The anti-cancer activity of an andrographolide analogue functions through a GSK-3β-independent Wnt/β-catenin signaling pathway in colorectal cancer cells

Reabroi, Somrudee; Saeeng, Rungnapha; Boonmuen, Nittaya; Kasemsuk, Teerapich; Saengsawang, Witchuda; Suksen, Kanoknetr; Zhu, Weiming; Piyachaturawat, Pawinee; Chairoungdua, Arthit

doi:10.1038/s41598-018-26278-8

Cited by 27 publications

(20 citation statements)

References 34 publications

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“…The overexpression of TCF12 is correlated with the metastasis of colorectal cancer (Lee et al, 2012). The TCF/LEF family is activated by β-catenin in response to TCFs during cell cycle progression (Reabroi et al, 2018). TCF12 interacts with EZH2 and histone deacetylases to transcriptionally repress VE-cadherin gene and thus facilitates endothelial-to-mesenchymal transition (EndoMT) to promote tumor growth and metastasis by secreting certain proteins (Fan et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: DEAD-Box Helicase 5 Interacts With Transcription Factor 12 and Promotes the Progression of Osteosarcoma by Stimulating Cell Cycle Progression

Chen

Wang

et al. 2019

Front. Pharmacol.

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Osteosarcoma (OS) is a common malignant primary bone tumor. Its mechanism of development and progression is poorly understood. Currently, there is no effective therapeutic regimens available for the treatment of OS. DEAD-box helicase 5 (DDX5) is involved in oncogenic processes. This study aimed to explore the role of DDX5 in the development and progression of OS and its relationship with transcription factor 12 (TCF12), which is as an important molecule of Wnt signaling pathway. We found that the expressions of DDX5 and TCF12 protein were significantly higher in OS patients tissues and in the MG63 cells than in the corresponding normal tissues and human osteoblast cell hFOB 1.19. Overexpressions of both DDX5 and TCF12 were associated with clinicopathological features and poor prognosis of OS patients. siRNA based knockdown of DDX5 inhibited the proliferation of MG63 cells as demonstrated by an in vitro MTS assay and 5-ethynyl-2-deoxyuridine DNA proliferation detection, and promoted apoptosis of MG63 cells measured by flow cytometry. In addition, DDX5 knockdown inhibited the MG63 cell migration and invasion on transwell assays. Further experiments showed that DDX5 knockdown not only inhibited the expression of TCF12 but also decreased the mRNA and protein levels of Cyclin E1, an important regulator of G1–S phase progression, suggesting that DDX5 was required for the entry of cells into S phase. Overexpression of TCF12 reversed the cell proliferation, migration and invasion in MG63 cells induced by DDX5 knockdown accompanied by the upregulation of Cyclin E1. Additionally, we observed that DDX5 interacted with TCF12 in both OS tissues and MG63 cells by Co-immunoprecipitation assays. Taken together, our study revealed that DDX5 interacts with TCF12 and promotes the progression of OS by stimulating cell cycle progression. Our results suggest that DDX5 and TCF12 could be potential biomarkers for the diagnosis and treatment of OS.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: DEAD-Box Helicase 5 Interacts With Transcription Factor 12 and Promotes the Progression of Osteosarcoma by Stimulating Cell Cycle Progression

Chen

Wang

et al. 2019

Front. Pharmacol.

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“…RS-PP-050 blocked the nuclear accumulation of phosphorylated β -catenin. Surprisingly, RS-PP-050 inhibited the activation of β -catenin independently of GSK-3 β -directed mechanism [ 31 ].…”

Section: Wnt/ β -Catenin Pathwaymentioning

confidence: 99%

The Prowess of Andrographolide as a Natural Weapon in the War against Cancer

Farooqı

Attar

Sabitaliyevich

et al. 2020

Cancers

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There has been a paradigm shift in our understanding about the multifaceted nature of cancer and a wealth of information has revealed that single-target drugs are not good enough to provide satisfactory clinical outcomes and therapeutic effects for complex diseases which involve multiple factors. Therefore, there has been a reignition to search for natural products having premium pharmacological activities aim to efficiently target multiple deregulated cellular signaling pathways. Andrographolide, a diterpene lactone from Andrographis paniculata was brought into to the limelight because of its ability to inhibit cancer cell proliferation and induce apoptosis. Here we review andrographolide on cellular pathways regulation including Wnt/β-catenin, mTOR, VEGF-mediated intracellular signaling, as well as TRAIL-mediated apoptosis to inhibit cancer development.

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“…Andrographolide and its derivatives have been shown to have anti-cancer activities in both in vitro and in vivo experimental models of cancer [ 39 – 41 ]. Recent studies demonstrated that andrographolide exerts inhibitory effects on malignant progression by repression of migration, matrix degradation, and invasion [ 42 , 43 ].…”

Section: Discussionmentioning

confidence: 99%

Andrographolide enhances the anti-metastatic effect of radiation in Ras-transformed cells via suppression of ERK–mediated MMP-2 activity

Chen

Fu³

et al. 2018

PLoS ONE

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BackgroundActivation of Ras oncogene in human tumors is associated with radiation-associated metastatic potential. Although ionizing radiation is one important method of cancer treatments, it has been shown to enhance matrix metalloproteinases (MMPs) activity and facilitates a more aggressive cancer phenotype. Our previous studies showed that andrographolide with lower dose rates of radiation could inhibit RAS-transformed cancer metastasis in vivo; however, the molecular mechanisms are not yet clear. In this study, we aimed to explore the anti-metastatic effect of andrographolide combined with radiation on Ras-transformed cells.MethodsRAS-transformed cells were treated with andrographolide in the presence or absence of irradiation (2–4 Gy) or angiotensin II to examine cell invasion. In vivo tumorigenesis assays were also performed. The MMP-2 activity was detected by using Gelatin zymography. Signal transduction of NF-κB subunit, p65 and phosphor-ERK 1/2, were examined by using Western blotting analysis.ResultsTreatment with andrographolide inhibited migration of Ras-transformed cells. Andrographolide treatment with radiation significantly inhibited cancer metastasis in vivo. We found that andrographolide exhibited anti-migration and anti-invasive ability against cancer metastasis via inhibition of MMP2 activity rather than affected MMP-9 and EMT. In addition, combined andrographolide with radiation appeared to be more effective in reducing MMP-2 expression, and this effect was accompanied by suppression of ERK activation that inhibits cancer cell migration and invasion.ConclusionsThese findings suggest that andrographolide enhances the anti-metastatic effect of radiation in Ras-transformed cells via suppression of ERK–mediated MMP-2 activity.

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The anti-cancer activity of an andrographolide analogue functions through a GSK-3β-independent Wnt/β-catenin signaling pathway in colorectal cancer cells

Cited by 27 publications

References 34 publications

RETRACTED: DEAD-Box Helicase 5 Interacts With Transcription Factor 12 and Promotes the Progression of Osteosarcoma by Stimulating Cell Cycle Progression

RETRACTED: DEAD-Box Helicase 5 Interacts With Transcription Factor 12 and Promotes the Progression of Osteosarcoma by Stimulating Cell Cycle Progression

The Prowess of Andrographolide as a Natural Weapon in the War against Cancer

Andrographolide enhances the anti-metastatic effect of radiation in Ras-transformed cells via suppression of ERK–mediated MMP-2 activity

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