Baicalin inhibits the metastasis of highly aggressive breast cancer cells by reversing epithelial-to-mesenchymal transition by targeting β-catenin signaling

Zhou, Tao; Zhang, Aijie; Kuang, Ge; Gong, Xia; Jiang, Rong; Lin, Dan; Li, Jie; Li, Hongzhong; Zhang, Xiang; Wan, Jingyuan; Li, Hongyuan

doi:10.3892/or.2017.6011

Cited by 37 publications

(33 citation statements)

References 38 publications

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“…Moreover, previous works provided that baicalin inhibited migration and invasion of BC cells by suppressing epithelial-to-mesenchymal transition or mitogen-activated protein kinase (MAPK) activity. 26,27 Consistently with these findings, we also proved the anti-metastasis role of baicalin in BC cells by trans-well assay. However, the potential pathway induced migration and invasion is absent in the current paper, which should be explored in future.…”

Section: Discussionsupporting

confidence: 86%

<p>Baicalin Inhibits Cell Viability, Migration and Invasion in Breast Cancer by Regulating miR-338-3p and MORC4</p>

Duan

Guo

Pei

et al. 2019

OTT

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Background: Baicalin is a natural compound from the roots of Scutellaria lateriflora Georgi, which plays anti-cancer role in multiple cancers. However, the exact role and potential underlying mechanism of baicalin in breast cancer (BC) remain poorly understood. Methods: Thirty BC patients were recruited in this study. MCF-10A, MCF-7 and MDA-MB-231 cells were used to investigate the anti-cancer role of baicalin in vitro. Cell viability, migration, invasion and apoptosis were measured by MTT, trans-well and flow cytometry, respectively. The expression levels of microRNA-338-3p (miR-338-3p) and microrchidia family CW-type zincfinger 4 (MORC4) were measured by quantitative real-time polymerase chain reaction or Western blot. The interaction between miR-338-3p and MORC4 was explored by luciferase reporter assay and RNA immunoprecipitation. Results: We found that Baicalin treatment inhibited cell viability, migration and invasion but promoted apoptosis of BC cells. The expression of miR-338-3p was decreased in BC tissues and cells and miR-338-3p overexpression suppressed cell viability, migration and invasion but induced apoptosis. MiR-338-3p expression was reversed by baicalin exposure and inhibition of miR-338-3p attenuated the role of baicalin in viability, apoptosis, migration and invasion. MORC4 mRNA level was increased in BC tissues and cells, which was decreased by baicalin exposure. MORC4 was a target of miR-338-3p and its overexpression alleviated the effect of miR-338-3p on cell viability, apoptosis, migration and invasion. Conclusion: In conclusion, baicalin suppressed cell viability, migration and invasion but promoted apoptosis in BC cells by regulating miR-338-3p and MORC4, indicating the promising pharmacological value of baicalin in BC treatment.

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Section: Discussionsupporting

confidence: 86%

<p>Baicalin Inhibits Cell Viability, Migration and Invasion in Breast Cancer by Regulating miR-338-3p and MORC4</p>

Duan

Guo

Pei

et al. 2019

OTT

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“…The effects of baicalin have been largely studied in vitro in transformed cell types, demonstrating various antitumor, hepatoprotective, anti-inflammatory and antibacterial properties (Chen et al 2012;Lin et al 2014b;Wang et al 2008;Yin et al 2011;Yu et al 2015;Zheng et al 2012). In mammary gland, studies have been dedicated to investigating the role of baicalin as a possible agent for the treatment of breast cancers, showing either no impact on cell viability (Zhou et al 2017) or a concentration-dependent (50 to 200 µM) decrease in cell viability (Zhou et al 2009) without affecting programmed cell death in human breast cancer MCF-7 and MDA-MB-231 cells (Zhou et al 2009). However, the potential beneficial effects of PeerJ reviewing PDF | (2018:11:32517:1:1:NEW 29 Jan 2019)…”

Section: Discussionmentioning

confidence: 99%

Peer Review #3 of "Effect of the flavonoid baicalin on the proliferative capacity of bovine mammary cells and their ability to regulate oxidative stress (v0.1)"

2019

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Background. High-yielding dairy cows are prone to oxidative stress due to the high metabolic needs of homeostasis and milk production. Oxidative stress and inflammation are tightly linked; therefore, anti-inflammatory and/or natural antioxidant compounds may help improve mammary cell health. Baicalin, one of the major flavonoids in Scutellaria baicalensis, has natural antioxidant and anti-inflammatory properties in various cell types, but its effects on bovine mammary epithelial cells (BMECs) have not been investigated. Methods. Explants from bovine mammary glands were collected by biopsy at the peak of lactation (approximately 60 days after the start of lactation) (n = 3 animals) to isolate BMECs corresponding to mature secretory cells. Cell viability, apoptosis, proliferative capacity and ROS production by BMECs were measured after increasing doses of baicalin were added to the culture media in the absence or presence of H 2 O 2 , which was used as an in vitro model of oxidative stress. Results. Low doses of baicalin (1 to 10 µg/mL) had no or only slightly positive effects on the proliferation and viability of BMECs, whereas higher doses (100 or 200 µg/mL) markedly decreased BMEC proliferation. Baicalin decreased apoptosis rate at low concentrations (10 µg/mL) but increased apoptosis at higher doses. ROS production was decreased in BMECs treated with increasing doses of baicalin compared with untreated cells, and this decreased production was associated with increased intracellular concentrations of catalase and NRF-2. Irrespective of the dose, baicalin pretreatment attenuated H 2 O 2-induced ROS production. Discussion. These results indicate that baicalin exerts protective antioxidant effects on bovine mammary cells. This finding suggests that baicalin could be used to prevent oxidative metabolic disorders in dairy cows.

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“…Baicalin (2 µM) can suppress TGF-1-mediated EMT in MCF10A cells by reducing the expression of slug [105]. Baicalin (12.5-25 µM) can inhibit the expression of TGF-1-induced EMT-related transcription factors in osteosarcoma cells and inhibit the aggressive metastasis of breast cancer by blocking EMT via inhibiting the activation of -catenin [106,107] Berberine found in Berberis can reduce the secretion of IL-1 and TNF-α [108,109]. Berberine (5-20 µM) can reverse EMT in uterine cancer, leading to suppression of cancer metastasis [110].…”

Section: Reversal Of Emt By Anti-inflammatory Natural Compoundsmentioning

confidence: 99%

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

Lee

2019

Cancers

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Epithelial mesenchymal transition (EMT) is a key process in the progression of malignant cancer. Therefore, blocking the EMT can be a critical fast track for the development of anticancer drugs. In this paper, we update recent research output of EMT and we explore suppression of EMT by natural anti-inflammatory compounds and pro-resolving lipids.A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the m ajor signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2) belongs to the runt-related transcription factor family [19]. Runx2 plays a key role in EMT of hepatocellular carcinoma (HCC) [20]. GATA transcription factors are also implicated in the EMT of cancer cells [21].A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the major signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2...

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Baicalin inhibits the metastasis of highly aggressive breast cancer cells by reversing epithelial-to-mesenchymal transition by targeting β-catenin signaling

Cited by 37 publications

References 38 publications

<p>Baicalin Inhibits Cell Viability, Migration and Invasion in Breast Cancer by Regulating miR-338-3p and MORC4</p>

<p>Baicalin Inhibits Cell Viability, Migration and Invasion in Breast Cancer by Regulating miR-338-3p and MORC4</p>

Peer Review #3 of "Effect of the flavonoid baicalin on the proliferative capacity of bovine mammary cells and their ability to regulate oxidative stress (v0.1)"

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

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