Daurisoline Inhibiting Tumor Angiogenesis and Epithelial-Mesenchymal Transition in Bladder Cancer by Mediating HAKAI Protein Stability

Huang, Keming; Chen, Qingke; Deng, Ling; Qi, Zhang; Min, Sufang

doi:10.5812/ijpr-129798

Cited by 4 publications

(2 citation statements)

References 32 publications

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“…Daurisoline has been demonstrated in several trials to trigger cancer cell death in a variety of cancers, including esophageal squamous cell carcinoma (Wang et al, 2023), cervical HeLa (Wu et al, 2017), and bladder cancer (Huang et al, 2022). Solasodin is also reported to have anticancer effectiveness in several cancer cells such as colon, hepatocellular, lung, cervix, stomach, glioblastoma, and breast cancer (Dey et al, 2019).…”

Section: Molecular Dockingmentioning

confidence: 99%

The Potency of Alkaloid Derivates as Anti-Breast Cancer Candidates: In Silico Study

Renadi,

Pratita,

Mardianingrum

et al. 2023

Valensi

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Breast cancer is the most frequent malignancy in women worldwide. One of the target receptors for the treatment of breast cancer are estrogen, progesterone, and HER2 receptors. An alternative treatment using natural ingredients has been developed, one of which is alkaloid compounds. This study aims to determine the activity of alkaloid compounds as anti-breast cancer agents through an in-silico method. Virtual screening (AutoDock Vina), molecular docking (AutoDock Tools), molecular dynamics (Desmond), scanning Lipinski's rule of five, as well as pharmacokinetic and toxicity parameters, were performed. The results of virtual screening, molecular docking, and molecular dynamics show that the compounds daurisoline, solasodine, and sambutoxin have stable interactions with the HER2 receptor, with the lowest values of RMSD (Root Mean Square Deviation) and RMSF (Root Mean Square Fluctuation) compared to other compounds. Based on the results of the study conducted, it was shown that daurisoline, solasodine, and sambutoxin were predicted to be used as anti-HER2 candidates for the treatment of breast cancer.

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Section: Molecular Dockingmentioning

confidence: 99%

The Potency of Alkaloid Derivates as Anti-Breast Cancer Candidates: In Silico Study

Renadi,

Pratita,

Mardianingrum

et al. 2023

Valensi

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show abstract

“…Natural products or derivatives exhibit exciting potential as a new class of agents for the cancer treatment (Vuorelaa et al, 2004). Daurisoline (DS) is an isoquinoline alkaloid isolated from the traditional Chinese herbal Rhizoma Menispermi, which has a broad range of pharmacological effects, including inhibition of tumor angiogenesis and epithelial–mesenchymal transition, suppression of cell proliferation and vasculogenic mimicry formation, modulation of autophagy and repression of early afterdepolarizations (Huang et al, 2022; Liu et al, 2010, 2012; Xue & Liu, 2021; Yuan et al, 2022; Zhang et al, 2021). Despite the extensive research on the anticancer activity of DS has been carried out, much less is known about its role against breast cancer.…”

Section: Introductionmentioning

confidence: 99%

Daurisoline inhibits proliferation, induces apoptosis, and enhances TRAIL sensitivity of breast cancer cells by upregulating DR5

Liu,

Wang,

Duan

et al. 2024

Cell Biology International

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Daurisoline (DS) is an isoquinoline alkaloid that exerts anticancer activities in various cancer cells. However, the underlying mechanisms through which DS affects the survival of breast cancer cells remain poorly understood. Therefore, the present study was undertaken to investigate the potential anticancer effect of DS on breast cancer cells and reveal the mechanism underlying the enhanced tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL)‐mediated apoptosis by DS. Cell counting kit‐8 (CCK‐8) and 5‐ethynyl‐2‐deoxyuridine (EdU) assay were used to evaluate the ability of cell proliferation. Flow cytometry was selected to examine the cell cycle distribution. TUNEL assay was used to detect the cell apoptosis. The protein expression was measured by Western blot analysis. DS was found to reduce the cell viability and suppress the proliferation of MCF‐7 and MDA‐MB‐231 cells by causing G1 phase cell cycle arrest. DS could trigger apoptosis by promoting the cleavage of caspase‐8 and PARP. The phosphorylation of ERK, JNK, and p38MAPK was upregulated clearly following DS treatment. Notably, SP600125 (JNK inhibitor) pretreatment significantly abrogated DS‐induced PARP cleavage. DS inactivated Akt/mTOR and Wnt/β‐catenin signaling pathway and upregulated the expression of ER stress‐related proteins. Additionally, DS amplified TRAIL‐caused viability reduction and apoptosis in breast cancer cells. Mechanismly, DS upregulated the protein level of DR4 and DR5, and knockdown of DR5 attenuated the cotreatment‐induced cleavage of PARP. Inhibition of JNK could block DS‐induced upregulation of DR5. This study provides valuable insights into the mechanisms of DS inhibiting cell proliferation, triggering apoptosis, and enhancing TRAIL sensitivity of breast cancer cells.

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Daurisoline suppress glioma progression by inhibiting autophagy through PI3K/AKT/mTOR pathway and increases TMZ sensitivity

Yin,

Hui-Lu,

Yang

et al. 2024

Biochemical Pharmacology

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Daurisoline Inhibiting Tumor Angiogenesis and Epithelial-Mesenchymal Transition in Bladder Cancer by Mediating HAKAI Protein Stability

Cited by 4 publications

References 32 publications

The Potency of Alkaloid Derivates as Anti-Breast Cancer Candidates: In Silico Study

The Potency of Alkaloid Derivates as Anti-Breast Cancer Candidates: In Silico Study

Daurisoline inhibits proliferation, induces apoptosis, and enhances TRAIL sensitivity of breast cancer cells by upregulating DR5

Daurisoline suppress glioma progression by inhibiting autophagy through PI3K/AKT/mTOR pathway and increases TMZ sensitivity

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