Evidence map›Paper›PMID 32316196›Full record

ArticleCells2020

Extracellular Acidosis Promotes Metastatic Potency via Decrease of the

Yong-Jin Kwon, Eun-Bi Seo, Sun-Ho Kwon, Song-Hee Lee, Seul-Ki Kim, Sang Ki Park, Kyungjin Kim, SaeGwang Park, In-Chul Park, Jong-Wan Park and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Melatonin and Breast Cancer: A Review Article.Chonnam medical journal · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Role of Melatonin in Cancer: Effect on Clock Genes.International journal of molecular sciences · 2023
    Review
  8. Major roles of the circadian clock in cancer.Cancer biology & medicine · 2023
    Review
  9. Article
  10. Article
  11. Circadian clock: a regulator of the immunity in cancer.Cell communication and signaling : CCS · 2021
    Review
  12. Article
  13. Article
  14. 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

11 authors at 5 institutions in 1 country.

Yong-Jin KwonDepartment of Pharmacology and Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
Eun-Bi SeoDepartment of Pharmacology and Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
Sun-Ho KwonDepartment of Pharmacology and Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
Song-Hee LeeDepartment of Pharmacology and Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
Seul-Ki KimDepartment of Pharmacology and Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
Sang Ki ParkDepartment of Life Sciences, Pohang University of Science and Technology, Pohang 37673, Korea.
Kyungjin KimDepartment of Brain and Cognitive Sciences, Daegu Gyeongbuk Institute of Science and Technology, Daegu 42988, Korea.
SaeGwang ParkDepartment of Microbiology and Immunology, INJE University College of Medicine, 633-165 GaegumDong, Busanjin Gu, Busan 614-735, Korea.
In-Chul ParkDivision of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, Nowon-gu, Seoul 01812, Korea.
Jong-Wan ParkDepartment of Pharmacology and Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
Sang-Kyu YeDepartment of Pharmacology and Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
Seoul National University · KRDaegu Gyeongbuk Institute of Science and Technology · KRInje University · KRKorea Institute of Radiological and Medical Sciences · KRPohang University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circadian oscillation is an essential process that influences many physiological and biological mechanisms and a decrease of circadian genes is associated with many diseases such as cancer. Despite many efforts to identify the detailed mechanism for decreasing circadian genes and recovering reduced circadian genes in cancer, it is still largely unknown. We found that BMAL1 was reduced in tumor hypoxia-induced acidosis, and recovered by selectively targeting acidic pH in breast cancer cell lines. Surprisingly, BMAL1 was reduced by decrease of protein stability as well as inhibition of transcription under acidosis. In addition, melatonin significantly prevented acidosis-mediated decrease of BMAL1 by inhibiting lactate dehydrogenase-A during hypoxia. Remarkably, acidosis-mediated metastasis was significantly alleviated by BMAL1 overexpression in breast cancer cells. We therefore suggest that tumor hypoxia-induced acidosis promotes metastatic potency by decreasing BMAL1, and that tumor acidosis could be a target for preventing breast cancer metastasis by sustaining BMAL1.

Indexed as

AcidosisARNTL Transcription FactorsBreast NeoplasmsCell HypoxiaCell Line, TumorCell SurvivalCircadian ClocksFemaleGene Expression RegulationHumansLactate Dehydrogenase 5MelatoninNeoplasm MetastasisRNA, Small InterferingUp-RegulationARNTL Transcription FactorsBMAL1 protein, humanLactate Dehydrogenase 5MelatoninRNA, Small InterferingacidosisBMAL1breast cancercircadian clockhypoxiametastasis

Identifiers

PMID32316196
PMCPMC7226966
OpenAlexW3016343742

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.