Evidence map›Paper›PMID 27388461›Full record

ArticleBMC cancer2016

Delphinidin-3-glucoside suppresses breast carcinogenesis by inactivating the Akt/HOTAIR signaling pathway.

Xiaohong Yang, En Luo, Xin Liu, Bin Han, Xiaoping Yu, Xiaoli Peng

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. HOTAIR in colorectal cancer: structure, function, and therapeutic potential.Medical oncology (Northwood, London, England) · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Delphinidin and Its Glycosides' War on Cancer: Preclinical Perspectives.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Long Non-Coding RNACancers · 2020
    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 2 institutions in 1 country.

Xiaohong YangDepartment of Public Health, Chengdu Medical College, Chengdu, China.
En LuoDepartment of General Surgery, The Fifth People's Hospital of Chengdu, Chengdu, China.
Xin LiuDepartment of Public Health, Chengdu Medical College, Chengdu, China.
Bin HanDepartment of Public Health, Chengdu Medical College, Chengdu, China.
Xiaoping YuDepartment of Public Health, Chengdu Medical College, Chengdu, China.
Xiaoli PengDepartment of Public Health, Chengdu Medical College, Chengdu, China. xiaopeng967@sohu.com.
Chengdu Medical College · CNChengdu Fifth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) plays a crucial role in cancer progression, which is regulated by the interferon regulatory factor-1 (IRF1) and up-streaming Akt activation. The present study evaluated the chemopreventive effects of delphinidin-3-glucoside (Dp), a major anthocyanin present in pigmented fruits and vegetables, on breast carcinogenesis, and investigate the role of the Akt/HOTAIR signaling pathway.

methodsHuman breast epithelial cells MCF10A were treated with carcinogens (NNK and B[a]P) or co-treated with carcinogens plus Dp for 30 days. Then, the cancer-associated properties of the treated cells were evaluated to assess the carcinogenesis and the effects of Dp. HOTAIR levels were detected by qRT-PCR. The proteins expression was measured by western blots, immunofluorescence and immunohistochemistry. Xenografted tumors were made by implanting breast cancer cells MDA-MB-231-Luc-GFP in athymic mice. ChIP-qPCR analysis was used to detect the IRF1 binding to the HOTAIR promoter.

resultsCarcinogens treatment induces apparent carcinogenic transformation in MCF10A cells including reduced dependence on growth factors, anchorage-independent cell growth and aberrant wound-healing ability, which is effectively suppressed by Dp co-treatment. The level of HOTAIR significantly increases in a time-dependent manner during chronic breast carcinogenesis. Dp treatment down-regulates HOTAIR expression in breast carcinogenesis and breast cancer cells. Furthermore, Dp administration inhibits the growth of xenografted breast tumors in athymic mice, and decreases HOTAIR in vivo. Further studies showed that Dp represses Akt activation, promotes IRF1 expression and increases IRF1 binding to the HOTAIR promoter. Silence of IRF1 expression via transfecting cells with IRF1 siRNAs significantly reduced the effects of Dp on HOTAIR, resulting in decreased cytotoxic effects of Dp on breast cancer cells.

conclusionsThese data suggest the effective chemopreventive effect of Dp on breast carcinogenesis, in which down-regulation of HOTAIR plays a critical role.

Indexed as

AnimalsAnthocyaninsBreast NeoplasmsCell Line, TumorCell ProliferationCell SurvivalCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticGlucosidesHumansMiceNitrosaminesPromoter Regions, GeneticProto-Oncogene Proteins c-aktRNA, Long Noncoding4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanoneAnthocyaninsdelphinidin 3-O-glucopyranosideGlucosidesHOTAIR long untranslated RNA, humanNitrosaminesProto-Oncogene Proteins c-aktRNA, Long NoncodingAnthocyaninBreast cancerCarcinogenesisHOTAIRlncRNAs

Identifiers

PMID27388461
PMCPMC4937537
OpenAlexW2464322022

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.