A Bioactive Compound from Sanguisorba officinalis L. Inhibits Cell Proliferation and Induces Cell Death in 5-Fluorouracil-Sensitive/Resistant Colorectal Cancer Cells

Zhang, Weijia; Chang, Peng; Shen, Xue; Yuan, Yuemei; Zhang, Wei; Yang, Chunjuan; Yao, Meicun

doi:10.3390/molecules26133843

Cited by 9 publications

(8 citation statements)

References 37 publications

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“…The triterpenoid compound named 3β-[(α-l-arabinopyranosyl) oxy]-urs-12,18(19)-dien-28-oic acid β-d-glupyranosylester (AGE) Both FU sensitive and resistant CRC cells showed strong activity. AGE induces cell death through the apoptosis pathway and autophagy, and inhibits cell proliferation through G0-G1 cell cycle arrest mediated by the Wnt signaling pathway [ 144 ]. Phytochemicals, especially anthocyanins/anthocyanins (A/A), have attracted the attention of the scientific community for their anti-inflammatory, anti-oxidant and anti-cancer properties.…”

Section: Drugs and Inhibitorsmentioning

confidence: 99%

Wnt signaling in colorectal cancer: pathogenic role and therapeutic target

et al. 2022

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Background The Wnt signaling pathway is a complex network of protein interactions that functions most commonly in embryonic development and cancer, but is also involved in normal physiological processes in adults. The canonical Wnt signaling pathway regulates cell pluripotency and determines the differentiation fate of cells during development. The canonical Wnt signaling pathway (also known as the Wnt/β-catenin signaling pathway) is a recognized driver of colon cancer and one of the most representative signaling pathways. As a functional effector molecule of Wnt signaling, the modification and degradation of β-catenin are key events in the Wnt signaling pathway and the development and progression of colon cancer. Therefore, the Wnt signaling pathway plays an important role in the pathogenesis of diseases, especially the pathogenesis of colorectal cancer (CRC). Objective Inhibit the Wnt signaling pathway to explore the therapeutic targets of colorectal cancer. Methods Based on studying the Wnt pathway, master the biochemical processes related to the Wnt pathway, and analyze the relevant targets when drugs or inhibitors act on the Wnt pathway, to clarify the medication ideas of drugs or inhibitors for the treatment of diseases, especially colorectal cancer. Results Wnt signaling pathways include: Wnt/β-catenin or canonical Wnt signaling pathway, planar cell polarity (Wnt-PCP) pathway and Wnt-Ca2+ signaling pathway. The Wnt signaling pathway is closely related to cancer cell proliferation, stemness, apoptosis, autophagy, metabolism, inflammation and immunization, microenvironment, resistance, ion channel, heterogeneity, EMT/migration/invasion/metastasis. Drugs/phytochemicals and molecular preparations for the Wnt pathway of CRC treatment have now been developed. Wnt inhibitors are also commonly used clinically for the treatment of CRC. Conclusion The development of drugs/phytochemicals and molecular inhibitors targeting the Wnt pathway can effectively treat colorectal cancer clinically.

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Section: Drugs and Inhibitorsmentioning

confidence: 99%

Wnt signaling in colorectal cancer: pathogenic role and therapeutic target

et al. 2022

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“…Similarly, Zhong et al evaluated TPL’s anti-tumor efficacy against SKOV3/DDP OC cells and discovered that TPL, which induces ROS production, strongly depressed the JAK2/STAT3 signaling pathway and promoted toxic autophagy [ 92 ]. Consistent with this evidence, terpenoids such as oleanolic acid (OA) [ 93 ], AGE [ 94 ], and demethylzeylasteral (ZST93) [ 95 ] have been demonstrated to overcome drug resistance by inducing lethal autophagy and cell apoptosis.…”

Section: Natural Products Overcome Autophagy-mediated Tumor Drug Resi...mentioning

confidence: 92%

“…The NPs andrographolide [ 59 ], α-hederin [ 62 ], jolkinolide B [ 63 ], PC3-15 [ 64 ], pristimerin [ 65 ], icariin [ 67 ], apigenin [ 69 ], tea polyphenol [ 70 ], genistein [ 71 ], phloretin [ 72 ], FMNT [ 73 ], rutin [ 74 ], berberine [ 86 , 87 ], matrine [ 88 ], ursolic acid [ 104 ], betulinic acid [ 90 ], triptolide [ 92 ], oleanolic acid [ 93 ], AGE [ 94 ], demethylzeylasteral [ 95 ], resveratrol [ 96 ], piceatannol [ 98 ], quercetin [ 99 ], hyperoside [ 100 ], scutellarin [ 101 ], chrysin [ 102 ], thymoquinone [ 103 ], tetrandrine [ 126 , 127 ], lycorine [ 134 ], carnosic acid [ 137 ], β-elemene [ 140 ], curcumin [ 141 ], luteolin [ 155 ], and epigallocatechin gallate [ 145 ] are associated with autophagy in tumor cells. These NPs can control autophagy in tumor cells such as those of the liver, pancreatic, gastric, breast, myeloma, lung, glioma, colorectal, ovarian, cervical, and oral malignancies, and thus combat drug resistance.…”

