Potential Strategies for Overcoming Drug Resistance Pathways Using Propolis and Its Polyphenolic/Flavonoid Compounds in Combination with Chemotherapy and Radiotherapy

Nutrients, Journal Year: 2024, Volume and Issue: 16(21), P. 3741 - 3741

Published: Oct. 31, 2024

Conventional cancer treatments include surgical resection, chemotherapy, hyperthermia, immunotherapy, hormone therapy, and locally targeted therapies such as radiation therapy. Standard often require the use of multiple agents, which can activate nuclear factor kappa B (NF-κB) in tumor cells, leading to reduced cell death increased drug resistance. Moreover, agents also contributes added toxicity, resulting poor treatment outcomes. Cancer cells gradually develop resistance almost all chemotherapeutics through various mechanisms, efflux, alterations metabolism transport, changes signal transduction pathways, enhanced DNA repair capacity, evasion apoptosis, mutations, reactivation targets, interaction with microenvironment, cell-stroma interactions, epithelial–mesenchymal transition (EMT)-mediated chemoresistance, epigenetic modifications, metabolic alterations, effect stem (CSCs). Developing new strategies improve chemotherapy sensitivity while minimizing side effects is essential for achieving better therapeutic outcomes enhancing patients’ quality life. One promising approach involves combining conventional propolis its flavonoids. These natural compounds may enhance response reducing toxicity. Propolis components sensitize chemotherapeutic likely by inhibiting NF-κB activation, reprogramming tumor-associated macrophages (TAMs; an M2-like phenotype), thereby release matrix metalloproteinase (MMP)-9, cytokines, chemokines, vascular endothelial growth (VEGF). By TAMs, overcome EMT-mediated disrupt crosstalk between CSCs, inhibit maintenance stemness, reverse acquired immunosuppression, thus promoting antitumor mediated cytotoxic T-cells. This review highlights potential flavonoids modulate responsiveness modalities. The evidence suggests that novel incorporating could be developed positive cytotoxicity peripheral blood leukocytes, liver, kidney cells. Therefore, polyphenolic/flavonoid hold combination clinical types cancers.

Language: Английский

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TNF-α Activates NF-κB Signalling Pathway in MG-63 Cells on Titanium and Zirconia Implant Surfaces

Materials, Journal Year: 2025, Volume and Issue: 18(4), P. 884 - 884

Published: Feb. 18, 2025

Dental implant therapy is a widely used clinical procedure for restoring missing teeth in patients. Zirconia implants were introduced as an alternative to titanium due their excellent biocompatibility and esthetic properties. The nuclear factor kappa B (NF-κB) signalling pathway responsible multiple aspects of innate adaptive immune functions serves significant crucial mediator inflammatory processes. dysregulation NF-κB activation induces pathological processes diseases. purpose this study was investigate the upon stimulation with tumour necrosis (TNF)-α osteoblast-like cells (MG-63) cultured on zirconia surfaces comparison surfaces. Several methods such immunoblot, immunofluorescence, MTT assay, flow cytometry study. We observed that human recombinant TNF-α caused strong both discs wells without any discs. This marked by upregulation MHC class I proteins MG-63 grown discs; however, there no effect II protein expression. In summary, present has shown equally activates

Language: Английский

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ALDH1A1 in breast cancer: A prospective target to overcome therapy resistance (Review)

Oncology Letters, Journal Year: 2025, Volume and Issue: 29(5), P. 1 - 17

Published: March 4, 2025

The expression of cytosolic aldehyde dehydrogenases (ALDHs), which mediate the last step in pathway synthesis all‑trans retinoic acid, is dysregulated various types human cancer, and has been associated with development cancer stem cells (CSCs) solid tumors hematological malignancies. CSCs are considered a minor fraction capacity to initiate neoplastic tumors. ALDH1A1 serves crucial role emergence CSC phenotype, induces malignant behavior promotes treatment resistance. Notably, ALDH1A1‑induced therapy resistance not exclusive just one group drugs, but affects diverse drugs that use different mechanisms kill cells. This diversity drug resistance‑inducing effects stemness‑supporting functions ALDH1A1. inhibition activity using chemicals or depletion via genetic approaches, such as small interfering RNA, can overcome pathways In context breast it critical only expected manifest stem‑like features, include increased From angle disease prognosis, extent association remains be determined through application cutting‑edge methods detect tracked biomarkers within

