Targeting MDR‐1 gene expression, BAX/BCL2, caspase‐3, and Ki‐67 by nanoencapsulated imatinib and hesperidin to enhance anticancer activity and ameliorate cardiotoxicity

El‐Sisi, Alaa E.; Sokkar, Samia Salem; Ibrahim, Hassan A.H.; Hamed, Mohamed F.; Abu-Risha, Sally

doi:10.1111/fcp.12549

Cited by 28 publications

(15 citation statements)

References 63 publications

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“…28 El Sisi et al reported that imatinib could increase the expression of Bax and decrease the expression of Bcl-2 by targeting Bax/Bcl-2, thus enhancing its antitumor activity. 29 In this study, it was demonstrated that the mRNA expression of PTEN in A549 cells and A549/DDP cells decreased. Moreover, Western blot assay showed that miR-29b-3p Mimics could up-regulate the protein expression of apoptosis-related gene Bax and tumor suppressor gene PTEN, and down-regulate the protein expression of Bcl-2 and COL1A1.…”

Section: Discussionmentioning

confidence: 61%

<p>MiR-29b-3p Reverses Cisplatin Resistance by Targeting COL1A1 in Non-Small-Cell Lung Cancer A549/DDP Cells</p>

Jia¹,

Wang²

2020

CMAR

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Objective: To investigate the expression of miR-29b-3p in tissues and cells of non-small-cell lung cancer (NSCLC) and its effect on cisplatin resistance in NSCLC cells and its mechanism. Methods: The mRNA expression of miR-29b-3p and COL1A1 in NSCLC tissue, cell line A549 and cisplatin-resistant cell line A549/DDP was detected by Mimics was transfected into A549/DDP cells, and the cell viability, proliferation, apoptosis and related protein expression were detected by CCK-8, flow cytometry and Western blot. Also, luciferase reporter gene assay was used to verify the targeting relationship between miR-29b-3p and COL1A1. Moreover, COL1A1 overexpression lentivirus and miR-29b-3p mimics (Mimics+COL1A1) were simultaneously transfected into A549/DDP cells, and then the cell viability and related protein expression were measured. Results: In NSCLC tissue and its cell line, miR-29b-3p was downregulated and COL1A1 was upregulated (P<0.05). After A549/DDP cell was transfected by mimics, its cell viability and proliferation rate decreased, apoptosis rate and the expression of tumor suppressor gene PTEN and apoptosis-related protein BAX were increased (P<0.05), which could be reversed by Mimics+COL1A1 co-transfection. Luciferase reporter gene assay indicated that COL1A1 was the target gene of miR-29b-3p. Conclusion: All in all, miR-29b-3p can reverse the cisplatin resistance of A549/DDP cells by inhibiting the expression of COL1A1 gene and increasing the expression of PTEN and BAX.

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Section: Discussionmentioning

confidence: 61%

<p>MiR-29b-3p Reverses Cisplatin Resistance by Targeting COL1A1 in Non-Small-Cell Lung Cancer A549/DDP Cells</p>

Jia¹,

Wang²

2020

CMAR

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“…On the other hand, El‐Sisi et al (2020) evaluated the in vivo anti-cancer efficacy and toxicity of poly (lactide-co-glycolide) (PLGA)-encapsulated imatinib mesylate and/or hesperidin in Swiss albino mice bearing solid Ehrlich carcinoma (SEC). The study showed that the intraperitoneal injection of nano-encapsulated imatinib mesylate (Nano-IM; 3.75 or 6.25 mg/mL) or nano-encapsulated hesperidin (Nano-HES; 6.25 mg/mL) induced a more significant reduction in both tumour volume and tumour weight than their respective treatment (50 mg/kg).…”

Section: Strategies To Enhance Bioavailability Of Hesperidin and Hesperetinmentioning

confidence: 99%

Hesperidin and its aglycone hesperetin in breast cancer therapy: A review of recent developments and future prospects