Section: Natural Products Overcome Autophagy-mediated Tumor Drug Resi...mentioning

confidence: 99%

Focusing on the Role of Natural Products in Overcoming Cancer Drug Resistance: An Autophagy-Based Perspective

Yao

Feng

et al. 2022

Biomolecules

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Autophagy is a critical cellular adaptive response in tumor formation. Nutritional deficiency and hypoxia exacerbate autophagic flux in established malignancies, promoting tumor cell proliferation, migration, metastasis, and resistance to therapeutic interventions. Pro-survival autophagy inhibition may be a promising treatment option for advanced cancer. Furthermore, excessive or persistent autophagy is cytotoxic, resulting in tumor cell death. Targeted autophagy activation has also shown significant promise in the fight against tumor drug resistance. Several research groups have examined the ability of natural products (NPs) such as alkaloids, terpenoids, polyphenols, and anthraquinones to serve as autophagy inhibitors or activators. The data support the capacity of NPs that promote lethal autophagy or inhibit pro-survival autophagy from being employed against tumor drug resistance. This paper discusses the potential applications of NPs that regulate autophagy in the fight against tumor drug resistance, some limitations of the current studies, and future research needs and priorities.

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“…After 24 h of treatment with S. officinalis extract (0, 50, and 100 μg/ml), the cells were harvested and incubated with PI/RNase solution (Beyotime, China). Then, cellular samples were immediately analyzed on flow cytometry (Temecula, CA, USA), see the details in a previous study ( 11 ).…”

Section: Methodsmentioning

confidence: 99%

Network Pharmacology and Transcriptomic Sequencing Analyses Reveal the Molecular Mechanism of Sanguisorba officinalis Against Colorectal Cancer

et al. 2022

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BackgroundColorectal cancer (CRC) is the most common malignant cancer worldwide. Sanguisorba officinalis has been shown to have anti-inflammatory, anti-bacterial, antioxidant, and anti-tumor effects, while its molecular mechanism against CRC remains unclear. The aim of this study is to explore the underlying mechanism of S. officinalis against CRC cell lines using network pharmacology and transcriptomic sequencing methods.MethodFirstly, the active ingredients and potential targets of S. officinalis against CRC were screened from databases. Secondly, the networks of ingredient–target, ingredient–target–CRC and protein–protein interaction were constructed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of network pharmacology and transcriptomic sequencing were performed. Finally, the effect of S. officinalis against CRC was verified by in vitro experiments.ResultsIn total, 14 active ingredients and 273 potential targets against CRC were identified in S. officinalis by network pharmacology. PI3K–Akt, HIF-1, and MAPK signaling pathways related to cell proliferation were regulated by S. officinalis in enrichment analyses and transcriptomic sequencing. In vitro, S. officinalis inhibited the proliferation and migration of CRC cells and arrested the cell cycle at the G0–G1 phase. The western blot showed that S. officinalis downregulated the expression of p-PI3K, p-Akt, HIF-1A, VEGFA, cyclin D1, c-Myc, and p-MAPK proteins in CRC cells.ConclusionIn conclusion, network pharmacology and transcriptomic sequencing analyses, in combination with in vitro studies, have been successfully applied to study the underlying mechanism of S. officinalis against CRC cells. Our results demonstrate that S. officinalis suppresses the proliferation, survival, and migration of CRC cells through regulating the PI3K–Akt, HIF-1, and MAPK signaling pathways.

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A Bioactive Compound from Sanguisorba officinalis L. Inhibits Cell Proliferation and Induces Cell Death in 5-Fluorouracil-Sensitive/Resistant Colorectal Cancer Cells

Cited by 9 publications

References 37 publications

Wnt signaling in colorectal cancer: pathogenic role and therapeutic target

Wnt signaling in colorectal cancer: pathogenic role and therapeutic target

Focusing on the Role of Natural Products in Overcoming Cancer Drug Resistance: An Autophagy-Based Perspective

Network Pharmacology and Transcriptomic Sequencing Analyses Reveal the Molecular Mechanism of Sanguisorba officinalis Against Colorectal Cancer

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