Xiaotansanjiefang inhibits the viability of colorectal cancer cells via Jagged 1/Notch 3/Snail signaling pathway

Ye, Min; Jia-qi, DU; Wang, Xiaowei; Xiu, Lijuan; Li, Xuan; Gu, Yufang; Pei, Bei; Sun, Dawei; Yue, Xupeng

doi:10.1002/tox.23651

Cited by 8 publications

(4 citation statements)

References 19 publications

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“…However, NOTCH3 ICD might interfere with NOTCH1-mediated activation of HES1 by competing with the NOTCH1 ICD to access the RBP-Jk transcriptional factor modulated by the Notch pathway (Beatus et al, 1999), and by competing for a common activator, DLL4 (Serafin et al, 2011) (Figure 3). This inhibition of the HES1 activation by NOTCH3 might be circumstantial though, since several in vitro and in vivo studies demonstrated the activation of HES1 by NOTCH3 (Bellavia et al, 2000;Shimizu et al, 2002;Ye et al, 2022).…”

Section: Notch Ligand-receptor Specificity and Colorectal Cancer Stem...mentioning

confidence: 96%

Notch receptor/ligand diversity: contribution to colorectal cancer stem cell heterogeneity

Brisset,

Mehlen,

Meurette

et al. 2023

Front. Cell Dev. Biol.

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Cancer cell heterogeneity is a key contributor to therapeutic failure and post-treatment recurrence. Targeting cell subpopulations responsible for chemoresistance and recurrence seems to be an attractive approach to improve treatment outcome in cancer patients. However, this remains challenging due to the complexity and incomplete characterization of tumor cell subpopulations. The heterogeneity of cells exhibiting stemness-related features, such as self-renewal and chemoresistance, fuels this complexity. Notch signaling is a known regulator of cancer stem cell (CSC) features in colorectal cancer (CRC), though the effects of its heterogenous signaling on CRC cell stemness are only just emerging. In this review, we discuss how Notch ligand-receptor specificity contributes to regulating stemness, self-renewal, chemoresistance and cancer stem cells heterogeneity in CRC.

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Section: Notch Ligand-receptor Specificity and Colorectal Cancer Stem...mentioning

confidence: 96%

Notch receptor/ligand diversity: contribution to colorectal cancer stem cell heterogeneity

Brisset,

Mehlen,

Meurette

et al. 2023

Front. Cell Dev. Biol.

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“…Accumulating evidence indicated that melatonin, 11 dichlorodiphenyltrichloroethane, 12 xiaotansanjiefang, 13 traditional Chinese medicine formula T33, 14 and some active ingredients and extracts of traditional Chinese medicine, such as xanthohumol, 15 hinokitiol, 16 bergapten, 17 lupeol, 18 tribulus terrestris fruit extract, 19 momordica balsamina crude acetone extract, 20 and crude extract of Rheum palmatum L 21,22 showed the anti‐cancer activity in colorectal cancer. In addition, the leguminous plant sophora flavescens has been used for more than 2000 years, as a traditional Chinese medicine, and matrine, an alkaloid, was extracted from it and exerted multiple pharmacological effects, such as antiviral, diuretic, anti‐inflammatory and anti‐allergic effects 23,24 .…”

Section: Introductionmentioning

confidence: 99%

Matrine restrains the development of colorectal cancer through regulating the AGRN/Wnt/β‐catenin pathway

Wen

et al. 2023

Environmental Toxicology

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Background Colorectal cancer is a common malignant digestive tract tumor. This study aimed to explore the biological role and potential underlying mechanism of matrine in colorectal cancer. Methods The mRNA expression of AGRN was measured using RT‐qPCR. Cell proliferation, migration, invasion and apoptosis were determined using CCK‐8, EdU, transwell assays and flow cytometry, respectively. Xenograft tumor experiment was performed to explore the action of matrine and AGRN on tumor growth in colorectal cancer in vivo. Immunohistochemistry (IHC) assay was applied for AGRN, β‐catenin, and c‐Myc expression in the tumor tissues from mice. Results Matrine dramatically repressed cell growth and reduced the level of AGRN in colorectal cancer cells. AGRN expression was boosted colorectal cancer tissues and cells. AGRN downregulation depressed cell proliferation, migration, invasion, and enhanced cell apoptosis in colorectal cancer cells. Moreover, matrine showed the anti‐tumor effects on colorectal cancer cells via regulating AGRN expression. AGRN knockdown could inactivate the Wnt/β‐catenin pathway in colorectal cancer cells. We found that AGRN downregulation exhibited the inhibition action in the progression of colorectal cancer by modulating the Wnt/β‐catenin pathway. In addition, matrine could inhibit the activation of the Wnt/β‐catenin pathway through regulating AGRN in colorectal cancer cells. Furthermore, xenograft tumor experiment revealed that matrine treatment or AGRN knockdown repressed the development of colorectal cancer via the Wnt/β‐catenin pathway in vivo. Conclusion Matrine retarded colorectal cancer development by modulating AGRN to inactivate the Wnt/β‐catenin pathway.

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“…Colorectal cancer (CRC) is the most common malignancy in both men and women, and the second leading cause of cancer-related death worldwide (1). Poor diet, lack of physical activity, obesity, drinking alcoholic beverages, and cigarette smoking are risk factors for CRC formation (2,3).…”

mentioning

confidence: 99%

Hyperforin Suppresses Oncogenic Kinases and Induces Apoptosis in Colorectal Cancer Cells

Hsu

Kuo

Hsu

et al. 2023

In Vivo

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Background/Aim: Signal transducer and activator of transcription 3 (STAT3), Janus Kinase 1 (JAK1), extracellular signal-regulated kinase (ERK), and protein kinase B (AKT) are essential for malignant transformation and progression in colorectal cancer (CRC) and can be considered as targets for therapeutic interventions. Hyperforin, an active constituent from Hypericum perforatum, has been reported to inhibit inflammation. However, whether hyperforin may suppress CRC progression via inactivation of JAK/STAT3, ERK or AKT signaling remains unclear. Materials and Methods: Human CRC cells were used to identify the treatment efficacy of hyperforin and its underlying mechanisms of action by MTT, flow cytometry, wound healing, and western blotting assays. Results: Hyperforin not only induced cytotoxicity, extrinsic/intrinsic apoptosis signaling, but also suppressed the invasion/migration ability of CRC. The phosphorylation of STAT3, JAK1, ERK and AKT was found to be decreased by hyperforin. Conclusion: Hyperforin inactivates multiple oncogenic kinases and induces apoptosis signaling in CRC cells.

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Xiaotansanjiefang inhibits the viability of colorectal cancer cells via Jagged 1/Notch 3/Snail signaling pathway

Cited by 8 publications

References 19 publications

Notch receptor/ligand diversity: contribution to colorectal cancer stem cell heterogeneity

Notch receptor/ligand diversity: contribution to colorectal cancer stem cell heterogeneity

Matrine restrains the development of colorectal cancer through regulating the AGRN/Wnt/β‐catenin pathway

Hyperforin Suppresses Oncogenic Kinases and Induces Apoptosis in Colorectal Cancer Cells

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