Endothelial cell autophagy in homeostasis and cancer

Verhoeven, Jelle; Baelen, Jef; Agrawal, Manju; Agostinis, Patrizia

doi:10.1002/1873-3468.14087

Cited by 8 publications

(7 citation statements)

References 110 publications

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“…21 The development of selective autophagy modulating drugs could be a useful therapeutic objective to improve therapeutic responses in cancer. 22 In this experiment, we found that Eleutheroside B can trigger the autophagy through regulating the expression of LC3 and p62 in SMMC-7721cells and HeLa cells.…”

Section: Discussionmentioning

confidence: 64%

Mitochondrial dysfunction is involved in the cellular activity inhibition by eleutheroside B in SMMC-7721 and HeLa cells

Sun

Zhang²,

et al. 2022

Hum Exp Toxicol

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Eleutheroside B, also known as syringin, has been shown to have various pharmacological activities such as anti-inflammatory, anti-irradiation and antidepressant, but there are few studies on its anti-cancer activity. Its anti-tumor effect on SMMC-7721 cells has not been revealed. Moreover, whether it induces autophagy is still unclear. Thus, the present study investigated whether Eleutheroside B induces apoptosis, autophagy and cellular motility in SMMC-7721 cells and HeLa cells, and explored the underlying molecular mechanisms. SMMC-7721 cells and HeLa cells treated with Eleutheroside B and cell viability measured by MTT assay and trypan blue dye exclusion assay. Apoptosis checked by flow cytometry combined, fluorescent staining. Apoptotic signal proteins and autophagy proteins were checked by Western blot. This study showed that Eleutheroside B inhibited the cell proliferation and blocked cell cycle, migration and invasion as well. Moreover, Eleutheroside B induced apoptosis in SMMC-7721 cells and HeLa cells. It upregulated Bax expression, while simultaneously decreasing Bcl-2 expression. Further elucidation of the mechanism revealed that Eleutheroside B induced mitochondrial dysfunction, with mitochondrial membrane potential collapse and cytochrome c release, suggesting that Eleutheroside B induced apoptosis by triggering mitochondrial pathway. Most importantly, Eleutheroside B could induce autophagy in SMMC-7721 cells and HeLa cells. Taken together, these results suggested Eleutheroside B is a potential therapeutic candidate for HCC and Human cervical cancer.

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Section: Discussionmentioning

confidence: 64%

Mitochondrial dysfunction is involved in the cellular activity inhibition by eleutheroside B in SMMC-7721 and HeLa cells

Sun

Zhang²,

et al. 2022

Hum Exp Toxicol

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“…68 Studies have shown that EC autophagy regulates the interaction between ECs and neutrophils under cellular stress conditions such as hypoxia, infection and trauma. 69 This result was further confirmed by a study by Natalia Reglero-Real et al 70 The researchers found that autophagy at the EC junctions in microvessels and venules was enhanced in IR/LPSstimulated wild-type mice, while autophagy at the EC junction was decreased in ATG5-deficient mice, and transendothelial cell migration (TEM) of PMNs was significantly increased. After the administration of an autophagy-inducing peptide (Tat-beclin-1/Tat-BECN1), autophagy was further increased in wild-type mice, and TEM was significantly inhibited, indicating that autophagy was involved in regulating TEM and tissue infiltration by modulating EC junctions.…”

Section: Autophagy and Endothelial Injury Autophagy And Neutrophil Tr...mentioning

confidence: 65%

Research Progress on Autophagy Regulation by Active Ingredients of Traditional Chinese Medicine in the Treatment of Acute Lung Injury

Dong¹,

Yin²,

Hao³

et al. 2023

JIR

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Autophagy is a highly conserved process that maintains cell stability in eukaryotes, participates in the turnover of intracellular substances to maintain cell function, helps to resist pathogen invasion, and improves cell tolerance to environmental changes. Autophagy has been observed in many diseases, and the symptoms of these diseases are significantly improved by regulating autophagy. Autophagy is also involved in the development of lung diseases. Studies have shown that autophagy may play a beneficial or harmful role in acute lung injury (ALI), and ALI has been treated with traditional Chinese medicine designed to promote or inhibit autophagy. In this paper, the molecular mechanism and common pathways regulating autophagy and the relationship between autophagy and ALI are introduced, and the active ingredients of traditional Chinese medicine that improve ALI symptoms by regulating autophagy are summarized.

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“…an amplified pro-inflammatory phenotype, characterized by an increased expression of inflammatory cytokines (Tellier et al, 2015). In the microenvironment of solid tumors, hypoxia has been shown to stimulate autophagy in tumor-associated blood vessels which in turn can alter metabolic pathways and surface markers of endothelial cells (Verhoeven et al, 2021). Additionally, hypoxic cancer-associated fibroblasts induced blood vessel abnormalities by altering the secretion of various pro-and anti-angiogenic factors leading to changes in endothelial cell function and promoting angiogenesis (Kugeratski et al, 2019).…”

Section: Tumor Vasculaturementioning

confidence: 99%

Targeting Angiogenesis in Breast Cancer: Current Evidence and Future Perspectives of Novel Anti-Angiogenic Approaches

et al. 2022

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Angiogenesis is a vital process for the growth and dissemination of solid cancers. Numerous molecular pathways are known to drive angiogenic switch in cancer cells promoting the growth of new blood vessels and increased incidence of distant metastasis. Several angiogenesis inhibitors are clinically available for the treatment of different types of advanced solid cancers. These inhibitors mostly belong to monoclonal antibodies or small-molecule tyrosine kinase inhibitors targeting the classical vascular endothelial growth factor (VEGF) and its receptors. Nevertheless, breast cancer is one example of solid tumors that had constantly failed to respond to angiogenesis inhibitors in terms of improved survival outcomes of patients. Accordingly, it is of paramount importance to assess the molecular mechanisms driving angiogenic signaling in breast cancer to explore suitable drug targets that can be further investigated in preclinical and clinical settings. This review summarizes the current evidence for the effect of clinically available anti-angiogenic drugs in breast cancer treatment. Further, major mechanisms associated with intrinsic or acquired resistance to anti-VEGF therapy are discussed. The review also describes evidence from preclinical and clinical studies on targeting novel non-VEGF angiogenic pathways in breast cancer and several approaches to the normalization of tumor vasculature by targeting pericytes, utilization of microRNAs and extracellular tumor-associate vesicles, using immunotherapeutic drugs, and nanotechnology.

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Endothelial cell autophagy in homeostasis and cancer

Cited by 8 publications

References 110 publications

Mitochondrial dysfunction is involved in the cellular activity inhibition by eleutheroside B in SMMC-7721 and HeLa cells

Mitochondrial dysfunction is involved in the cellular activity inhibition by eleutheroside B in SMMC-7721 and HeLa cells

Research Progress on Autophagy Regulation by Active Ingredients of Traditional Chinese Medicine in the Treatment of Acute Lung Injury

Targeting Angiogenesis in Breast Cancer: Current Evidence and Future Perspectives of Novel Anti-Angiogenic Approaches

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