New Advancements in Cisplatin-Based Treatments

Gentilin, Erica

doi:10.3390/ijms24065920

Cited by 3 publications

(2 citation statements)

References 11 publications

(13 reference statements)

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“…In clinical oncology, chemotherapy is still a vital treatment option. Cisplatin (Cp), a well-known and broad-spectrum anticancer medication, is regarded as one of the most effective chemotherapy agents now used in clinical practice [ 4 ]. As a low molecular weight platinum compound with high reactivity and strong accumulation properties [ 5 ], cisplatin is irreversibly bound to plasma proteins upon administration, leading to its low bioavailability.…”

Section: Introductionmentioning

confidence: 99%

Gelatin-Functionalized Carbon Nanotubes Loaded with Cisplatin for Anti-Cancer Therapy

Bao

Wang

et al. 2023

Polymers

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Cisplatin (Cp), a chemotherapeutic agent, interacts with purines on tumor DNA, causing tumor cell apoptosis. However, cisplatin has the characteristics of non-specific distribution and lack of selectivity, resulting in systemic toxicity. Moreover, it cannot maintain the drug’s high concentration in the tumor-weak acid environment. These flaws of cisplatin restrict its use in clinical applications. Therefore, a pH-responsive carbon nanotube-modified nano-drug delivery system (CNTs/Gel/Cp) was constructed in this study using gelatin (Gel)-modified carbon nanotubes (CNTs/Gel) loaded with cisplatin to release drugs precisely and slowly, preventing premature inactivation and maintaining an effective concentration. When MCp:MCNTs/Gel = 1:1, the drug reaches the highest loading rate and entrapment efficiency. To achieve the sustained-release effect, CNTs/Gel/Cp can release the medicine steadily for a long time in a pH environment of 6.0. Additionally, CNTs/Gel/Cp display antitumor properties comparable to cisplatin in a manner that varies with the dosage administered. These findings indicate that CNTs/Gel/Cp have an effective, sustained release of cisplatin and a good antitumor effect, providing a theoretical and experimental basis for the clinical application of modified carbon nanotubes (CNTs) as a new drug delivery system.

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Section: Introductionmentioning

confidence: 99%

Gelatin-Functionalized Carbon Nanotubes Loaded with Cisplatin for Anti-Cancer Therapy

Bao

Wang

et al. 2023

Polymers

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“…Among them chemotherapy is widely used for cancer treatment and includes neoadjuvant, adjuvant and combination chemotherapies [ 1 ]. The platinum-based drug cisplatin (cis-diaminedichloroplatinum) is one of the most effective anti-cancer agents and is a standard treatment for a wide range of cancer types [ 2 – 4 ]. Cisplatin goes through a process called aquation during which cisplatin becomes highly reactive where one or two chlorides in cisplatin will be replaced with water molecule inside the cell.…”

Section: Introductionmentioning

confidence: 99%

USP28 promotes tumorigenesis and cisplatin resistance by deubiquitinating MAST1 protein in cancer cells

Karapurkar,

Colaco,

Suresh

et al. 2024

Cell. Mol. Life Sci.

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Cisplatin is a chemotherapy drug that causes a plethora of DNA lesions and inhibits DNA transcription and replication, resulting in the induction of apoptosis in cancer cells. However, over time, patients develop resistance to cisplatin due to repeated treatment and thus the treatment efficacy is limited. Therefore, identifying an alternative therapeutic strategy combining cisplatin treatment along with targeting factors that drive cisplatin resistance is needed. CRISPR/Cas9 system-based genome-wide screening for the deubiquitinating enzyme (DUB) subfamily identified USP28 as a potential DUB that governs cisplatin resistance. USP28 regulates the protein level of microtubule-associated serine/threonine kinase 1 (MAST1), a common kinase whose expression is elevated in several cisplatin-resistant cancer cells. The expression level and protein turnover of MAST1 is a major factor driving cisplatin resistance in many cancer types. Here we report that the USP28 interacts and extends the half-life of MAST1 protein by its deubiquitinating activity. The expression pattern of USP28 and MAST1 showed a positive correlation across a panel of tested cancer cell lines and human clinical tissues. Additionally, CRISPR/Cas9-mediated gene knockout of USP28 in A549 and NCI-H1299 cells blocked MAST1-driven cisplatin resistance, resulting in suppressed cell proliferation, colony formation ability, migration and invasion in vitro. Finally, loss of USP28 destabilized MAST1 protein and attenuated tumor growth by sensitizing cells to cisplatin treatment in mouse xenograft model. We envision that targeting the USP28-MAST1 axis along with cisplatin treatment might be an alternative therapeutic strategy to overcome cisplatin resistance in cancer patients.

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MST1 interactomes profiling across cell death in esophageal squamous cell carcinoma

Zhang,

Gao,

et al. 2024

Medical Review

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Objectives Resistance to apoptosis in esophageal squamous cell carcinoma (ESCC) constitutes a significant impediment to treatment efficacy. Exploring alternative cell death pathways and their regulatory factors beyond apoptosis is crucial for overcoming drug resistance and enhancing therapeutic outcomes in ESCC. Methods Mammalian Ste 20-like kinase 1 (MST1) is implicated in regulating various cell deaths, including apoptosis, autophagy, and pyroptosis. Employing enhanced ascorbate peroxidase 2 (APEX2) proximity labeling coupled with immunoprecipitation-mass spectrometry (IP-MS), we elucidated the interactomes of MST1 across these three cell death paradigms. Results Proteomic profiling unveiled the functional roles and subcellular localization of MST1 and its interacting proteins during normal proliferation and various cell death processes. Notably, MST1 exhibited an expanded interactome during cell death compared to normal proliferation and chromosome remodeling functions consistently. In apoptosis, there was a notable increase of mitosis-associated proteins such as INCENP, ANLN, KIF23, SHCBP1 and SUPT16H, which interacted with MST1, alongside decreased expression of the pre-apoptotic protein STK3. During autophagy, the bindings of DNA repair-related proteins CBX8 and m6A reader YTHDC1 to MST1 were enhanced. In pyroptosis, LRRFIP2 and FLII which can inhibit pyroptosis increasingly binding to MST1. Conclusions Our findings delineate potential mechanisms through which MST1 and its interactomes regulate cell death, paving the way for further investigation to validate and consolidate these observations.

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New Advancements in Cisplatin-Based Treatments

Abstract: Cisplatin (cis-diamminedichloroplatinum (II)) is one of the most broadly used chemotherapies worldwide [...]

Cited by 3 publications

References 11 publications

Gelatin-Functionalized Carbon Nanotubes Loaded with Cisplatin for Anti-Cancer Therapy

Gelatin-Functionalized Carbon Nanotubes Loaded with Cisplatin for Anti-Cancer Therapy

USP28 promotes tumorigenesis and cisplatin resistance by deubiquitinating MAST1 protein in cancer cells

MST1 interactomes profiling across cell death in esophageal squamous cell carcinoma

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