Evidence map›Paper›PMID 26068969›Full record

ArticleOncotarget2015

The potential utility of acetyltanshinone IIA in the treatment of HER2-overexpressed breast cancer: Induction of cancer cell death by targeting apoptotic and metabolic signaling pathways.

Mounia Guerram, Zhen-Zhou Jiang, Bashir Alsiddig Yousef, Aida Mejda Hamdi, Hozeifa Mohamed Hassan, Zi-Qiao Yuan, Hou-Wei Luo, Xiong Zhu, Lu-Yong Zhang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
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  5. Frontiers in pharmacology · 2022
    Review
  6. Study on the Antibreast Cancer Mechanism and Bioactive Components ofEvidence-based complementary and alternative medicine : eCAM · 2020
    Article
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  8. Article
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  10. Article
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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

9 authors at 1 institution in 1 country.

Mounia GuerramJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
Zhen-Zhou JiangJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
Bashir Alsiddig YousefJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
Aida Mejda HamdiJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
Hozeifa Mohamed HassanJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
Zi-Qiao YuanJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
Hou-Wei LuoDepartment of Natural Medicinal Chemistry, China Pharmaceutical University, Nanjing 210009, China.
Xiong ZhuMedical and Chemical Institute, China Pharmaceutical University, Nanjing 210009, China.
Lu-Yong ZhangJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
China Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased lipogenesis and protein synthesis is a hallmark of cancer cell proliferation, survival, and metastatic progression and is under intense investigation as a potential antineoplastic target. Acetyltanshinone IIA (ATA) is a compound that was obtained from chemical modifications of tanshinone IIA (TIIA), a potent anticancer agent extracted from the dried roots of the Chinese herbal medicine Salvia miltiorrhiza Bunge. A previous investigation indicated that ATA is more effective in inhibiting the growth of breast cancer especially cells with HER2 overexpression. However, the molecular mechanism(s) mediating this cytotoxic effect on HER2-positive breast cancer remained undefined. Studies described here report that ATA induced G1/S phase arrest and apoptosis in the HER2-positive MDA-MB-453, SK-BR-3, and BT-474 breast cancer cell lines. Mechanistic investigations revealed that the ATA-induced apoptosis effect is associated with remarkably down-regulation of receptor tyrosine kinases (RTKs) EGFR/HER2 and inhibition of their downstream pro-survival signaling pathways. Interestingly, ATA was found to trigger oxidative and endoplasmic reticulum (ER) stresses and to activate AMP activated protein kinase (AMPK) leading to inactivation of key enzymes involved in lipid and protein biogenesis. Intraperitoneal administration of ATA significantly inhibited the growth of MDA-MB-453 xenografts in athymic mice without causing weight loss and any other side effects. Additionally, transwell migration, invasion, and wound healing assays revealed that ATA could suppress tumor angiogenesis in vitro. Taken together, our data suggest that ATA may have broad utility in the treatment of HER2-overexpressed breast cancers.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBiological ProductsBreast NeoplasmsCell Cycle CheckpointsCell Growth ProcessesCell Line, TumorDown-RegulationEndoplasmic ReticulumErb-b2 Receptor Tyrosine KinasesFemaleHumansLipidsMiceMice, Inbred BALB Cacetyltanshinone IIAAntineoplastic AgentsBiological ProductsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesLipidsPhenanthrenesATAbreast cancerHER2metabolismsignaling pathways

Identifiers

PMID26068969
PMCPMC4673132
OpenAlexW1693151270

What OpenQuestion holds

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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.