Novel silicene-mesoporous silica nanoparticles conjugated Gemcitabine induced cellular apoptosis via upregulating NF-κB p65 nuclear translocation suppresses pancreatic cancer growth in vitro and in vivo.
Yuhang ChenChien-Shan ChengPeiwen YangShu DongLianyu Chen ChenPublished in: Nanotechnology (2024)
Pancreatic cancer's high fatality rates stem from its resistance to systemic drug delivery and aggressive metastasis, limiting the efficacy of conventional treatments. In this study, two-dimensional ultrathin silicene nanosheets (SN) were initially synthesized and near-infrared-responsive two-dimensional silicene-mesoporous silica nanoparticles (SMSNs) were successfully constructed to load the clinically-approved conventional pancreatic cancer chemotherapeutic drug Gemcitabine. Experiments on nanoparticle characterization show that they have excellent photothermal conversion ability and stability. Then silicene-mesoporous silica nanoparticles loaded with Gemcitabine nanoparticles (SMSN@G NPs) were employed in localized photothermal therapy to control pancreatic tumor growth and achieve therapeutic effects. Our research confirmed the functionality of SMSN@G NPs through immunoblotting and apoptotic assays, demonstrating its capacity to enhance the nuclear translocation of the NF-κB p65, further affect the protein levels of apoptosis-related genes, induce the apoptosis of tumor cells, and ultimately inhibit the growth of the tumor. Additionally, the study assessed the inhibitory role of SMSN@G NPs on pancreatic neoplasm growth in vivo, revealing its excellent biocompatibility. SMSN@G NPs have a nice application prospect for anti-pancreatic tumors.
Keyphrases
- drug delivery
- oxidative stress
- cell death
- cancer therapy
- signaling pathway
- endoplasmic reticulum stress
- cell cycle arrest
- oxide nanoparticles
- pi k akt
- photodynamic therapy
- nuclear factor
- emergency department
- drug induced
- squamous cell carcinoma
- walled carbon nanotubes
- gold nanoparticles
- immune response
- high grade
- single cell
- amino acid
- binding protein
- stress induced
- transition metal