Baicalein Induces Beclin 1- and Extracellular Signal-Regulated Kinase-Dependent Autophagy in Ovarian Cancer Cells

Wang, Ya Fang; Xu, Yali; Tang, Zheng; Li, Ting; Zhang, Le‐Le; Chen, Xiuping; Lu, Jia; Leung, Chi Hung; Ma, Dik‐Lung; Qiang, Wenan; Wang, Yi Tao

doi:10.1142/s0192415x17500094

Cited by 37 publications

(16 citation statements)

References 51 publications

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“…As a previous study reported that baicalein may regulate the ERK signaling pathway (24), the present study tested the effect of baicalein on the ERK signaling pathway and related proteins in HeLa cells. RT-qPCR results demonstrated that baicalein obviously declined ERK1/2, MMP2 and MMP9 levels in HeLa cells.…”

Section: Baicalein and U0126 Affected Erk Signaling Pathway And Apoptmentioning

confidence: 99%

The restraining effect of baicalein and U0126 on human cervical cancer cell line HeLa

Zhang

Wang

et al. 2017

Molecular Medicine Reports

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To explore the restraining effect of baicalein and the mitogen-activation protein kinase kinase inhibitor, U0126, on human cervical cell line HeLa proliferation, apoptosis and migration. HeLa cells were treated by different concentrations of baicalein or U0126. A Cell Counting Kit (CCK)‑8 assay was applied to examine cell viability. Flow cytometry was used to determine cell cycle and apoptosis. A wound healing assay was performed to detect cell migration. A terminal deoxynucleotidyl transferase dUTP nick end labeling assay was adopted to test cell apoptosis. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis was used to detect apoptosis gene and protein expression. CCK‑8 assay demonstrated that baicalein and U0126 suppressed HeLa cell viability by dose dependence. TUNEL, Annexin V‑fluorescein isothiocyanate/propidium iodide, and ratio of Bcl‑2‑associated X protein and B cell lymphoma 2 indicated that baicalein and U0126 induced HeLa cell apoptosis. Flow cytometry revealed that baicalein blocked the cell cycle of HeLa in G0/G1 phase. A wound healing assay demonstrated that baicalein significantly inhibited HeLa cell migration compared with control. Baicalein and U0126 markedly downregulated extracellular signal‑regulated kinase 1/2, matrix metalloproteinase (MMP) 2 and MMP9 levels both in mRNA and protein. In the present study, the authors demonstrated that baicalein and U0126 may be used in cervical cancer treatment by inhibiting cell migration and inducing cell apoptosis.

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Section: Baicalein and U0126 Affected Erk Signaling Pathway And Apoptmentioning

confidence: 99%

The restraining effect of baicalein and U0126 on human cervical cancer cell line HeLa

Zhang

Wang

et al. 2017

Molecular Medicine Reports

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“…Baicalein (5, 6, 7-trihydroxyflavone) is a bioactive flavone, originally isolated from the roots of Scutellaria baicalensis and Scutellaria lateriflora which are traditionally used to treat various inflammatory diseases. In particular, it has been shown that baicalein the displays anticancer properties against various cancers such as pancreatic cancer (7,8), ovarian cancer (9), and gastric cancer (10) through the induction of cancer cell apoptosis, cell-cycle arrest, inhibition of angiogenesis, metastasis, and inflammation (11,12). Thus, baicalein has great potential as an agent for the treatment and prevention of cancer without causing severe side effects.…”

mentioning

confidence: 99%

Anticancer Effects of Baicalein in FRO Thyroid Cancer Cells Through the Up-regulation of ERK/p38 MAPK and Akt Pathway

Han

Park

Nam-Goong

et al. 2019

In Vivo

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Background/Aim: The aim of the study was to evaluate the anticancer effects of baicalein in FRO anaplastic thyroid cancer (ATC) cells. Materials and Methods: FRO cells were treated with baicalein and viability was measured by the MTT assay. Cell apoptosis was observed by staining with Hoechst dye. The expression of apoptotic proteins (Bax, Bcl-2, PARP, cytochrome c, and caspase-3) and the inflammatory protein Cox-2 and the phosphorylation of MAPKs and Akt were determined by western blot. Results: Treatment with baicalein inhibited cell proliferation in a time-dependent manner and increased DNA fragmentation and apoptosis in FRO cells. Baicalein at 50 and 100 μM inhibited the expression of Bax, PARP, cytochrome c, cleaved caspase-3, and Cox-2, and increased the expression of Bcl-2. Baicalein increased the phosphorylation of ERK, p38 MAPK, and Akt and decreased JNK phosphorylation. Conclusion: Baicalein caused anticancer effects in FRO ATC cells through induction of apoptosis and regulation of the MAPK and Akt pathway.

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“…Baicalein significantly increased the level of autophagy in cancer [35] and liver disease [36]. 6 However, other studies report that baicalein attenuated autophagy [37].…”

Section: Discussionmentioning

confidence: 92%

Calcium-dependent serine-threonine phosphatase, calcineurin inactivation mediated by baicalein attenuates prion protein-mediated neuronal cell damage

Hong

Moon

Park

2020

Preprint

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Prion diseases are a group of fatal neurodegenerative disorders characterized by neuronal cell death.Calcineurin and autophagy mediate prion-induced neurodegeneration, suggesting that inhibition of calcineurin and autophagy could be a target for therapy. Baicalein has been reported to exert neuroprotective effects against calcium-dependent neuronal cell death. In this study, we investigated the effects of baicalein on the development of prion diseases. We found that baicalein treatment inhibits prion protein-induced apoptosis. Baicalein inhibited calcium up-regulation and protected the cells against prion peptide-induced neuron cell death by calcineurin inactivation. Furthermore, baicalein increased p62 protein levels and decrease LC3-II protein levels indicating autophagic flux inhibition and baicalein inhibited prion protein-induced neurotoxicity through autophagy flux inhibition. Taken together, this study demonstrated that baicalein attenuated prion peptide-induced neurotoxicity via calcineurin inactivation and autophagic flux reduction, and also suggest that baicalein may be an effective therapeutic drug against neurodegenerative diseases, including prion diseases.

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Baicalein Induces Beclin 1- and Extracellular Signal-Regulated Kinase-Dependent Autophagy in Ovarian Cancer Cells

Cited by 37 publications

References 51 publications

The restraining effect of baicalein and U0126 on human cervical cancer cell line HeLa

The restraining effect of baicalein and U0126 on human cervical cancer cell line HeLa

Anticancer Effects of Baicalein in FRO Thyroid Cancer Cells Through the Up-regulation of ERK/p38 MAPK and Akt Pathway

Calcium-dependent serine-threonine phosphatase, calcineurin inactivation mediated by baicalein attenuates prion protein-mediated neuronal cell damage

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