Evidence map›Paper›PMID 30510404›Full record

ArticleDrug design, development and therapy2018

Baicalein induces apoptosis and autophagy of breast cancer cells via inhibiting PI3K/AKT pathway in vivo and vitro.

Wanjun Yan, Xingcong Ma, Xiaoyao Zhao, Shuqun Zhang

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 1 pooled it
10.4field-weighted citation impact, top 1% 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

120 citing papers in PubMed, 1 synthesis or guideline pooled it, 241 citations in OpenAlex.

  1. Pooled it
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  7. Cancer management and research · 2026
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  18. Inhibiting SNX10 induces autophagy to suppress invasion and EMT and inhibits the PI3K/AKT pathway in cervical cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
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60 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Wanjun YanDepartment of Oncology, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China, zhangshuqun19711@aliyun.com.
Xingcong MaDepartment of Oncology, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China, zhangshuqun19711@aliyun.com.
Xiaoyao ZhaoDepartment of Oncology, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China, zhangshuqun19711@aliyun.com.
Shuqun ZhangDepartment of Oncology, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China, zhangshuqun19711@aliyun.com.
Second Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeBaicalein, a widely used Chinese herbal medicine, has shown anticancer effects on many types of human cancer cell lines. However, little is known about the underlying mechanism in human breast cancer cells. In this study, we examined the apoptotic and autophagic pathways activated following baicalein treatment in human breast cancer cells in vitro and in vivo. MATERIALS AND

methodsIn in vitro study, we used MTT and clone formation assay to confirm the inhibitory role of baicalein on proliferation of MCF-7 and MDA-MB-231 breast cancer cells. Apoptosis was detected employing Hoechst 33258 staining, JC-1 staining, and flow cytometry. Autophagy was monitored by acridine orange staining and transmission electron microscopy observation. Quantitative real-time PCR and Western blot analysis were employed to study the effects of baicalein on PI3K/AKT signaling components of MCF-7 and MDA-MB-231 breast cancer cells. In in vivo study, the effect of baicalein was tested with a breast cancer cells transplantation tumor model.

resultsOur study showed that baicalein has the potential to suppress cell proliferation, induce apoptosis and autophagy of breast cancer cells in vitro and in vivo. Furthermore, baicalein significantly downregulated the expression of p-AKT, p-mTOR, NF-κB, and p-IκB while enhancing the expression of IκB in MCF-7 and MDA-MB-231 cells. It also decreased the p-AKT/AKT and p-mTOR/mTOR ratios.

conclusionOur study demonstrated that baicalein induces apoptosis and autophagy of breast cancer cells via inhibiting the PI3K/AKT signaling pathway in vivo and vitro. Our study revealed that baicalein may be a potential therapeutic agent for breast cancer.

Indexed as

Phosphoinositide-3 Kinase InhibitorsAnimalsAntineoplastic AgentsApoptosisBreast NeoplasmsCell ProliferationCell SurvivalDose-Response Relationship, DrugDrug Screening Assays, AntitumorFemaleFlavanonesHumansMammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, Inbred BALB CAntineoplastic AgentsbaicaleinFlavanonesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktAKTapoptosisautophagybaicaleinbreast cancerPI3K

Identifiers

PMID30510404
PMCPMC6248272
OpenAlexW2900863907

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.