A triple-drug combination induces apoptosis in cervical cancer-derived cell lines

Delgado-Waldo, Izamary; Contreras-Romero, Carlos; Salazar-Aguilar, Sandra; Pessoa, João; Mitre-Aguilar, Irma B.; García-Castillo, Verónica; Pérez‐Plasencia, Carlos; Jacobo-Herrera, Nadia

doi:10.3389/fonc.2023.1106667

Cited by 3 publications

(2 citation statements)

References 68 publications

(92 reference statements)

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“…Micelle‐mediated combination therapy and the use of nanocarriers for controlled delivery of CDDP have shown promising results [91] . Combined therapy is a cornerstone of cancer treatment that uses two or more therapeutic agents to get superior therapeutic effects in cancer patients including drug efflux inhibition, increased DNA damage and synergistic induced cell death, [92,93] which are as shown in Figure 7.…”

Section: Strategies To Overcome Cddp Resistancementioning

confidence: 99%

Cisplatin Resistance in Cancer Therapy: Causes and Overcoming Strategies

Shruthi,

Bhasker Shenoy

2024

ChemistrySelect

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Dr. S. Shruthi, Prof. Dr. K. Bhasker Shenoy. Cisplatin (CDDP) is the first metal‐based drug and has been a popular drug in the treatment of various types of cancer for decades. Cancer cell death is promoted by this platinum‐based drug by generating DNA adducts and activating apoptotic signaling pathways. The development of drug resistance is the foremost clinical concern that compromises its efficacy. The mechanism of CDDP resistance encompasses changes in drug influx and efflux, drug accumulation reduction, enhanced drug detoxification, and repair which may affect its therapeutic value. Researchers have paid significant attention to overcoming CDDP resistance, which provides an opportunity to enhance clinical outcomes. Combinational therapy, use of CDDP analogs, phytochemicals, nanoparticle‐mediated drug delivery, gene targeting and regulation of drug induced epigenetic changes are the specific regimens to overcome CDDP resistance and treatment burden. In this review, we summarize the mechanisms involved in CDDP resistance and strategies considered to overcome these hurdles concerning preclinical and clinical studies. This may provide insights into the further development of novel approaches to uproot CDDP resistance, to ascertain a safer and more effective cancer therapy.

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Section: Strategies To Overcome Cddp Resistancementioning

confidence: 99%

Cisplatin Resistance in Cancer Therapy: Causes and Overcoming Strategies

Shruthi,

Bhasker Shenoy

2024

ChemistrySelect

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“…HeLa cells were obtained from American Type Culture Collection (ATCC ® CCL-2™) (ATCC, 2023;Becit et al, 2020;Delgado-Waldo et al, 2023;Sariaydin et al, 2021). HeLa cells were cultured in DMEM, containing fetal bovine serum (10%) and penicillin-streptomycin (1%).…”

Section: Cell Culturementioning

confidence: 99%

Pitavastatin induces caspase‐mediated apoptotic death through oxidative stress and DNA damage in combined with cisplatin in human cervical cancer cell line

Hacıseyitoğlu,

Doğan,

Dilsiz

et al. 2023

J of Applied Toxicology

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Pitavastatin (PITA) is a 3‐hydroxy‐3‐methylglutaryl‐CoA (HMG‐CoA) reductase inhibitor to treat hypercholesterolemia and in recent studies is focused that its potential anti‐cancer effect. This study was aimed to elucidate the effect of PITA alone and in combination with cisplatin on cervical cancer cells (HeLa) in vitro. Cytotoxicity of PITA (5–200 μM) was evaluated by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) and neutral red uptake (NRU) assays for 24, 48, and 72 h. Cell apoptosis and cell cycle analyses were performed in flow cytometry (0.1–100 μM). The evaluation of genotoxic effects and oxidative DNA damage of PITA (2–200 μM) were performed with standard comet assay, formamidopyrimidine glycosylase (fpg)‐modified comet assay, and reactive oxygen species (ROS) activation in HeLa cells. PITA alone reduced cell viability in a dose‐dependent manner (20–200, 20–200, and 5–200 μM for 24, 48, and 72 h, respectively, in MTT). The combined treatment of PITA with cisplatin resulted in significantly greater inhibition of cell viability. ROS and DNA damage increased significantly at 100 μM for 4 h and 20 μM for 24 h, respectively. PITA‐induced apoptosis, an increased proportion of sub G1 cells, was monitored, and also, it increased the expression of active caspase‐9 and caspase‐3 and upregulated cleaved poly adenosine diphosphate ribose polymerase (PARP) by western blotting and caspase 3/8/9 multiple assay kit. We conclude that PITA can be used to efficiently cervical cancer studies, and promising findings have been obtained for further studies.

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Metformin (The Miracle Drug) Kinetics in Different Diseases such as Cancer

Tolou-Ghamari

2024

CCTR

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Metformin, a miracle drug that was introduced a century ago, could be considered for various aspects of diseases such as diabetes (type 1 and 2), cancer prevention or chemotherapy, and metabolic and neurodegenerative disease. It is well known that the frequency of cancer is higher in patients with type 2 diabetes mellitus. This review aims to provide updated information regarding clinical pharmacokinetics and the mechanism of action of Metformin in different diseases such as cancer. Diabetes type 1 is another chronic autoimmune disease detected usually in early childhood due to immune-mediated devastation of insulin-producing pancreatic beta-cells. Because of the lack of effective therapeutic approaches, its prevalence is increasing. Regarding cancer, an estimated 19.3 million new cancer cases and almost 10.0 million cancer deaths were reported in 2020 worldwide. By 50-60% bioavailability, the main route of metformin excretion is through urine. Its mechanism of action is based on 1) initiation of adenosine monophosphate-activated kinase, 2) block proinflammatory paths in perivascular adipose tissue, 3) decrease in monocyte-to-macrophage differentiation in vascular tissues, and 4) improvement in endothelial function. Metformin induces adenosine monophosphate-activated protein kinase signaling and suppresses gluconeogenesis. Antitumor properties of Metformin include a decrease in reactive oxygen species generation and inducing autophagy. In addition to glucose-lowering effects, Metformin has moderate anti-inflammatory and antioxidative effects. It could improve lipid profile and reduce overweight individuals' body mass and arterial blood pressure. In type 1 diabetes, Metformin reduces the requirement for daily insulin and improves glycemia. Its long-term use decreases cardiovascular events. In addition to inhibiting the synthesis of lipids via a reduction in oxidative stress, Metformin inhibits inflammation and increases energy metabolism. Finally, by reducing micro- and macro-vascular consequences, mortality-related diabetes and cancer decline by metformin administration. Therefore, in addition to diabetes, Metformin could reduce the proliferation of cancer cells and the possibility of malignancies in different types of cancer.

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A triple-drug combination induces apoptosis in cervical cancer-derived cell lines

Cited by 3 publications

References 68 publications

Cisplatin Resistance in Cancer Therapy: Causes and Overcoming Strategies

Cisplatin Resistance in Cancer Therapy: Causes and Overcoming Strategies

Pitavastatin induces caspase‐mediated apoptotic death through oxidative stress and DNA damage in combined with cisplatin in human cervical cancer cell line

Metformin (The Miracle Drug) Kinetics in Different Diseases such as Cancer

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