The effects and mechanisms of aloe‐emodin on reversing adriamycin‐induced resistance of <scp>MCF</scp>‐7/<scp>ADR</scp> cells

Cheng, Guorong; Pi, Zifeng; Zhuang, Xiaoyu; Zheng, Zhong; Liu, Shu; Liu, Zhiqiang; Song, Fengrui

doi:10.1002/ptr.7096

Cited by 14 publications

(15 citation statements)

References 38 publications

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“…Emodin plays an important role in inducing cell cycle arrest in a variety of cancer cells. Cheng et al reported that aloe-emodin can strengthen the sensitivity of adriamycin to breast cancer cell by inhibiting G2/M phase, inducing apoptosis through DNA damage, ROS accumulation, and caspase-3 activation [ 29 ]. Dong et al found that emodin exerts inhibitory effects on the proliferation of HCC cells through restraint of S and G2/M phases [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Emodin inhibits invasion and migration of hepatocellular carcinoma cells via regulating autophagy-mediated degradation of snail and β-catenin

Qin

Zeng

et al. 2022

BMC Cancer

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Background Previous studies reported that emodin extracted from Rheum palmatum L. exerts antiproliferation and antimetastatic effects in a variety of human cancer types. However, the role of emodin in hepatocellular carcinoma (HCC) remain unknown. Methods EdU and colony formation assays were performed to evaluate the effects of emodin on proliferation. The mobility capacities of HCC treated with emodin were evaluated using wound healing assay. Transwell invasion and migration assays were performed to evaluate anti-migratory and anti-invasive effects of emodin on HCC. Annexin V-FITC/PI was performed to analyze the apoptosis. PI stain was performed to analyze cell cycle. RNA sequencing technology was used to identify the differentially expressed genes (DEGs) induced by emodin in HCC. The impact of emodin on autophagic flux in HepG2 cells was examined by mCherry-GFP-LC3 analysis. Western blot was used to assess the protein expressions of epithelial-mesenchymal transition (EMT), autophagy, PI3K/AKT/mTOR and Wnt/β-catenin signaling pathway. Results We found that emodin inhibited the growth of HepG2 cells in a dose- and time-dependent manner. In addition, emodin inhibited cell proliferation, induced S and G2/M phases arrest, and promoted apoptosis in HepG2 cells. The migration and invasion of HepG2 cells were also suppressed by emodin. Enrichment analysis revealed that DEGs involved in cell adhesion, cancer metastasis and cell cycle arrest. Moreover, western bolt results show that emodin-induced autophagy promotes Snail and β-catenin degradation. We also found that blocking autophagic flux after emodin treatment caused EMT reversal. Furthermore, the PI3K agonist Y-P 740 significantly reversed the phosphorylation levels of GSK3β and mTOR. These results indicated that emodin induced autophagy and inhibited the EMT in part through suppression of the PI3K/AKT/mTOR and Wnt/β-catenin pathways. Conclusion Our study indicated that emodin inhibited cell metastasis in HCC via the crosstalk between autophagy and EMT.

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Section: Discussionmentioning

confidence: 99%

Emodin inhibits invasion and migration of hepatocellular carcinoma cells via regulating autophagy-mediated degradation of snail and β-catenin

Qin

Zeng

et al. 2022

BMC Cancer

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“…Cheng et al. presented that AE sensitized tumor cells to chemotherapeutic agents, indicating the potential of AE for improving drug resistance ( 18 ). In this study, AE could improve the drug resistance of PC9-GR cells and xenograft models.…”

Section: Discussionmentioning

confidence: 99%

“…Dou et al reported that AE could alleviate renal fibrosis by repressing PI3K/Akt/mTOR signaling pathway both in vivo and in vitro ( 17 ). Additionally, it has been demonstrated that AE could mitigate drug resistance of breast cancer cells and melanoma cells, indicating a regulatory role of AE in drug resistance ( 18 , 19 ). Nonetheless, effects of AE on drug resistance of NSCLCs have not been fully explored.…”

Section: Introductionmentioning

confidence: 99%

Sensitization of Non-Small Cell Lung Cancer Cells to Gefitinib and Reversal of Epithelial–Mesenchymal Transition by Aloe-Emodin Via PI3K/Akt/TWIS1 Signal Blockage

et al. 2022

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ObjectiveTo explore the impacts of AE (aloe-emodin) in gefitinib-resistant NSCLC (non-small cell lung cancer) cells and the corresponding mechanism.MethodsPC9 and PC9-GR cells were cultured and treated by gefitinib, AE, or the combination of the two drugs. Then, viability, apoptosis, migration and invasion of cells were investigated using CCK-8, TUNEL, wound healing assay, and transwell assay, respectively. Female BALB/c nude mice were employed for the establishment of xenograft tumor models to examine the role of AE in tumor growth.ResultsPC9-GR cells showed reduced apoptosis and enhanced cell viability, migration and invasion upon treatment by gefitinib, compared with PC9 cells. E-cahherin in PC9-GR cells was down-regulated, while Vimentin, Snail2 (or Slug) and Twist1 in PC9-GR cells were up-regulated, compared with PC9 cells. Meanwhile, treatment by a combination of gefitinib and AE significantly strengthened apoptosis of PC9-GR cells, while attenuated their migration and invasion, compared with the control group or treatment by gefitinib or AE alone. WB results showed that AE could reverse EMT and activation of PI3K/AKT signalling pathway in PC9-GR cells. In vivo experiments showed that tumor growth and EMT of PC9-GR cells were dramatically repressed after treatment by a combination of AE and gefitinib. Additionally, the use of SC97 (a PI3K/Akt pathway activator) could counteract the effects of AE in gefitinib-resistant PC9 cells.ConclusionsAE could enhance the gefitinib sensitivity of PC9-GR cells and reverse EMT by blocking PI3K/Akt/TWIS1 signal pathway.

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“…Interestingly, Cheng et al found that AE also enhanced protective autophagy in reversing ADM-induced drug resistance. By supplementing AE with autophagy inhibitors, anti-tumor activity and sensibility may be enhanced (in vitro: MCF-7/ADR cell line, 20 μM, 48 h) [ 109 ].…”

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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The effects and mechanisms of aloe‐emodin on reversing adriamycin‐induced resistance of MCF‐7/ADR cells

Cited by 14 publications

References 38 publications

Emodin inhibits invasion and migration of hepatocellular carcinoma cells via regulating autophagy-mediated degradation of snail and β-catenin

Emodin inhibits invasion and migration of hepatocellular carcinoma cells via regulating autophagy-mediated degradation of snail and β-catenin

Sensitization of Non-Small Cell Lung Cancer Cells to Gefitinib and Reversal of Epithelial–Mesenchymal Transition by Aloe-Emodin Via PI3K/Akt/TWIS1 Signal Blockage

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

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