Formation and evaluation of doxorubicin and cromoglycate metal–organic framework for anti-cancer activity DOI

Ebaa Abu Saleem,

Zainab Lafi, Naeem Shalan

et al.

Nanomedicine, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 13

Published: Jan. 31, 2025

We develop and evaluate copper-based metal-organic frameworks (Cu-MOFs) incorporating cromolyn as a linker to enhance structural stability, drug delivery efficiency, therapeutic potential, particularly for breast cancer treatment. Two Cu-MOF formulations were synthesized: Cu-MOFs-BDC-DOX (using terephthalic acid) Cu-MOFs-CROMO-DOX linker). Characterization was performed using SEM/TEM morphology, FTIR, XRD, TGA confirm integrity. Drug encapsulation efficiency release profiles assessed, followed by in vitro cytotoxicity, cell migration, colony formation assays MDA-MB-231 cells. Both demonstrated high (83-91%) sustained over 48 h at pH 7.4. exhibited superior cytotoxicity with an IC50 of 0.88 ± 0.07 µM compared 7.1 0.11 Cu-MOFs-BDC-DOX. inhibit migration dose-dependent manner. The formulation enhanced outperforming its counterpart targeting This study highlights the promise MOF-based nanocarriers overcoming limitations conventional chemotherapy, offering pathway more effective targeted treatments reduced side effects.

Language: Английский

Semaglutide attenuates doxorubicin-induced cardiotoxicity by ameliorating BNIP3-Mediated mitochondrial dysfunction DOI Creative Commons
Xiaoping Li, Wenbin Luo,

Yang Tang

et al.

Redox Biology, Journal Year: 2024, Volume and Issue: 72, P. 103129 - 103129

Published: March 19, 2024

Doxorubicin is a powerful chemotherapeutic agent for cancer, whose use limited due to its potential cardiotoxicity. Semaglutide (SEMA), novel analog of glucagon-like peptide-1 (GLP-1), has received widespread attention the treatment diabetes. However, increasing evidence highlighted therapeutic benefits on cardiac function. Therefore, objective this study was examine efficacy semaglutide in ameliorating doxorubicin-induced

Language: Английский

Citations

16

Drug resistance mechanisms and treatment strategies mediated by Ubiquitin-Specific Proteases (USPs) in cancers: new directions and therapeutic options DOI Creative Commons
Hongli Gao, Zhuo Xi, Jingwei Dai

et al.

Molecular Cancer, Journal Year: 2024, Volume and Issue: 23(1)

Published: May 3, 2024

Abstract Drug resistance represents a significant obstacle in cancer treatment, underscoring the need for discovery of novel therapeutic targets. Ubiquitin-specific proteases (USPs), subclass deubiquitinating enzymes, play pivotal role protein deubiquitination. As scientific research advances, USPs have been recognized as key regulators drug across spectrum treatment modalities, including chemotherapy, targeted therapy, immunotherapy, and radiotherapy. This comprehensive review examines complex relationship between mechanisms, focusing on specific strategies highlighting influence DNA damage repair, apoptosis, characteristics stem cells, immune evasion, other crucial biological functions. Additionally, highlights potential clinical significance USP inhibitors means to counter treatment. By inhibiting particular USP, cells can become more susceptible variety anti-cancer drugs. The integration with current therapies offers promising strategy circumvent resistance. Therefore, this emphasizes importance viable targets insight into fruitful directions future development. Targeting presents an effective method combat various types, leading enhanced better patient outcomes.

Language: Английский

Citations

16

Rnd3 protects against doxorubicin-induced cardiotoxicity through inhibition of PANoptosis in a Rock1/Drp1/mitochondrial fission-dependent manner DOI Creative Commons
Ge Wen, Xiaohua Zhang,

Jie Lin

et al.

