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1.
Med Oncol ; 41(10): 244, 2024 Sep 11.
Artículo en Inglés | MEDLINE | ID: mdl-39259412

RESUMEN

The likelihood of survival for cancer patients has greatly improved due to chemotherapy medicines. However, these antitumor agents might also have unfavorable effects on the cardiovascular system, which could result in sudden or gradual cardiac failure. The production of free radicals that result in oxidative stress appears to be the key mechanism by which chemotherapy-induced cardiotoxicity (CIC) happens. Reports suggest that the Sirtuin-1 (Sirt1)/Nuclear factor E2-associated factor 2 (Nrf2) signaling pathway has been considered an alternative path for counteracting cardiotoxicity by suppressing oxidative stress, inflammation, and apoptosis. This review concludes recent knowledge about CIC with a special focus on the anti-oxidative regulation properties of the Sirt1/Nrf2 pathway.


Asunto(s)
Antineoplásicos , Cardiotoxicidad , Factor 2 Relacionado con NF-E2 , Transducción de Señal , Sirtuina 1 , Humanos , Sirtuina 1/metabolismo , Factor 2 Relacionado con NF-E2/metabolismo , Cardiotoxicidad/etiología , Transducción de Señal/efectos de los fármacos , Antineoplásicos/efectos adversos , Estrés Oxidativo/efectos de los fármacos , Animales , Neoplasias/tratamiento farmacológico , Neoplasias/metabolismo
2.
Pathol Res Pract ; 260: 155424, 2024 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-38909406

RESUMEN

Breast cancer is one of the most common causes of cancer-related mortality globally, and its aggressive phenotype results in poor treatment outcomes. Growth Arrest-Specific 5 long non-coding RNA has attracted considerable attention due to its pivotal function in apoptosis regulation and tumor aggressiveness in breast cancer. Gas5 enhances apoptosis by regulating apoptotic proteins, such as caspases and BCL2 family proteins, and the sensitivity of BCCs to chemotherapeutic agents. At the same time, low levels of GAS5 increased invasion, metastasis, and overall tumor aggressiveness. GAS5 also regulates EMT markers, critical for cancer metastasis, and influences tumor cell proliferation by regulating various signaling components. As a result, GAS5 can be restored to suppress tumor development as a possible therapeutic strategy, which might present promising prospects for a patient's treatment. Its activity levels might also be a crucial indicator and diagnostic parameter for prediction. This review highlights the significant role of GAS5 in modulating apoptosis and tumor aggressiveness in breast cancer, emphasizing its potential as a therapeutic target for breast cancer treatment and management.


Asunto(s)
Apoptosis , Biomarcadores de Tumor , Neoplasias de la Mama , ARN Largo no Codificante , Humanos , ARN Largo no Codificante/genética , Neoplasias de la Mama/genética , Neoplasias de la Mama/patología , Neoplasias de la Mama/terapia , Femenino , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , Apoptosis/genética , Regulación Neoplásica de la Expresión Génica
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