Tenofovir alone or combined with doxorubicin abrogates DMBA-induced mammary cell carcinoma: An insight into its modulatory impact on oxidative/Notch/apoptotic signaling

Abouelezz, Hadeer M.; El‐Kashef, Dalia H.; Abdеlaziz, Rania R.; Nader, Manar A.

doi:10.1016/j.lfs.2023.121798

Cited by 3 publications

(1 citation statement)

References 73 publications

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“…Historically, clinical BC therapies have been developed using some of the earliest established rat models. DMBAinduced tumor models have facilitated pharmacological studies testing a range of drugs, such as letrozole, palbocyclib, lapatinib, tenofovir alone or in combination with doxorubicin, and sodium channel inhibitors [158,159,[305][306][307]. Furthermore, NMU-induced models have been used to study BC prevention, [308] as well as for nutritional and pharmacological studies focusing on hormone-related effects, [309][310][311] and as a preclinical validation system for immunotherapy responses [101].…”

Section: Development and Testing Of Breast Cancer Treatment Strategiesmentioning

confidence: 99%

Rat Models of Hormone Receptor-Positive Breast Cancer

Nicotra,

Lutz,

Messal

et al. 2024

J Mammary Gland Biol Neoplasia

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Hormone receptor-positive (HR+) breast cancer (BC) is the most common type of breast cancer among women worldwide, accounting for 70–80% of all invasive cases. Patients with HR+ BC are commonly treated with endocrine therapy, but intrinsic or acquired resistance is a frequent problem, making HR+ BC a focal point of intense research. Despite this, the malignancy still lacks adequate in vitro and in vivo models for the study of its initiation and progression as well as response and resistance to endocrine therapy. No mouse models that fully mimic the human disease are available, however rat mammary tumor models pose a promising alternative to overcome this limitation. Compared to mice, rats are more similar to humans in terms of mammary gland architecture, ductal origin of neoplastic lesions and hormone dependency status. Moreover, rats can develop spontaneous or induced mammary tumors that resemble human HR+ BC. To date, six different types of rat models of HR+ BC have been established. These include the spontaneous, carcinogen-induced, transplantation, hormone-induced, radiation-induced and genetically engineered rat mammary tumor models. Each model has distinct advantages, disadvantages and utility for studying HR+ BC. This review provides a comprehensive overview of all published models to date.

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Section: Development and Testing Of Breast Cancer Treatment Strategiesmentioning

confidence: 99%

Rat Models of Hormone Receptor-Positive Breast Cancer

Nicotra,

Lutz,

Messal

et al. 2024

J Mammary Gland Biol Neoplasia

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Potential to use of viral reverse transcriptase inhibitors in oncology

Vlasova,

Antonova,

Magomedova

et al. 2024

Usp. mol. onkol

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In preparing the review, articles on the functioning of the reverse transcriptase enzyme of endogenous repeat sequences LINE1, the mechanisms of action and antitumor activity of viral reverse transcriptase inhibitors. Articles available in the biomedical literature information databases SciVerse Scopus, PubMed, Web of Science, Russian Science CitationIndex (RSCI) were analyzed. The review used information from 140 publications, of which 95 and 39 were published, respectively, over the last ten and three years, 2 articles present the results of clinical studies, and 45 articles refer to results demonstrating the anticancer properties of the studied compounds in various models in vitro and in vivo. Aim. Based on data on the functional properties of the reverse transcriptase enzyme of endogenous repeat sequences LINE1 (long interspersed nuclear elements 1), analyze the potential use of viral reverse transcriptase inhibitors in oncology, presenting their classification and main mechanisms of action. About 98 % of the human genome consists of repetitive sequences, most of which are represented by mobil genetic elements, the activation of which leads to increased genome instability. These include long (LINE) and short (SINE) interspersed nuclear element repeated DNA sequences interspersed nuclear elements, respectively, which occupy about 45 % of the human genome. Increased expression levels of these sequences in the genome have been identified in many forms of malignant neoplasms. Their transposition occurs due to the expression of LINE1-encoded reverse transcriptase, whichis homologous to viral reverse transcriptase. To date, reverse transcriptase inhibitors of viruses of nucleoside and non-nucleoside structure have been developed and are successfully used in the clinic. These drugs demonstrate an inhibitory effect on both LINE1 reverse transcriptase and telomerase, which provides the tumor cell with the ability to overcome replicative senescence. Due to these properties, these compounds are expected to exhibit both their own antitumor activity and increase the sensitivity of tumor cells to the therapy of malignant neoplasms, which is experimentally confirmed in models of malignant tumors in vitro and in vivo. Use of reverse transcriptase inhibitors in combination therapy seems advisable both to prevent further genome rearrangements caused by LINE1 and to suppress the survival of tumor cells by inhibiting telomerase activity.

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Antiretroviral Drugs Impact Autophagy: Opportunities for Drug Repurposing

Cheney,

Barbaro,

McDermott

et al. 2024

Front. Biosci. (Landmark Ed)

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Autophagy is an evolutionarily conserved process in which intracellular macromolecules are degraded in a lysosomal-dependent manner. It is central to cellular energy homeostasis and to quality control of intracellular components. A decline in autophagic activity is associated with aging, and contributes to the development of various age-associated pathologies, including cancer. There is an ongoing need to develop chemotherapeutic agents to improve morbidity and mortality for those diagnosed with cancer, as well as to decrease the cost of cancer care. Autophagic programs are altered in cancer cells to support survival in genetically and metabolically unstable environments, making autophagy an attractive target for new chemotherapy. Antiretroviral drugs, which have dramatically increased the life- and health spans of people with human immunodeficiency virus (HIV) (PWH), have offered promise in the treatment of cancer. One mechanism underlying the antineoplastic effects of antiretroviral drugs is the alteration of cancer cell autophagy that can potentiate cell death. Antiretroviral drugs could be repurposed into the cancer chemotherapy arsenal. A more complete understanding of the impact of antiretroviral drugs on autophagy is essential for effective repurposing. This review summarizes our knowledge of the effects of antiretroviral drugs on autophagy as potential adjunctive chemotherapeutic agents, and highlights gaps to be addressed to reposition antiretroviral drugs into the antineoplastic arsenal successfully.

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Tenofovir alone or combined with doxorubicin abrogates DMBA-induced mammary cell carcinoma: An insight into its modulatory impact on oxidative/Notch/apoptotic signaling

Cited by 3 publications

References 73 publications

Rat Models of Hormone Receptor-Positive Breast Cancer

Rat Models of Hormone Receptor-Positive Breast Cancer

Potential to use of viral reverse transcriptase inhibitors in oncology

Antiretroviral Drugs Impact Autophagy: Opportunities for Drug Repurposing

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