Evidence map›Paper›PMID 26496737›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

RIP1K and RIP3K provoked by shikonin induce cell cycle arrest in the triple negative breast cancer cell line, MDA-MB-468: necroptosis as a desperate programmed suicide pathway.

Zahra Shahsavari, Fatemeh Karami-Tehrani, Siamak Salami, Mehran Ghasemzadeh

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Cells · 2023
    Article
  9. Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022
    Review
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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

4 authors at 3 institutions in 1 country.

Zahra ShahsavariCancer Research Laboratory, Department of Clinical Biochemistry, Faculty of Medical Science, Tarbiat Modares University, P.O. Box: 14115-331, Tehran, Iran.
Fatemeh Karami-TehraniCancer Research Laboratory, Department of Clinical Biochemistry, Faculty of Medical Science, Tarbiat Modares University, P.O. Box: 14115-331, Tehran, Iran. karamitf@modares.ac.ir.
Siamak SalamiDepartment of Clinical Biochemistry, Faculty of Medical Science, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mehran GhasemzadehBlood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran.
Tarbiat Modares University · IRHigh Institute for Education and Research in Transfusion Medicine · IRShahid Beheshti University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance to cell death and reprogramming of metabolism are important in neoplastic cells. Increased resistance to apoptosis and recurrence of tumors are the major roadblocks to effective treatment of triple negative breast cancer. It has been thought that execution of necroptosis involves ROS generation and mitochondrial dysfunction in malignant cells. In this study, the effect of shikonin, an active substance from the dried root of Lithospermum erythrorhizon, on the induction of necroptosis or apoptosis, via RIP1K-RIP3K expressions has been examined in the triple negative breast cancer cell line. The expression levels of RIP1K and RIP3K, caspase-3 and caspase-8 activities, the levels of ROS, and mitochondrial membrane potential have been studied in the shikonin-treated MDA-MB-468 cell line. An increase in the ROS levels and a reduction in mitochondrial membrane potential have been observed in the shikonin-treated cells. Cell death has mainly occurred through necroptosis with a significant increase in the RIP1K and RIP3K expressions, and characteristic morphological changes have been observed. In the presence of Nec-1, caspase-3 mediating apoptosis has occurred in the shikonin-treated cells. The current findings have revealed that shikonin provoked mitochondrial ROS production in the triple negative breast cancer cell line, which works as a double-edged executioner's ax in the execution of necroptosis or apoptosis. The main route of cell death induced by shikonin is RIP1K-RIP3K-mediated necroptosis, but in the presence of Nec-1, apoptosis has prevailed. The present results shed a new light on the possible treatment of drug-resistant triple negative breast cancer.

Indexed as

Antineoplastic AgentsApoptosisCaspase 3Caspase 8Cell Cycle CheckpointsCell Line, TumorCell ShapeCell SurvivalFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansMembrane Potential, MitochondrialNaphthoquinonesReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesAntineoplastic AgentsCASP3 protein, humanCASP8 protein, humanCaspase 3Caspase 8NaphthoquinonesReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanRIPK3 protein, humanshikoninApoptosisNecroptosisRIP1KRIP3KROSTriple negative breast cancer cell line

Identifiers

PMID26496737
OpenAlexW1823204499

What OpenQuestion holds

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Registered trials

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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.