Yap

Sekar

et al. 2021

Saudi Journal of Biological Sciences

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Breast cancer (BC) has high incidence and mortality rates, making it a major global health issue. BC treatment has been challenging due to the presence of drug resistance and the limited availability of therapeutic options for triple-negative and metastatic BC, thereby urging the exploration of more effective anti-cancer agents. Hesperidin and its aglycone hesperetin, two flavonoids from citrus species, have been extensively evaluated for their anti-cancer potentials. In this review, available literatures on the chemotherapeutic and chemosensitising activities of hesperidin and hesperetin in preclinical BC models are reported. The safety and bioavailability of hesperidin and hesperetin as well as the strategies to enhance their bioavailability are also discussed. Overall, hesperidin and hesperetin can inhibit cell proliferation, migration and BC stem cells as well as induce apoptosis and cell cycle arrest in vitro . They can also inhibit tumour growth, metastasis and neoplastic changes in tissue architecture in vivo . Moreover, the co-administration of hesperidin or hesperetin with doxorubicin, letrozole or tamoxifen can enhance the efficacies of these clinically available agents. These chemotherapeutic and chemosensitising activities of hesperidin and hesperetin have been linked to several mechanisms, including the modulation of signalling pathways, glucose uptake, enzymes, miRNA expression, oxidative status, cell cycle regulatory proteins, tumour suppressor p53, plasma and liver lipid profiles as well as DNA repair mechanisms. However, poor water solubility, extensive phase II metabolism and apical efflux have posed limitations to the bioavailability of hesperidin and hesperetin. Various strategies for bioavailability enhancement have been studied, including the utilisation of nano-based drug delivery systems and the co-administration of hesperetin with other flavonoids. In particular, nanoformulated hesperidin and hesperetin possess greater chemotherapeutic and chemosensitising activities than free compounds. Despite promising preclinical results, further safety and efficacy evaluation of hesperidin and hesperetin as well as their nanoformulations in clinical trials is required to ascertain their potentials to be developed as clinically useful agents for BC treatment.

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“…It has also been evaluated to work in combination with cisplatin to treat non-small-cell lung cancer (NSCLC) patients in clinical trials, as ginseng is able to enhance the cytotoxicity of multiple chemotherapy drugs [ 26 ]. Regarding breast cancer, hesperidin was shown to increase the cytotoxicity of tamoxifen, a selective estrogen receptor modulator, and imatinib mesylate, a platelet-derived growth factor (PDGF) receptor inhibitor, when treating breast cancer cells [ 27 , 28 ]. In addition, combination with hesperidin could potentially prevent the resistance of MCF-7 to doxorubicin treatment in breast cancers [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Hesperidin and Chlorogenic Acid Synergistically Inhibit the Growth of Breast Cancer Cells via Estrogen Receptor/Mitochondrial Pathway

Hsu

Chen

Juan-Lu

et al. 2021

Life

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Breast cancer is the most common cancer in women worldwide. Hesperidin (Hes) and chlorogenic acid (CA) are traditional medicinal molecules that abundantly exist in natural plants or foods. These compounds have been shown to prevent and suppress various cancers and therefore can be utilized as adjunctive therapies to aid cancer treatment. Here, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays show a greater synergistic inhibitory effect on the growth of breast cancer cells, MCF-7, but not normal breast cells, MCF-10A, than hesperidin or chlorogenic acid alone. We present the possible molecular signaling pathways in MCF-7 cells with or without herbal molecule treatments via proteomic approaches. The data were further analyzed by Ingenuity Pathway Analysis (IPA) and confirmed by quantifying mRNA associated with the estrogen-receptor signaling pathway and mitochondrial functions. We demonstrated that the expression of CYC1, TFAM, ATP5PB, mtATP6, mtDNA, and NRF-1 were decreased upon 12 h treatment, and subsequent ATP production was also significantly decreased at 24 h. These results identified a synergistic effect induced by combinational treatment with hesperidin and chlorogenic acid, which can regulate mitochondria and ATP production through the estrogen receptor pathway in MCF-7 cells. However, none of the treatments induced the generation of reactive oxygen species (ROS), suggesting that ROS likely plays no role in the observed pharmacological activities. Overall, our study sheds light on the adequacy of hesperidin and chlorogenic acid to serve as an adjunctive therapy when co-administrated with chemotherapy drugs in breast cancer patients.

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Targeting MDR‐1 gene expression, BAX/BCL2, caspase‐3, and Ki‐67 by nanoencapsulated imatinib and hesperidin to enhance anticancer activity and ameliorate cardiotoxicity

Cited by 28 publications

References 63 publications

<p>MiR-29b-3p Reverses Cisplatin Resistance by Targeting COL1A1 in Non-Small-Cell Lung Cancer A549/DDP Cells</p>

<p>MiR-29b-3p Reverses Cisplatin Resistance by Targeting COL1A1 in Non-Small-Cell Lung Cancer A549/DDP Cells</p>

Hesperidin and its aglycone hesperetin in breast cancer therapy: A review of recent developments and future prospects

Hesperidin and Chlorogenic Acid Synergistically Inhibit the Growth of Breast Cancer Cells via Estrogen Receptor/Mitochondrial Pathway

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