Language: Английский

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Potential of Carbon Nanodots (CNDs) in Cancer Treatment

Nanomaterials, Journal Year: 2025, Volume and Issue: 15(7), P. 560 - 560

Published: April 6, 2025

Carbon Nanodots (CNDs) are characterized by their nanoscale size (<10 nm), biocompatibility, stability, fluorescence, and photoluminescence, making them a promising candidate for cancer therapy. The difference in the methods of synthesis CNDs, whether top-down or bottom-up, affects formation, visual, surface characteristics which crucial biomedical pharmaceutical applications. urgent need innovative therapeutic strategies from CNDs is due to limitations barriers posed conventional therapies including drug resistance cytotoxicity. Nano-loaded chemotherapy treatments highly effective can enhance solubility targeted delivery chemotherapeutic agents, generate reactive oxygen species (ROS) induce cell cytotoxicity, regulate intracellular signaling pathways. Their ability be designed cellular uptake exact localization further improves potential. In addition working on delivery, highlighted dual functionality imaging therapy, allows real-time observing treatment efficacy. Despite development these results future, challenges still exist treatment.

Language: Английский

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Age-Dependent Differences in Radiation-Induced DNA Damage Responses in Intestinal Stem Cells

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(18), P. 10213 - 10213

Published: Sept. 23, 2024

Age at exposure is a critical modifier of the risk radiation-induced cancer. However, effects age on carcinogenesis remain poorly understood. In this study, we focused tissue stem cells using

Language: Английский

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RNA expression data suggest ALDH2 inhibition as a concept for killing acute myeloid leukemia cells that are resistant to ALDH1 inhibitors: the example of NPM1 mutant AML

Published: Nov. 10, 2024

Abstract In this data paper we present a study of RNA expression in association with the disease course acute myeloid leukemia (AML). We have previously identified aldehyde dehydrogenase genes ALDH1A1 and ALDH2 as prospective actionable targets AML. is expected to key functions stem-like cells that are prone dormant state terms metabolic activity proliferation. Cells higher metabolism whole mitochondria particular, likely generate abundance formaldehyde acetaldehyde. Cell survival necessitates removal acetaldehyde, which substantial degree function ALDH2. AML mutant NPM1 gene permit MYC would lead increased activity. Extended allowed by protein, compared wild-type. Here, show analysis patients yields hazard ratio for than , not case wild-type NPM1. This result consistent difference enzymatic between ALDH1A1, latter suited small aldehydes, especially formaldehyde. should open door examination inhibitors such clinically approved disulfiram, treatment proves refractory inhibition.

Language: Английский

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Investigating the biology of microRNA links to ALDH1A1 reveals candidates for preclinical testing in acute myeloid leukemia

International Journal of Oncology, Journal Year: 2024, Volume and Issue: 65(6)

Published: Oct. 30, 2024

Aldehyde dehydrogenase 1 family member A1 (ALDH1A1) is a of the aldehyde gene subfamily that encode enzymes with ability to oxidize retinaldehyde. It was recently shown high ALDH1A1 RNA abundance correlates poor prognosis in acute myeloid leukemia (AML). AML hematopoietic malignancy associated morbidity and mortality rates. Although there are number agents inhibit ALDH activity, it would be crucial develop methodologies for adjustable genetic interference, which permit interventions on several oncogenic pathways parallel. Intervention multiple theoretically possible microRNAs (miRNAs or miRs), class small non‑coding RNAs have emerged as key regulators expression AML. A miRNAs interfere directly solid tumor cells, these can evaluated model systems. There indications few actually do an association disease course, rendering them promising target intervention cells.

Language: Английский

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