Molecular avenues in targeted doxorubicin cancer therapy

Roychoudhury, Sayantani; Kumar, Ajay; Bhatkar, Devyani; Sharma, Nilesh Kumar

doi:10.2217/fon-2019-0458

Cited by 39 publications

(22 citation statements)

References 123 publications

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“…Nevertheless, DOX could negatively affect non-cancer cells; therefore, its clinical practice is limited. In the context of its mechanical action, DOX has more capabilities to target cancer cell growth and inhibit free radical production and DNA intercalation, as shown in in-vitro and in-vivo systems [ 3 , 4 ]. It can induce toxicities, as shown by redox signaling on mitochondria and drastic generation of superoxide radicals and ROS, causing oxidative stress [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Diosmin Alleviates Doxorubicin-Induced Liver Injury via Modulation of Oxidative Stress-Mediated Hepatic Inflammation and Apoptosis via NfkB and MAPK Pathway: A Preclinical Study

et al. 2021

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Hepatotoxicity caused by chemotherapeutic drugs (e.g., doxorubicin) is of critical concern in cancer therapy. This study focused on investigating the modulatory effects of diosmin against doxorubicin-induced hepatotoxicity in Male Wistar rats. Male Wistar rats were randomly divided into four groups: Group I was served as control, Group II was treated with doxorubicin (20 mg/kg, intraperitoneal, i.p.), Group III was treated with a combination of doxorubicin and low-dose diosmin (100 mg/kg orally), and Group IV was treated with a combination of doxorubicin and high-dose diosmin (200 mg/kg orally) supplementation. A single dose of doxorubicin (i.p.) caused hepatic impairment, as shown by increases in the concentrations of serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase. Doxorubicin produced histological abnormalities in the liver. In addition, a single injection of doxorubicin increased lipid peroxidation and reduced glutathione, catalase, and superoxide dismutase (SOD) levels. Importantly, pre-treatment with diosmin restored hepatic antioxidant factors and serum enzymatic activities and reduced the inflammatory and apoptotic-mediated proteins and genes. These findings demonstrate that diosmin has a protective effect against doxorubicin-induced hepatotoxicity.

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Section: Introductionmentioning

confidence: 99%

Diosmin Alleviates Doxorubicin-Induced Liver Injury via Modulation of Oxidative Stress-Mediated Hepatic Inflammation and Apoptosis via NfkB and MAPK Pathway: A Preclinical Study

et al. 2021

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“…Doxorubicyn (DOX) is an anthracycline antibiotic, widely used in therapy of the number of different cancers. The main characteristics of it as a therapeutic agent is its genotoxisity, caused by intercalation between complementary bases in double-stranded DNA helix and induction of oxidative stress via ROS formation [43]. It is known that oxidative stress induces epigenetic changes, including aberrant hypermethylation of tumor suppressor genes' (TSGs') promoters [44].…”

Section: Discussionmentioning

confidence: 99%

Tristetraproline in breast cancer: treat or trick?

Serhii

Anastasiia

Oksana

et al. 2022

Preprint

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Breast cancer is one of the most common types of cancer. It is very heterogeneous, hence still complicated to diagnose despite of decades of research. Post-transcriptional regulation of gene expression is crucial for modulation of cell networking and is performed via different regulatory molecules. Tristetraproline (TTP) is RNA-binding protein which binds to AU-rich elements within its target mRNAs and negatively regulates multiple transcripts, including pro-inflammatory and pro-oncogenic. Its expression level correlates with patient outcomes in different types of cancer and is considered as a potential molecular marker. Here we examined TTPs expression level in different molecular subtypes of breast cancer. Our findings show that TTP expression is significantly higher in HER2-enriched breast cancer compared to other types and adjacent tissues. We also investigated changes in the TTPs methylation status under temozolomide and doxorubicin treatment in MCF-7 cell line and found that temozolomide decreased TTPs methylation, which can potentially improve patient prognosis. In contrast, another well-known anticancer agent, doxorubicin, promoted TTPs methylation, which may impair an expected therapeutic effect of this drug.

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“…The treatment with doxorubicin causes many side effects, including cardiotoxicity[ 186 ], infertility[ 187 ], genotoxicity[ 188 ], amenorrhea[ 189 ], thrombophlebitis[ 190 ] and lung embolism[ 191 ]. Regarding cardiotoxicity, the additional challenge is that it can occur 10 years after chemotherapy treatment, appearing as a progressive congestive cardiac failure secondary to a non-ischemic dilated cardiomyopathy, and is irreversible and usually fatal[ 192 , 193 ].…”

Section: Chemotherapeutic Drugs Interacting With Machrsmentioning

confidence: 99%

Breast cancer: Muscarinic receptors as new targets for tumor therapy

Español¹,

Salem²,

Sanchez³

et al. 2021

WJCO

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The development of breast cancer is a complex process that involves the participation of different factors. Several authors have demonstrated the overexpression of muscarinic acetylcholine receptors (mAChRs) in different tumor tissues and their role in the modulation of tumor biology, positioning them as therapeutic targets in cancer. The conventional treatment for breast cancer involves surgery, radiotherapy, and/or chemotherapy. The latter presents disadvantages such as limited specificity, the appearance of resistance to treatment and other side effects. To prevent these side effects, several schedules of drug administration, like metronomic therapy, have been developed. Metronomic therapy is a type of chemotherapy in which one or more drugs are administered at low concentrations repetitively. Recently, two chemotherapeutic agents usually used to treat breast cancer have been considered able to activate mAChRs. The combination of low concentrations of these chemotherapeutic agents with muscarinic agonists could be a useful option to be applied in breast cancer treatment, since this combination not only reduces tumor cell survival without affecting normal cells, but also decreases pathological neo-angiogenesis, the expression of drug extrusion proteins and the cancer stem cell fraction. In this review, we focus on the previous evidences that have positioned mAChRs as relevant therapeutic targets in breast cancer and analyze the effects of administering muscarinic agonists in combination with conventional chemotherapeutic agents in a metronomic schedule.

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Molecular avenues in targeted doxorubicin cancer therapy

Cited by 39 publications

References 123 publications

Diosmin Alleviates Doxorubicin-Induced Liver Injury via Modulation of Oxidative Stress-Mediated Hepatic Inflammation and Apoptosis via NfkB and MAPK Pathway: A Preclinical Study

Diosmin Alleviates Doxorubicin-Induced Liver Injury via Modulation of Oxidative Stress-Mediated Hepatic Inflammation and Apoptosis via NfkB and MAPK Pathway: A Preclinical Study

Tristetraproline in breast cancer: treat or trick?

Breast cancer: Muscarinic receptors as new targets for tumor therapy

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