WZB117 Decorated Metformin-Carboxymethyl Chitosan Nanoparticles for Targeting Breast Cancer Metabolism

De, Anindita; Wadhwani, Ashish; Sauraj, .; Roychowdhury, Parikshit; Kang, Ji Hee; Ko, Young Tag; Kuppusamy, Gowthamarajan

doi:10.3390/polym15040976

Cited by 12 publications

(7 citation statements)

References 54 publications

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“…Metformin improves hepatic insulin sensitivity and is therefore recommended in the treatment of polycystic ovary syndrome in obese patients with insulin resistance [ 14 ]. Some researchers reported the potential anticancer activity of metformin against breast cancer [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Formulation and Evaluation of Xanthan Gum Microspheres for the Sustained Release of Metformin Hydrochloride

et al. 2023

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This work aimed to formulate xanthan gum microspheres for the encapsulation of metformin hydrochloride, according to the process of ionotropic gelation. The obtained microparticles, based on various fractions of xanthan gum (0.5–1.25), were subjected to different physico-chemical tests and a drug release study. Microspheres with an average size varying between 110.96 μm and 208.27 μm were obtained. Encapsulation efficiency reached 93.11% at a 1.25% biopolymer concentration. The swelling study showed a swelling rate reaching 29.8% in the gastric medium (pH 1.2) and 360% in the intestinal medium (pH 6.8). The drug release studies showed complete metformin hydrochloride release from the beads, especially those prepared from xanthan gum at the concentration of 1.25%, in intestinal medium at 90.00% after 6 h. However, limited and insignificant drug release was observed within the gastric medium (32.50%). The dissolution profiles showed sustained release kinetics.

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Section: Introductionmentioning

confidence: 99%

Formulation and Evaluation of Xanthan Gum Microspheres for the Sustained Release of Metformin Hydrochloride

et al. 2023

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“…Some studies have unveiled that metformin can affect cancer progression through the AMPK and JNK signalling pathways. 21 , 22 Thus, western blots were utilized to evaluate the effects of low-dose metformin on the expression levels of AMPK and JNK pathways in HCC cells. The results uncovered that low-dose metformin dose-dependently promoted phosphorylated AMPK (p-AMPK) expression and inhibited phosphorylated JNK (p-JNK) expression, but the levels of total AMPK and JNK weren’t changed ( Figure 4(c) ).…”

Section: Resultsmentioning

confidence: 99%

Low-dose metformin suppresses hepatocellular carcinoma metastasis via the AMPK/JNK/IL-8 pathway

Zhao,

Zheng,

et al. 2024

Int J Immunopathol Pharmacol

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Background and objectives Metformin, an oral hypoglycemic drug, has been suggested to possess antitumour activity in several types of cancers. Additionally, interleukin-8 (IL-8) has been reported to be involved in the development and metastasis of many cancers. However, the effect of metformin on IL-8 expression in hepatocellular carcinoma (HCC) remains unclear. Therefore, this study aimed to investigate whether metformin could inhibit IL-8 expression to exert an inhibitory effect on HCC progression. Materials and methods The IL-8 levels were measured in the plasma of 159 HCC patients (86 men, 73 women; average age 56 years) and in the culture supernatant of HCC cells (Hep3B and HuH7) using flow cytometry. In addition, the protein expression levels of IL-8 were also validated by the Human Protein Atlas (HPA) database. The prognostic value of IL-8 was evaluated using the Kaplan–Meier Plotter database. The association between IL-8 expression and immune checkpoints was estimated using the TIMER and The Cancer Genome Atlas (TCGA) databases. What’s more, bioinformatics analysis, western blotting, and transwell assays were conducted to illustrate the molecular mechanism of metformin (≤1 mM) on IL-8 in HCC. Results IL-8 expression was found to be increased in the plasma of HCC patients, which is consistent with the expression of IL-8 in HCC cells and tissues. High expression of IL-8 was significantly related to poor prognosis. In addition, IL-8 was positively correlated with immune checkpoints in HCC. Notably, we found that low-dose metformin could inhibit the secretion of IL-8 by HCC cells and the migration of HCC cells. Mechanistically, low-dose metformin significantly suppresses HCC metastasis mainly through the AMPK/JNK/IL-8/MMP9 pathway. Conclusion The results indicate that low-dose metformin can inhibit HCC metastasis by suppressing IL-8 expression. Targeting the AMPK/JNK/IL-8 axis may be a promising treatment strategy for patients with HCC metastasis.

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“…Several studies have been administrated by combining glycolytic reprogramming strategies with chemotherapy and photothermal therapy (PTT), , which significantly reduced the chemotherapy and radiotherapy resistance of tumors, enhancing the therapeutic effect of doxorubicin and PTT. In addition, De et al coupled the GLUT1 inhibitor WZB117 to OCMC (O-carboxymethyl chitosan)-MET nanopolymers to obtain the conjugated polymer nanoparticle WZB117-OCMC-MET, reprogramming tumor metabolism by dual-targeting GLUT1 and mTOR pathways, thereby improving the therapeutic effect. Furthermore, Wu et al designed dual gate-controlled “nano-enabled energy interrupter” HZ@GD nanoparticles .…”

Section: Nanodelivery Systems Based On Glucose Metabolism Reprogrammi...mentioning

confidence: 99%

Advances in Nanodelivery Systems Based on Metabolism Reprogramming Strategies for Enhanced Tumor Therapy

Zhang,

Liang,

Yang

et al. 2024

ACS Appl. Mater. Interfaces

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Tumor development and metastasis are closely related to the complexity of the metabolism network. Recently, metabolism reprogramming strategies have attracted much attention in tumor metabolism therapy. Although there is preliminary success of metabolism therapy agents, their therapeutic effects have been restricted by the effective reaching of the tumor sites of drugs. Nanodelivery systems with unique physical properties and elaborate designs can specifically deliver to the tumors. In this review, we first summarize the research progress of nanodelivery systems based on tumor metabolism reprogramming strategies to enhance therapies by depleting glucose, inhibiting glycolysis, depleting lactic acid, inhibiting lipid metabolism, depleting glutamine and glutathione, and disrupting metal metabolisms combined with other therapies, including chemotherapy, radiotherapy, photodynamic therapy, etc. We further discuss in detail the advantages of nanodelivery systems based on tumor metabolism reprogramming strategies for tumor therapy. As well as the opportunities and challenges for integrating nanodelivery systems into tumor metabolism therapy, we analyze the outlook for these emerging areas. This review is expected to improve our understanding of modulating tumor metabolisms for enhanced therapy.

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WZB117 Decorated Metformin-Carboxymethyl Chitosan Nanoparticles for Targeting Breast Cancer Metabolism

Cited by 12 publications

References 54 publications

Formulation and Evaluation of Xanthan Gum Microspheres for the Sustained Release of Metformin Hydrochloride

Formulation and Evaluation of Xanthan Gum Microspheres for the Sustained Release of Metformin Hydrochloride

Low-dose metformin suppresses hepatocellular carcinoma metastasis via the AMPK/JNK/IL-8 pathway

Advances in Nanodelivery Systems Based on Metabolism Reprogramming Strategies for Enhanced Tumor Therapy

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