Evidence map›Paper›PMID 27248319›Full record

ArticleOncotarget2016

Immunogenicity of mammary tumor cells can be induced by shikonin via direct binding-interference with hnRNPA1.

Shu-Yi Yin, Thomas Efferth, Feng-Yin Jian, Yung-Hsiang Chen, Chia-I Liu, Andrew H J Wang, Yet-Ran Chen, Pei-Wen Hsiao, Ning-Sun Yang

RetractedErratum issuedOpen 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. It has been retracted, and should not be counted. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Plant-derived natural products for drug discovery: current approaches and prospects.The Nucleus : an international journal of cytology and allied topics · 2022
    Review
  8. Review
  9. Review
  10. Article
  11. Shikonin Inhibites Migration and Invasion of Thyroid Cancer Cells by Downregulating DNMT1.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  12. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Shu-Yi YinAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan, ROC.
Thomas EfferthInstitute of Pharmacy and Biochemistry, University of Mainz, Germany.
Feng-Yin JianAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan, ROC.
Yung-Hsiang ChenAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan, ROC.
Chia-I LiuSchool of Medical Laboratory Science and Biotechnology, Taipei Medical University, Taipei, Taiwan, ROC.
Andrew H J WangInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan, ROC.
Yet-Ran ChenAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan, ROC.
Pei-Wen HsiaoAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan, ROC.
Ning-Sun YangAgricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan, ROC.
Agricultural Biotechnology Research Center, Academia Sinica · TWInstitute of Biological Chemistry, Academia Sinica · TWJohannes Gutenberg University Mainz · DETaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunogenic cell death (ICD) of tumor cells occurs via various pathways that activate immune cell systems against cancer. Previous studies have demonstrated that shikonin (SK), a plant secondary metabolite, can confer strong pharmacological activities that activate ICD and strong immunogenicity of tumor cells. However, the exact hierarchical regulatory mechanisms including the molecular targets of SK-activated immunogenicity are still unknown. Here, the heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) was revealed to serve as a specific protein target for SK. This binding plays a key role in SK-stimulated ICD activity and the suppression of post-transcriptional mRNA processing, including nuclear export activity of newly synthesized mRNAs in mammary carcinoma cells in vitro. Moreover, it also mechanistically mediates the anti-metastatic effect of a tumor cell lysate (TCL) vaccine, which can be readily generated from SK-treated 4T1 tumor cells (SK-TCL), and the derived tumor-immunogenicity of SK-TCL-treated dendritic cells in vivo. Together, the identification of hnRNPA1 as the intracellular molecular target provides compelling pharmacology-based knowledge for the potential clinical use of SK-induced immunogenicity. In addition, SK may also serve as a potent suppressor that interferes with specific post-transcriptional activities, a mechanism which may be useful for exploitation in cancer therapeutics.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBreast NeoplasmsCancer VaccinesCell Line, TumorDendritic CellsFemaleHeterogeneous Nuclear Ribonucleoprotein A1HumansMiceMice, Inbred BALB CMolecular Docking SimulationNaphthoquinonesRNA, MessengerRNA Processing, Post-TranscriptionalAntineoplastic AgentsCancer VaccinesHeterogeneous Nuclear Ribonucleoprotein A1hnRNPA1 protein, humanHnrnpa1 protein, mouseNaphthoquinonesRNA, Messengershikoninheterogeneous nuclear ribonucleoprotein A1immunogenic cell deathshikonintumor immunogenicity

Identifiers

PMID27248319
PMCPMC5190049
OpenAlexW2401153021

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.