Galangin Induces Apoptosis in MCF-7 Human Breast Cancer Cells Through Mitochondrial Pathway and Phosphatidylinositol 3-Kinase/Akt Inhibition

Liú, Dan; Peng, You; Luo, Yan; Yang, Min; Liu, Yanwen

doi:10.1159/000489564

Cited by 50 publications

(36 citation statements)

References 49 publications

(58 reference statements)

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“…Additionally, we also explored the effect of PI3K/AKT pathway on tumor cell growth and apoptosis. From the previous studies, 22 – 25 we concluded that the activation of the PI3K/AKT pathway can increase the proliferation of tumor cells and inhibit the apoptosis of cells, which is consistent with our study. In our study, we added PI3K inhibitor or PI3K activator to explore the effect of PI3K/AKT pathway.…”

Section: Discussionsupporting

confidence: 92%

Peroxiredoxin 1 silencing inhibited the growth and promoted apoptosis of pancreatic cancer cells via targeting <em>FOXO3</em> gene

Sun¹,

Kong²,

Li³

et al. 2018

CMAR

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ObjectiveOur study aimed to investigate the interaction between peroxiredoxin 1 (Prx1) and forkhead box O3 (FOXO3) and to explore the role of PI3K/AKT pathway in the development of pancreatic cancer.Material and methodsHuman pancreatic normal cells HPDE6-C7 and pancreatic cancer cells PANC-1 were randomly divided into control group, Prx1-silencing (si-Prx1) group, Prx1/FOXO3 dual-silencing (si-Prx1/FOXO3) group, and negative control group. Cell proliferation assay, clone formation assay, and cell apoptosis assay were performed to investigate the effects of Prx1 silencing and FOXO3 silencing on the proliferation and apoptosis ability of pancreatic cancer cells. qRT-PCR and Western blot were performed to study the Prx1 and FOXO3 mRNA in the two cells and FOXO3 protein expression in PANC-1 cells.ResultWe found Prx1 silencing could inhibit growth and promote apoptosis of PANC-1 cells. And Prx1 silencing could decrease the Prx1 mRNA level and increase FOXO3 mRNA level. To further explore the role of Prx1 in PI3K/AKT, we study the cell proliferation and apoptosis ability after adding the PI3K inhibitor and PI3K activator. We observed that PI3K inhibitor could inhibit tumor cell growth and promote cell apoptosis. And PI3K inhibitor also downregulated Prx1 protein expression.ConclusionWe concluded that the Prx1 silencing inhibited the growth and promoted apoptosis of pancreatic cancer cells via modulation of PI3K/AKT pathway by targeting FOXO3 gene.

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Section: Discussionsupporting

confidence: 92%

Peroxiredoxin 1 silencing inhibited the growth and promoted apoptosis of pancreatic cancer cells via targeting <em>FOXO3</em> gene

Sun¹,

Kong²,

Li³

et al. 2018

CMAR

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“…It can significantly inhibit the proliferation of TNBC cell lines (MDA-MB-231, BT-549, HCC70, and HCC1806) compared with non-tumorigenic BC lines (MCF-10A and AG11132) through downregulating the expression of CDK1 [159]. Moreover, Galangin, another plant anticancer compound, inhibits the survival of MCF-7 cells and induces apoptosis by downregulating CDK1, CDK2, and CDK4, leading to cell-cycle arrest [160]. The 5,7-dihydroxy-2-[4 -hydroxy-3 -(methoxymethyl)phenyl]-6-C-β-glucopyranosyl flavone (from Urginea indica bulb) induces G0/G1 arrest and apoptosis, as well as inhibits angiogenesis in BC cells through targeting CDK1 and CDK6 [161].…”

Section: The Novel Cdk Inhibitors In Bcmentioning

confidence: 99%

The Roles of Cyclin-Dependent Kinases in Cell-Cycle Progression and Therapeutic Strategies in Human Breast Cancer

