A promising natural product, pristimerin, results in cytotoxicity against breast cancer stem cells in vitro and xenografts in vivo through apoptosis and an incomplete autopaghy in breast cancer

Cevatemre, Buse; Erkısa, Merve; Aztopal, Nazlıhan; Karakaş, Didem; Alper, Pınar; Tsimplouli, Chrisiida; Sereti, Evangelia; Dimas, Konstantinos; Armutak, Elif Ilkay; Gürevin, Ebru Gürel; Uvez, Ayca; Mori, Mattia; Berardozzi, Simone; Ingallina, Cinzia; D’Acquarica, Ilaria; Botta, Bruno; Özpolat, Bülent; Ulukaya, Engin

doi:10.1016/j.phrs.2017.11.027

Cited by 67 publications

(45 citation statements)

References 58 publications

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“…Several studies have documented the anticancer activity of pristimerin in vitro and in vivo. [8][9][10][11][12][13] For example, pristimerin inhibits cell proliferation and induces apoptosis through suppression of proteasome activity and NF-κB pathway signaling. [22,23] In addition, pristimerin induced ROS generation and subsequent JNK activation during cell death.…”

Section: Pristimerin Triggers Apoptosis and Autophagy By Ros/jnk Pathmentioning

confidence: 99%

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Pristimerin Induces Autophagy‐Mediated Cell Death in K562 Cells through the ROS/JNK Signaling Pathway

Liu

Ren

et al. 2019

Chemistry & Biodiversity

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Chronic myeloid leukemia (CML) is a lethal malignancy, and the progress toward long‐term survival has stagnated in recent decades. Pristimerin, a quinone methide triterpenoid isolated from the Celastraceae and Hippocrateaceae families, is well‐known to exert potential anticancer activities. In this study, we investigated the effects and the mechanisms of action on CML. We found that pristimerin inhibited cell proliferation of K562 CML cells by causing G1 phase arrest. Furthermore, we demonstrated that pristimerin triggered autophagy and apoptosis. Intriguingly, pristimerin‐induced cell death was restored by an autophagy inhibitor, suggesting that autophagy is cross‐linked with pristimerin‐induced apoptosis. Further studies revealed that pristimerin could produce excessive reactive oxygen species (ROS), which then induce JNK activation. These findings provide clear evidence that pristimerin might be clinical benefit to patients with CML.

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Section: Pristimerin Triggers Apoptosis and Autophagy By Ros/jnk Pathmentioning

confidence: 99%

“…[6,7] Recently, pristimerin has been reported to exert promising therapeutic effect on several malignancies. [8][9][10][11][12][13] Although pristimerin exhibits a variety of anticancer activities, its effects and mechanisms on CML have not been completely explored.…”

Section: Introductionmentioning

confidence: 99%

Pristimerin Induces Autophagy‐Mediated Cell Death in K562 Cells through the ROS/JNK Signaling Pathway

Liu

Ren

et al. 2019

Chemistry & Biodiversity

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“…Considering that pericytes recruitment to the newly formed endothelial cells networks is critical for new blood vessel maturation during the angiogenesis late-stage 33 , we performed adhesion assay and 3D coculture assay of HUVECs and HBVPs to ascertain the effect of pristimerin on pericyte recruitment. The result showed that Shh stimulated a dramatic increase of HBVPs adhesion, and pristimerin treatment attenuated Shh-induced HBVPs adhesion (Fig.…”

