Abstract Smart nanoparticles, which can respond to biological cues or be guided by them, are emerging as a promising drug delivery platform for precise cancer treatment. The field of oncology, nanotechnology, and biomedicine has witnessed rapid progress, leading to innovative developments in smart nanoparticles for safer and more effective cancer therapy. In this review, we will highlight recent advancements in smart nanoparticles, including polymeric nanoparticles, dendrimers, micelles, liposomes, protein nanoparticles, cell membrane nanoparticles, mesoporous silica nanoparticles, gold nanoparticles, iron oxide nanoparticles, quantum dots, carbon nanotubes, black phosphorus, MOF nanoparticles, and others. We will focus on their classification, structures, synthesis, and intelligent features. These smart nanoparticles possess the ability to respond to various external and internal stimuli, such as enzymes, pH, temperature, optics, and magnetism, making them intelligent systems. Additionally, this review will explore the latest studies on tumor targeting by functionalizing the surfaces of smart nanoparticles with tumor-specific ligands like antibodies, peptides, transferrin, and folic acid. We will also summarize different types of drug delivery options, including small molecules, peptides, proteins, nucleic acids, and even living cells, for their potential use in cancer therapy. While the potential of smart nanoparticles is promising, we will also acknowledge the challenges and clinical prospects associated with their use. Finally, we will propose a blueprint that involves the use of artificial intelligence-powered nanoparticles in cancer treatment applications. By harnessing the potential of smart nanoparticles, this review aims to usher in a new era of precise and personalized cancer therapy, providing patients with individualized treatment options. 

Smart nanoparticles for cancer therapy

Rational combinations of targeted cancer therapies: background, advances and challenges

The great clinical success of cisplatin and its derivatives has convinced people that metal complexes could play a more significant role in human cancer therapy. However, targeting and drug resistance are still two dominant problems that need to be urgently solved for metallodrugs' efficacy and clinical translation. As an important component of metal complexes, organometallics have been experiencing rapid development in recent years. Compared with platinum drugs, emerging anti-tumor organometallics targeting dynamic bioprocesses provide an effective strategy to overcome conventional problems. This review focuses on burgeoning anti-tumor strategies and provides up-to-date advances in anti-tumor organometallics development based on their action mechanisms. Specifically, important tumor-overexpressed proteins and nucleic acids as organometallics' anti-tumor targets are systematically presented, followed by organometallics that exert their anti-tumor activity by perturbing tumor intracellular energy/redox/metal/immune homeostasis. Finally, nine cell death pathways including apoptosis, paraptosis, autophagy, oncosis, necrosis, necroptosis, ferroptosis, pyroptosis, and immunogenic cell death (ICD) that can be induced by organometallics are reviewed, and their morphological and biochemical features are summarised. This review at the interface of chemistry, biology, and medicine aims to enlighten the rational development of organometallic anti-tumor agents.

Organometallic anti-tumor agents: targeting from biomolecules to dynamic bioprocesses.

Triple-negative breast cancer (TNBC) is still the most aggressive cancer in women. Combination chemotherapy holds great potential for cancer therapy; however, the off-target and side effects of free chemotherapy administration remain a major challenge. In this study, we developed a photo/thermo-responsive nanoplatform that can be used for TNBC treatment via photothermic therapy in combination with multidrug therapy. By conjugating the chemotherapy drug PTX prodrug on the surface of mesoporous silica-coated gold nanorod nanoparticles and then loading another chemotherapy drug, CPT, the Au@MSN-PTX@CPT nanoparticles exhibited great photothermal response, redox response drug release and cancer cell inhibition abilities. Otherwise, we further coated the Au@MSN-PTX@CPT nanoparticle with a temperature-sensitive polymer poly(N-isopropylacrylamide-co-methacrylic acid) (p(NIPAM-co-MAAc)), and the polymer-coated Au@MSN-PTX@TPT@polymer nanoparticles showed perfect near-infrared (NIR) light controlled drug release. Finally, the Au@MSN-PTX@CPT@polymer nanoparticles were injected into the 4T1 breast cancer mouse model. The Au@MSN-PTX@CPT@polymer nanoparticles preferably accumulated at the tumor site and had reduced chemotherapy injuries and great antitumor activity when combined with 650 nm laser treatment. In summary, our developed Au@MSN-PTX@CPT@polymer nanoparticles served as a good method for controlled chemodrug delivery and provided a good choice for TNBC combination therapy. 

Co‐delivery CPT and PTX prodrug with a photo/thermo‐responsive nanoplatform for triple‐negative breast cancer therapy

Abstract Glioblastoma multiforme (GBM) is the most lethal primary brain tumor with a poor median survival of less than 15 months. However, clinical strategies and effective therapies are limited. Here, we found that the second-generation small molecule multi-CDK inhibitor AT7519 is a potential drug for GBM treatment according to high-throughput screening via the Approved Drug Library and Clinical Compound Library (2718 compounds). We found that AT7519 significantly inhibited the cell viability and proliferation of U87MG, U251, and patient-derived primary GBM cells in a dose-dependent manner. Furthermore, AT7519 also inhibited the phosphorylation of CDK1/2 and arrested the cell cycle at the G1-S and G2-M phases. More importantly, AT7519 induced intrinsic apoptosis and pyroptosis via caspase-3-mediated cleavage of gasdermin E (GSDME). In the glioblastoma intracranial and subcutaneous xenograft assays, tumor volume was significantly reduced after treatment with AT7519. In summary, AT7519 induces cell death through multiple pathways and inhibits glioblastoma growth, indicating that AT7519 is a potential chemical available for GBM treatment. 

/pdf/the-cdk-inhibitor-at7519-inhibits-human-glioblastoma-cell-2z37j3w2.pdf

The CDK inhibitor AT7519 inhibits human glioblastoma cell growth by inducing apoptosis, pyroptosis and cell cycle arrest

Abstract Combinations of anti-cancer drugs can overcome resistance and provide new treatments 1,2 . The number of possible drug combinations vastly exceeds what could be tested clinically. Efforts to systematically identify active combinations and the tissues and molecular contexts in which they are most effective could accelerate the development of combination treatments. Here we evaluate the potency and efficacy of 2,025 clinically relevant two-drug combinations, generating a dataset encompassing 125 molecularly characterized breast, colorectal and pancreatic cancer cell lines. We show that synergy between drugs is rare and highly context-dependent, and that combinations of targeted agents are most likely to be synergistic. We incorporate multi-omic molecular features to identify combination biomarkers and specify synergistic drug combinations and their active contexts, including in basal-like breast cancer, and microsatellite-stable or KRAS -mutant colon cancer. Our results show that irinotecan and CHEK1 inhibition have synergistic effects in microsatellite-stable or KRAS – TP53 double-mutant colon cancer cells, leading to apoptosis and suppression of tumour xenograft growth. This study identifies clinically relevant effective drug combinations in distinct molecular subpopulations and is a resource to guide rational efforts to develop combinatorial drug treatments. 

/pdf/effective-drug-combinations-in-breast-colon-and-pancreatic-2dvvo9m0.pdf

Effective drug combinations in breast, colon and pancreatic cancer cells

/pdf/effective-drug-combinations-in-breast-colon-and-pancreatic-1qx97xoh.pdf

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Effective drug combinations in breast, colon and pancreatic cancer cells

Effective drug combinations in breast, colon and pancreatic cancer cells