Cell Death and Disease, Journal Year: 2025, Volume and Issue: 16(1)

Published: Jan. 4, 2025

Abstract Doxorubicin, a representative drug of the anthracycline class, is widely used in cancer treatment. However, Doxorubicin-induced cardiotoxicity (DIC) presents significant challenge its clinical application. Mitochondrial dysfunction plays central role DIC, primarily through disrupting mitochondrial dynamics. This study aimed to investigate impact Rnd3 (a Rho family GTPase 3) on with focus Cardiomyocyte-specific transgenic mice (Rnd3-Tg) and LSP/LSP (N-Tg) were established for vivo experiments, adenoviruses harboring (Ad-Rnd3) or negative control (Ad-Control) injected myocardium vitro experiments. The DIC model was using wild-type, N-Tg, Rnd3-Tg mice, subsequent intraperitoneal injection Dox 4 weeks. molecular mechanism explored RNA sequencing, immunofluorescence staining, co-immunoprecipitation assay, protein-protein docking. administration induced injury cardiac dysfunction, which ameliorated by overexpression. Further, augmentation expression mitigated fragmentation mediated dynamin-related protein 1 (Drp1), thereby ameliorating PANoptosis (pyroptosis, apoptosis, necroptosis) response Dox. Mechanically, interaction between Rho-associated kinase (Rock1) may impede Rock1-induced Drp1 phosphorylation at Ser616, thus inhibiting fission dysfunction. Interestingly, Rock1 knockdown nullified effects cardiomyocytes PANoptosis, as well Dox-induced remodeling elicited Rnd3. enhances resilience against stabilizing dynamics reducing PANoptosis. Our findings suggest that Rnd3/Rock1/Drp1 signaling pathway represents novel target mitigating modulating could be strategic approach safeguarding function patients undergoing

Language: Английский

Citations

2

Chloroquine and Chemotherapeutic Compounds in Experimental Cancer Treatment DOI Open Access
Natalia I. Agalakova

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(2), P. 945 - 945

Published: Jan. 12, 2024

Chloroquine (CQ) and its derivate hydroxychloroquine (HCQ), the compounds with recognized ability to suppress autophagy, have been tested in experimental works clinical trials as adjuvant therapy for treatment of tumors different origin increase efficacy cytotoxic agents. Such a strategy can be effective overcoming resistance cancer cells standard chemotherapy or anti-angiogenic therapy. This review presents results combined application CQ/HCQ conventional drugs (doxorubicin, paclitaxel, platinum-based compounds, gemcitabine, tyrosine kinases PI3K/Akt/mTOR inhibitors, other agents) malignancies obtained experiments on cultured cells, animal xenografts models, few trials. The effects such an approach viability tumor growth, well autophagy-dependent -independent molecular mechanisms underlying cellular responses CQ/HCQ, are summarized. Although majority vitro vivo studies shown that effectively sensitize agents potential chemotherapy, often inconsistent. Nevertheless, pharmacological suppression autophagy remains promising tool increasing development more specific inhibitors is required.

Language: Английский

Citations

13

Baicalin-peptide supramolecular self-assembled nanofibers effectively inhibit ferroptosis and attenuate doxorubicin-induced cardiotoxicity DOI
Yinghua Zeng, Xu Liao, Yuting Guo

et al.

Journal of Controlled Release, Journal Year: 2024, Volume and Issue: 366, P. 838 - 848

Published: Feb. 1, 2024

Language: Английский

Citations

11

A comprehensive review on doxorubicin: mechanisms, toxicity, clinical trials, combination therapies and nanoformulations in breast cancer DOI

Anjali Bisht,

Dubey Avinash,

Kantrol Kumar Sahu

et al.

Drug Delivery and Translational Research, Journal Year: 2024, Volume and Issue: unknown

Published: June 17, 2024

Language: Английский

Citations

9

A Targeted and Responsive Nanoprodrug Delivery System for Synergistic Glioma Chemotherapy DOI

Weiling Zhuo,

Wanyu Wang, Wenjie Zhou

et al.