Ding

Cao

Lin

et al. 2020

IJMS

347

216

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Cyclin-dependent kinases (CDKs) are serine/threonine kinases whose catalytic activities are regulated by interactions with cyclins and CDK inhibitors (CKIs). CDKs are key regulatory enzymes involved in cell proliferation through regulating cell-cycle checkpoints and transcriptional events in response to extracellular and intracellular signals. Not surprisingly, the dysregulation of CDKs is a hallmark of cancers, and inhibition of specific members is considered an attractive target in cancer therapy. In breast cancer (BC), dual CDK4/6 inhibitors, palbociclib, ribociclib, and abemaciclib, combined with other agents, were approved by the Food and Drug Administration (FDA) recently for the treatment of hormone receptor positive (HR+) advanced or metastatic breast cancer (A/MBC), as well as other sub-types of breast cancer. Furthermore, ongoing studies identified more selective CDK inhibitors as promising clinical targets. In this review, we focus on the roles of CDKs in driving cell-cycle progression, cell-cycle checkpoints, and transcriptional regulation, a highlight of dysregulated CDK activation in BC. We also discuss the most relevant CDK inhibitors currently in clinical BC trials, with special emphasis on CDK4/6 inhibitors used for the treatment of estrogen receptor-positive (ER+)/human epidermal growth factor 2-negative (HER2−) M/ABC patients, as well as more emerging precise therapeutic strategies, such as combination therapies and microRNA (miRNA) therapy.

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“…Cell apoptosis is induced by multiple signaling pathways, including the Akt signaling pathway which has a central role in cell apoptosis. Therefore, anticancer drugs often induce cancer apoptosis through inhibiting the AKT signaling pathway (39,40). It has been reported that Pris is a potential anticancer drug that can induce apoptosis in pancreatic cancer cells and colorectal cancer cells (15,41).…”

Section: Discussionmentioning

confidence: 99%

Pristimerin enhances the effect of cisplatin by inhibiting the miR‑23a/Akt/GSK3β signaling pathway and suppressing autophagy in lung cancer cells

et al. 2019

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Lung cancer is a common type of cancer with a high mortality rate in China. Cisplatin (Cis) is one of the most effective broad-spectrum chemotherapeutic drugs for the treatment of advanced lung cancer. However, Cis resistance remains an obstacle in the treatment of advanced lung cancer. Pristimerin (Pris), a naturally occurring triterpenoid quinone compound, not only possesses anticancer properties, but also enhances chemosensitivity. Therefore, the present study aimed to investigate whether Pris can enhance the chemosensitivity of lung cancer cells to Cis and identify the underlying mechanism. A Cell Counting kit-8 and flow cytometry were used to determine cell viability, cell cycle progression and apoptosis in A549 and NCI-H446 cells. Western blotting was used to determine cell apoptosis-related, cell cycle-related and autophagy-related proteins. The results showed that Pris inhibited cell proliferation, and induced G0/G1 arrest and cell apoptosis in A549 and NCI-H446 cells. The western blotting revealed that Pris effectively synergized with Cis to induce cell apoptosis by inhibiting the microRNA-23a/Akt/glycogen synthase kinase 3β signaling pathway and suppressing autophagy. In vivo xenograft experiments confirmed that Pris effectively synergized with Cis to suppress tumor growth. Collectively, these results indicate that Pris synergized with Cis and that this may be a potential therapeutic strategy to overcome lung cancer.

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Galangin Induces Apoptosis in MCF-7 Human Breast Cancer Cells Through Mitochondrial Pathway and Phosphatidylinositol 3-Kinase/Akt Inhibition

Cited by 50 publications

References 49 publications

Peroxiredoxin 1 silencing inhibited the growth and promoted apoptosis of pancreatic cancer cells via targeting <em>FOXO3</em> gene

Peroxiredoxin 1 silencing inhibited the growth and promoted apoptosis of pancreatic cancer cells via targeting <em>FOXO3</em> gene

The Roles of Cyclin-Dependent Kinases in Cell-Cycle Progression and Therapeutic Strategies in Human Breast Cancer

Pristimerin enhances the effect of cisplatin by inhibiting the miR‑23a/Akt/GSK3β signaling pathway and suppressing autophagy in lung cancer cells

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