Section: Pristimerin Attenuates the Adhesion And Recruitment Of Pericmentioning

confidence: 99%

Identification of a novel tumor angiogenesis inhibitor targeting Shh/Gli1 signaling pathway in Non-small cell lung cancer

et al. 2020

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Although angiogenesis inhibitors targeting VEGF/VEGFR2 have been applied for tumor therapy, the outcomes are still unsatisfactory. Thus, it is urgent to develop novel angiogenesis inhibitor for cancer therapy from new perspectives. Identification of novel angiogenesis inhibitor from natural products is believed to be one of most promising strategy. In this study, we showed that pristimerin, an active agent isolated from traditional Chinese herbal medicine Celastrus aculeatus Merr, was a novel tumor angiogenesis inhibitor that targeting sonic hedgehog (Shh)/glioma associated oncogene 1 (Gli1) signaling pathway in non-small cell lung cancer (NSCLC). We showed that pristimerin affected both the early-and late-stage of angiogenesis, suggesting by that pristimerin inhibited Shh-induced endothelial cells proliferation, migration, invasion as well as pericytes recruitment to the endothelial tubes, which is critical for the new blood vessel maturation. It also suppressed tube formation, vessel sprouts formation and neovascularization in chicken embryo chorioallantoic membrane (CAM). Moreover, it significantly decreased microvessel density (MVD) and pericyte coverage in NCI-H1299 xenografts, resulting in tumor growth inhibition. Further research revealed that pristimerin suppressed tumor angiogenesis by inhibiting the nucleus distribution of Gli1, leading to inactivation of Shh/Gli1 and its downstream signaling pathway. Taken together, our study showed that pristimerin was a promising novel antiangiogenic agent for the NSCLC therapy and targeting Shh/Gli1 signaling pathway was an effective approach to suppress tumor angiogenesis.

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“…Here, we collect natural telomerase inhibitors reported in the literature and summarize their telomerase inhibition effects, structures, possible mechanisms, and provide references for pharmaceutical chemists searching for suitable lead compounds. Table and Figures and show natural products and chemical structures that target the telomere elongation process …”

Section: Small Molecule Inhibitorsmentioning

confidence: 99%

“…Pristimerins ( 55 ) is a highly reversible monoacylglycerol lipase inhibitor that belongs to quinone methyl triterpenoids with broad biological activities. The studies found that it has antiproliferative effects on a variety of tumor cell lines (multiple myeloma, prostate cancer, lung cancer, cervical cancer, and breast cancer) . Deeb et al reported that it inhibits telomere elongation and induces apoptosis, which may be caused by the reduction in the transcription factors and nuclear factor κB associated with the expression of hTERT.…”

Section: Small Molecule Inhibitorsmentioning

confidence: 99%

Therapeutic strategies for targeting telomerase in cancer

Chen

Tang

Shi

et al. 2019

Medicinal Research Reviews

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Telomere and telomerase play important roles in abnormal cell proliferation, metastasis, stem cell maintenance, and immortalization in various cancers. Therefore, designing of drugs targeting telomerase and telomere is of great significance. Over the past two decades, considerable knowledge regarding telomere and telomerase has been accumulated, which provides theoretical support for the design of therapeutic strategies such as telomere elongation. Therefore, the development of telomere‐based therapies such as nucleoside analogs, non‐nucleoside small molecules, antisense technology, ribozymes, and dominant negative human telomerase reverse transcriptase are being prioritized for eradicating a majority of tumors. While the benefits of telomere‐based therapies are obvious, there is a need to address the limitations of various therapeutic strategies to improve the possibility of clinical applications. In this study, current knowledge of telomere and telomerase is discussed, and therapeutic strategies based on recent research are reviewed.

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A promising natural product, pristimerin, results in cytotoxicity against breast cancer stem cells in vitro and xenografts in vivo through apoptosis and an incomplete autopaghy in breast cancer

Cited by 67 publications

References 58 publications

Pristimerin Induces Autophagy‐Mediated Cell Death in K562 Cells through the ROS/JNK Signaling Pathway

Pristimerin Induces Autophagy‐Mediated Cell Death in K562 Cells through the ROS/JNK Signaling Pathway

Identification of a novel tumor angiogenesis inhibitor targeting Shh/Gli1 signaling pathway in Non-small cell lung cancer

Therapeutic strategies for targeting telomerase in cancer

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