Cisplatin-based combination therapy for cancer

Kumar, Rakesh; Shah, Ruchi; Minerva,; Bhat, Amrita; Verma, Sonali; Chander, Gresh; Jamwal, RajeshwerSingh; Sharma, Bhawani Shankar; Bhat, Audesh; Katyal, Taruna

doi:10.4103/jcrt.jcrt_792_22

Cited by 11 publications

(5 citation statements)

References 80 publications

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“…DNA damage was evaluated by the expression of the phosphorylated form of the histone H2AX (Ser139-H2AX, i.e., γH2AX), a sensitive and well-established marker for DNA DSB . As a positive control for drug-induced DSB, the alkylating agent cisplatin was used. , Cisplatin treatment in THP-1 monocytes clearly shows an expected strong dose-dependent DNA damage, associated with reduced cell viability (Figure B). SMIP-031 as well as SMIP-30 do not induce any observable DNA damage and do not affect cell viability in both monocytes and macrophages, supporting a safety profile in highly proliferating as well as in differentiated cells (Figure B, C).…”

Section: Results and Discussionmentioning

confidence: 99%

Small Molecule Targeting PPM1A Activates Autophagy for Mycobacterium tuberculosis Host-Directed Therapy

Yu,

Liang,

Berton

et al. 2024

J. Med. Chem.

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Mycobacterium tuberculosis (Mtb), the infectious agent of tuberculosis (TB), causes over 1.5 million deaths globally every year. Host-directed therapies (HDT) for TB are desirable for their potential to shorten treatment and reduce the development of antibiotic resistance. Previously, we described a modular biomimetic strategy to identify SMIP-30, targeting PPM1A (IC 50 = 1.19 μM), a metal-dependent phosphatase exploited by Mtb to survive intracellularly. SMIP-30 restricted the survival of Mtb in macrophages and lungs of infected mice. Herein, we redesigned SMIP-30 to create SMIP-031, which is a more potent inhibitor for PPM1A (IC 50 = 180 nM). SMIP-031 efficiently increased the level of phosphorylation of S403-p62 and the expression of LC3B-II to activate autophagy, resulting in the dose-dependent clearance of Mtb in infected macrophages. SMIP-031 possesses a good pharmacokinetic profile and oral bioavailability (F = 74%). In vivo, SMIP-031 is well tolerated up to 50 mg/kg and significantly reduces the bacteria burden in the spleens of infected mice.

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Section: Results and Discussionmentioning

confidence: 99%

Small Molecule Targeting PPM1A Activates Autophagy for Mycobacterium tuberculosis Host-Directed Therapy

Yu,

Liang,

Berton

et al. 2024

J. Med. Chem.

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“…Non-anthracyclines drugs have been shown to trigger cardiovascular side effects [ 355 ] also through the alteration of mitochondrial activity and function. This is the case for cisplatin, an alkylating agent used alone or combination with other antineoplastic agents to treat diverse types of tumors [ 356 ]. By prompting organelles’ structural and ultrastructural modifications and alterations of ΔΨm, together enhanced ROS generation, cisplatin elicits cumulative cardiotoxicity, which is frequently associated with remarkable nephrological side effects [ 357 ]).…”

Section: Anticancer Therapies and Cardiotoxicity: A Role For Mitochon...mentioning

confidence: 99%

Mitochondrial dysfunction at the crossroad of cardiovascular diseases and cancer

Rocca,

Soda,

De Francesco

et al. 2023

J Transl Med

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A large body of evidence indicates the existence of a complex pathophysiological relationship between cardiovascular diseases and cancer. Mitochondria are crucial organelles whose optimal activity is determined by quality control systems, which regulate critical cellular events, ranging from intermediary metabolism and calcium signaling to mitochondrial dynamics, cell death and mitophagy. Emerging data indicate that impaired mitochondrial quality control drives myocardial dysfunction occurring in several heart diseases, including cardiac hypertrophy, myocardial infarction, ischaemia/reperfusion damage and metabolic cardiomyopathies. On the other hand, diverse human cancers also dysregulate mitochondrial quality control to promote their initiation and progression, suggesting that modulating mitochondrial homeostasis may represent a promising therapeutic strategy both in cardiology and oncology. In this review, first we briefly introduce the physiological mechanisms underlying the mitochondrial quality control system, and then summarize the current understanding about the impact of dysregulated mitochondrial functions in cardiovascular diseases and cancer. We also discuss key mitochondrial mechanisms underlying the increased risk of cardiovascular complications secondary to the main current anticancer strategies, highlighting the potential of strategies aimed at alleviating mitochondrial impairment-related cardiac dysfunction and tumorigenesis. It is hoped that this summary can provide novel insights into precision medicine approaches to reduce cardiovascular and cancer morbidities and mortalities.

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“…Cisplatin is the more commonly used platinum-based chemotherapy agent in the treatment of OS than other platinum-based chemotherapy drugs ( Qi et al, 2019 ). Cisplatin, also known as cis-diamine dichloroplatin, mainly binds to the N7 position on the purine ring and causes DNA damage to tumor cells by blocking cell division leading to apoptosis ( Minerva et al, 2023 ). After DNA damage, tumors lose their ability to proliferate, thereby inducing oxidative stress, upregulating p53, mitogen-activated protein kinase (MAPK) and Jun N-terminal kinase (JNK) or Akt pathways, and inducing apoptosis ( Gupta and Nebreda, 2015 ).…”

Section: Cardiotoxicity Of First-line Chemotherapy Drugs For Osteosar...mentioning

confidence: 99%

Engineered biomaterial delivery strategies are used to reduce cardiotoxicity in osteosarcoma

Hou,

Wang,

Wang

2023

Front. Pharmacol.

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Osteosarcoma (OS) is the most common malignant bone tumor in children and adolescents. Chemotherapy drugs play an integral role in OS treatment. Preoperative neoadjuvant chemotherapy and postoperative conventional adjuvant chemotherapy improve survival in patients with OS. However, the toxic side effects of chemotherapy drugs are unavoidable. Cardiotoxicity is one of the common side effects of chemotherapy drugs that cannot be ignored. Chemotherapy drugs affect the destruction of mitochondrial autophagy and mitochondria-associated proteins to cause a decrease in cardiac ejection fraction and cardiomyocyte necrosis, which in turn causes heart failure and irreversible cardiomyopathy. Biomaterials play an important role in nanomedicine. Biomaterials act as carriers to deliver chemotherapy drugs precisely around tumor cells and continuously release carriers around the tumor. It not only promotes anti-tumor effects but also reduces the cardiotoxicity of chemotherapy drugs. In this paper, we first introduce the mechanism by which chemotherapy drugs commonly used in OS cause cardiotoxicity. Subsequently, we introduce biomaterials for reducing cardiotoxicity in OS chemotherapy. Finally, we prospect biomaterial delivery strategies to reduce cardiotoxicity in OS.

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Cisplatin-based combination therapy for cancer

Cited by 11 publications

References 80 publications

Small Molecule Targeting PPM1A Activates Autophagy for Mycobacterium tuberculosis Host-Directed Therapy

Small Molecule Targeting PPM1A Activates Autophagy for Mycobacterium tuberculosis Host-Directed Therapy

Mitochondrial dysfunction at the crossroad of cardiovascular diseases and cancer

Engineered biomaterial delivery strategies are used to reduce cardiotoxicity in osteosarcoma

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