Evidence map›Paper›PMID 25085901›Full record

ArticleCarcinogenesis2014

A signaling pathway consisting of miR-551b, catalase and MUC1 contributes to acquired apoptosis resistance and chemoresistance.

Xiuling Xu, Alexandria Wells, Mabel T Padilla, Kosuke Kato, Kwang Chul Kim, Yong Lin

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 76 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Targeting catalase in cancer.Redox biology · 2024
    Review
  5. MicroRNAs in metabolism for precision treatment of lung cancer.Cellular & molecular biology letters · 2024
    Review
  6. MicroRNAs as Regulators of Radiation-Induced Oxidative Stress.Current issues in molecular biology · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Micro RNAs in Regulation of Cellular Redox Homeostasis.International journal of molecular sciences · 2021
    Review
  14. Evodiamine suppresses non-small cell lung cancer by elevating CD8Journal of experimental & clinical cancer research : CR · 2020
    Article
  15. Review
  16. Review
  17. Comprehensive analysis of the mechanism and treatment significance of Mucins in lung cancer.Journal of experimental & clinical cancer research : CR · 2020
    Review
  18. Review
  19. MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases.International journal of molecular sciences · 2020
    Review
  20. The Yin-Yang Regulation of Reactive Oxygen Species and MicroRNAs in Cancer.International journal of molecular sciences · 2019
    Review
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

6 authors at 1 institution in 1 country.

Xiuling XuMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive, Albuquerque, NM 87108, USA and Department of Physiology & Lung Center, Temple University School of Medicine, 3420 North Broad Street, Philadelphia, PA 19140, USA.
Alexandria WellsMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive, Albuquerque, NM 87108, USA and Department of Physiology & Lung Center, Temple University School of Medicine, 3420 North Broad Street, Philadelphia, PA 19140, USA.
Mabel T PadillaMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive, Albuquerque, NM 87108, USA and Department of Physiology & Lung Center, Temple University School of Medicine, 3420 North Broad Street, Philadelphia, PA 19140, USA.
Kosuke KatoDepartment of Physiology & Lung Center, Temple University School of Medicine, 3420 North Broad Street, Philadelphia, PA 19140, USA.
Kwang Chul KimDepartment of Physiology & Lung Center, Temple University School of Medicine, 3420 North Broad Street, Philadelphia, PA 19140, USA.
Yong LinMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive, Albuquerque, NM 87108, USA and Department of Physiology & Lung Center, Temple University School of Medicine, 3420 North Broad Street, Philadelphia, PA 19140, USA ylin@lrri.org.
Temple University · US

Funding

SIGNALING MECHANISM OF MUC1 MUCINR01HL047125 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI KIM, KWANG CHUL · 1991 to 2015
$4.5M
Bridging Inflammation and Cigarette Smoke-associated Lung Carcinogenesis by MUC1R01ES017328 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI LIN, YONG · 2010 to 2014
$2.2M
NHLBI NIH HHS R01 HL047125NIEHS NIH HHS R01 ES017328NIEHS NIH HHS R01ES017328
6 · The paper itself

Abstract

Acquired chemoresistance is a major challenge in cancer therapy. While the oncoprotein Mucin-1 (MUC1) performs multiple roles in the development of diverse human tumors, whether MUC1 is involved in acquired chemoresistance has not been determined. Using an acquired chemoresistance lung cancer cell model, we show that MUC1 expression was substantially increased in cells with acquired apoptosis resistance (AR). Knockdown of MUC1 expression effectively increased the sensitivity of these cells to the apoptotic cytotoxicity of anticancer therapeutics, suggesting that MUC1 contributes to acquired chemoresistance. Decreased catalase expression and increased cellular reactive oxygen species (ROS) accumulation were found to be associated with MUC1 overexpression. Scavenging ROS with butylated hydroxyanisole or supplying exogenous catalase dramatically suppressed MUC1 expression through destabilizing MUC1 protein, suggesting that reduced catalase expression mediated ROS accumulation is accounted for MUC1 overexpression. Further, we found that increased miR-551b expression in the AR cells inhibited the expression of catalase and potentiated ROS accumulation and MUC1 expression. Finally, by manipulating MUC1 expression, we found that MUC1 promotes EGFR-mediated activation of the cell survival cascade involving Akt/c-FLIP/COX-2 in order to protect cancer cells from responding to anticancer agents. Thus, our results establish a pathway consisting of miR-551b/catalase/ROS that results in MUC1 overexpression, and intervention against this pathway could be exploited to overcome acquired chemoresistance.

Indexed as

ApoptosisCatalaseCell Line, TumorDrug Resistance, NeoplasmErbB ReceptorsGene Expression Regulation, NeoplasticHumansLung NeoplasmsMicroRNAsMucin-1Reactive Oxygen SpeciesSignal TransductionCatalaseEGFR protein, humanErbB ReceptorsMicroRNAsMIRN-551 microRNA, humanMUC1 protein, humanMucin-1Reactive Oxygen Species

Identifiers

PMID25085901
PMCPMC4216053
OpenAlexW2138189882

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.