Small, Journal Year: 2024, Volume and Issue: 20(30)

Published: March 3, 2024

Abstract Doxorubicin (DOX) is widely used as a chemotherapeutic agent for both hematologic and solid tumors reasonable candidate glioma treatment. However, its effectiveness hindered by significant toxicity drug resistance. Moreover, the presence of blood–brain barrier (BBB) brings crucial challenge to therapy. In response, GSH‐responsive actively targeted nanoprodrug delivery system (cRGD/PSDOX‐Cur@NPs) are developed. this system, disulfide bond‐bridged DOX prodrug (PEG‐SS‐DOX) designed release specifically in high glutathione (GSH) tumor environment, markedly reducing cardiotoxicity associated with DOX. To further address resistance, curcumin, serving P‐glycoprotein (P‐gp) inhibitor, effectively increased cellular concentration. Consequently, cRGD/PSDOX‐Cur@NPs exhibited synergistic anti‐tumor effects vitro. Furthermore, vivo experiments validated superior BBB penetration brain‐targeting abilities cRGD/PSDOX‐Cur@NPs, showcasing remarkable potential treating subcutaneous orthotopic gliomas. This research underscores that presents novel approach inhibiting while addressing resistance systemic toxicity.

Language: Английский

Citations

8

Combating cisplatin-resistant lung cancer using a coiled-coil lipopeptides modified membrane fused drug delivery system DOI
Xi Wang,

Guiquan Liu,

Xueyu Pu

et al.

Journal of Controlled Release, Journal Year: 2025, Volume and Issue: 379, P. 45 - 58

Published: Jan. 8, 2025

Language: Английский

Citations

1

Cannabidiol Ameliorates Doxorubicin-Induced Myocardial Injury via Activating Hippo Pathway DOI Creative Commons

Tianwei Dong,

Jinlian Li,

Xinfang Liang

et al.

Drug Design Development and Therapy, Journal Year: 2025, Volume and Issue: Volume 19, P. 569 - 583

Published: Jan. 1, 2025

Background: Doxorubicin (DOX) is a chemotherapeutic agent widely used for cancer treatment and has non-negligible cardiotoxicity.Some previous studies have reported that cannabidiol (CBD) cardioprotective effects.In this study, we evaluated the protective effects of CBD against DOX-induced cardiomyocyte injury, explored downstream molecular mechanism.Methods Materials: GSE193861, containing healthy myocardial tissues with was analyzed to screen involved proteins pathways.Molecular docking performed identify candidate drugs.After H9c2 cells were treated DOX CBD, their viability, oxidative stress, apoptosis assessed.After YAP depletion, role Hippo pathway in function investigated.C57BL/6 mice establish an vivo model, verteporfin (VP) treat mice.Histological analyses immunofluorescence evaluate tissue stress also analyzed.Western blotting investigate regulatory on apoptosis-related pathways.Results: Bioinformatic analysis suggested crucial injury.Molecular showed targeted multiple regulators pathway.CBD injury both vitro regulated activity cardiomyocytes.After inactivation by knockdown or VP intervention, reversed.Conclusion: For first time, revealed likely reduce regulating signaling pathway.

Language: Английский

Citations

1

Exercise, cancer, and the cardiovascular system: clinical effects and mechanistic insights DOI Creative Commons
Simon Wernhart, Tienush Rassaf

Basic Research in Cardiology, Journal Year: 2024, Volume and Issue: unknown

Published: Feb. 14, 2024

Abstract Cardiovascular diseases and cancer are the leading causes of death in Western world share common risk factors. Reduced cardiorespiratory fitness (CRF) is a major determinant cardiovascular morbidity survival. In this review we discuss cancer- induced disturbances parenchymal, cellular, mitochondrial function, which limit CRF may be antagonized attenuated through exercise training. We show impact on survival its attenuating effects cardiotoxicity cancer-related treatment. Tailored programs not yet available for each tumor entity as several trials were performed heterogeneous populations without adequate cardiopulmonary testing (CPET) prior to prescription with wide variation modalities. There emerging evidence that crucial pillar treatment tool mitigate cardiotoxic effects. modalities aerobic resistance training their potential improve patients provide an example periodization model cancer.

Language: Английский

Citations

7