The effects and mechanisms of isoliquiritigenin loaded nanoliposomes regulated AMPK/mTOR mediated glycolysis in colorectal cancer

Wang, Gang; Yu, Yinhua; Wang, Yuzhu; Yin, Peihao; Xu, Kecheng; Zhang, Heng

doi:10.1080/21691401.2020.1825092

Cited by 19 publications

(13 citation statements)

References 63 publications

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“…In our study, we found that ENO1 silencing inhibited the migration and invasion of ESCC. Some studies have reported that the possible mechanisms involved in ENO1 induced metastasis include the P13K/AKT pathway and its downstream signals 24 (including glycolysis, cell cycle progression and epithelial-mesenchymal transition related genes). Our bioinformatics results showed that ENO1 was involved in the Wnt signaling pathway in ESCC.…”

Section: Discussionmentioning

confidence: 99%

Relationship between ENO1 and Metastasis Risk and Prognosis in Esophageal squamous cell carcinoma

Bai

Xiang

Tian

et al. 2022

Preprint

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Objective Esophageal cancer (EC), a common gastrointestinal malignancy, ranks as the sixth leading cause of cancer death worldwide. Esophageal squamous cell carcinoma (ESCC) is the predominant histological subtype of EC. Lack of potential biomarkers for treatment and prognosis is a limitation for early diagnosis and treatment of ESCC. Methods Based on The Cancer Genome Atlas (TCGA) database, the weighted gene co-expression network analysis (WGCNA) was constructed to identify gene modules associated with the metastasis in ESCC. The LASSO algorithm was used to construct a prognosis genes model. After the collinearity test, all independent prognostic parameters and important clinical parameters were included in the prognostic nomogram constructed by the Cox regression model. The nomogram was used to evaluate the prognostic significance of these parameters in ESCC. Finally, we used biological experiments to preliminary investigate the impact of ENO1 on the metastasis risk of ESCC. Results A total of 16 genetic modules were identified, and the brown module is considered the most relevant to tumor metastasis. (P = 0.02, R2 = 0.30). Protein-protein interaction (PPI) network was performed to identify the hub nodes in the brown module. The univariate and multivariate Cox regression analysis indicated that ENO1 and SUPT5H were independent prognostic factors. Expression data of ENO1 was pipelined along with patients’ clinic pathological data for nomogram construction 1-, and 2-OS forecasting. ENO1 gene was regarded as "real" hub genes for cancer metastasis risk. Low-expressed ENO1 inhibited migration and invasion of human ESCC cells in vitro. The mechanism may involve the Wnt signaling pathway and the influence of EMT. Conclusion ENO1 might be a novel metastasis risk biomarker for ESCC.

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Section: Discussionmentioning

confidence: 99%

Relationship between ENO1 and Metastasis Risk and Prognosis in Esophageal squamous cell carcinoma

Bai

Xiang

Tian

et al. 2022

Preprint

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“…A combination of ISL and docosahexaenoic acid induces apoptosis in colorectal cancer via enhancing ROS levels and mediating phosphorylation of JNK and ERK [ 181 ]. The ISL-loaded liposomes suppress colorectal tumor progression via inhibiting AMPK-mediated glycolysis [ 182 ]. This section focuses on anti-tumor activity of ISL via targeting CSCs.…”

Section: Dietary Agents and Cancer Stem Cellsmentioning

confidence: 99%

Targeting Cancer Stem Cells by Dietary Agents: An Important Therapeutic Strategy against Human Malignancies

Paskeh

Asadi²,

Zabolian

et al. 2021

IJMS

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As a multifactorial disease, treatment of cancer depends on understanding unique mechanisms involved in its progression. The cancer stem cells (CSCs) are responsible for tumor stemness and by enhancing colony formation, proliferation as well as metastasis, and these cells can also mediate resistance to therapy. Furthermore, the presence of CSCs leads to cancer recurrence and therefore their complete eradication can have immense therapeutic benefits. The present review focuses on targeting CSCs by natural products in cancer therapy. The growth and colony formation capacities of CSCs have been reported can be attenuated by the dietary agents. These compounds can induce apoptosis in CSCs and reduce tumor migration and invasion via EMT inhibition. A variety of molecular pathways including STAT3, Wnt/β-catenin, Sonic Hedgehog, Gli1 and NF-κB undergo down-regulation by dietary agents in suppressing CSC features. Upon exposure to natural agents, a significant decrease occurs in levels of CSC markers including CD44, CD133, ALDH1, Oct4 and Nanog to impair cancer stemness. Furthermore, CSC suppression by dietary agents can enhance sensitivity of tumors to chemotherapy and radiotherapy. In addition to in vitro studies, as well as experiments on the different preclinical models have shown capacity of natural products in suppressing cancer stemness. Furthermore, use of nanostructures for improving therapeutic impact of dietary agents is recommended to rapidly translate preclinical findings for clinical use.

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“…The release of the drug paclitaxel was possible only under conditions similar to the TME, e.g., acid pH and overexpressed hyaluronic acid [165]. A third example are nanoliposomes loaded with isoliquiritigenin to affect AMPK/mTOR mediated glycolysis in colorectal cancer [166].…”

Section: Strategies For Intervention With the Tmementioning

confidence: 99%

Mitochondria at Work: New Insights into Regulation and Dysregulation of Cellular Energy Supply and Metabolism

Schirrmacher¹

2020

Biomedicines

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Mitochondria are of great relevance to health, and their dysregulation is associated with major chronic diseases. Research on mitochondria—156 brand new publications from 2019 and 2020—have contributed to this review. Mitochondria have been fundamental for the evolution of complex organisms. As important and semi-autonomous organelles in cells, they can adapt their function to the needs of the respective organ. They can program their function to energy supply (e.g., to keep heart muscle cells going, life-long) or to metabolism (e.g., to support hepatocytes and liver function). The capacity of mitochondria to re-program between different options is important for all cell types that are capable of changing between a resting state and cell proliferation, such as stem cells and immune cells. Major chronic diseases are characterized by mitochondrial dysregulation. This will be exemplified by cardiovascular diseases, metabolic syndrome, neurodegenerative diseases, immune system disorders, and cancer. New strategies for intervention in chronic diseases will be presented. The tumor microenvironment can be considered a battlefield between cancer and immune defense, competing for energy supply and metabolism. Cancer cachexia is considered as a final stage of cancer progression. Nevertheless, the review will present an example of complete remission of cachexia via immune cell transfer. These findings should encourage studies along the lines of mitochondria, energy supply, and metabolism.

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The effects and mechanisms of isoliquiritigenin loaded nanoliposomes regulated AMPK/mTOR mediated glycolysis in colorectal cancer

Cited by 19 publications

References 63 publications

Relationship between ENO1 and Metastasis Risk and Prognosis in Esophageal squamous cell carcinoma

Relationship between ENO1 and Metastasis Risk and Prognosis in Esophageal squamous cell carcinoma

Targeting Cancer Stem Cells by Dietary Agents: An Important Therapeutic Strategy against Human Malignancies

Mitochondria at Work: New Insights into Regulation and Dysregulation of Cellular Energy Supply and Metabolism

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