinal Diseases.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Review
  18. Targeting PGC1α to wrestle cancer: a compelling therapeutic opportunity.Journal of cancer research and clinical oncology · 2022
    Review
  19. Article
  20. Activation of PPARPPAR research · 2022
    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

3 authors at 1 institution in 1 country.

Chul Won YunMedical Science Research Institute, Soonchunhyang University Seoul Hospital, Seoul 336-745, Korea. skydbs113@naver.com.
Yong-Seok HanMedical Science Research Institute, Soonchunhyang University Seoul Hospital, Seoul 336-745, Korea. format7000@naver.com.
Sang Hun LeeMedical Science Research Institute, Soonchunhyang University Seoul Hospital, Seoul 336-745, Korea. ykckss1114@nate.com.
Soonchunhyang University Hospital · KR

Funding

National Research Foundation of Korea NRF-2016R1D-1A3B01007727National Research Foundation of Korea NRF-2017M3A9B4032528
6 · The paper itself

Abstract

Anti-cancer drug resistance is a serious issue for patients with colorectal cancer (CRC). Although recent studies have shown the mechanism by which CRC cells become drug resistant, novel strategies for overcoming this drug resistance have not yet been developed. To address this problem, we characterized 5-fluorouracil (5FU)-resistant CRC cells after treatment with 5FU, and focused on the expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) in these cells. In 5FU-resistant CRC cells, the 5FU did not considerably decrease the mitochondrial biogenesis or mitochondrial complex I and IV activities, and only partially decreased the antioxidant enzymatic activity, oxygen consumption ratio, and cell survival. The expression of PGC-1α was remarkably increased in the 5FU-resistant CRC cells compared with the 5FU-sensitive CRC cells. The 5FU-resistant CRC cells displayed enhanced mitochondrial biogenesis, oxidative phosphorylation, and antioxidant enzyme activities against 5FU-induced reactive oxygen species, because of the increased expression of PGC-1α. PGC-1α inhibited 5FU-induced endoplasmic reticulum (ER) stress in the 5FU-resistant CRC cells, resulting in the suppression of apoptosis. These findings reveal that PGC-1α plays an important role in drug resistance in 5FU-resistant CRC cells. Moreover, PGC-1α could serve as a novel target in patients with 5FU-resistant CRC.

Indexed as

Drug Resistance, NeoplasmEndoplasmic Reticulum StressOrganelle BiogenesisAntioxidantsApoptosisCell Line, TumorColorectal NeoplasmsCytoprotectionFluorouracilHumansMitochondriaModels, BiologicalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaReactive Oxygen SpeciesAntioxidantsFluorouracilPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaReactive Oxygen Speciesapoptosiscolorectal cancer cellsdrug resistanceendoplasmic reticulum stressmitochondrial biogenesisPGC-1α

Identifiers

PMID30959809
PMCPMC6480203
OpenAlexW2931360703

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.