Mesoporous Silica Nanoparticles Are Nanocarrier for Drug Loading and Induces Cell Death in Breast Cancer

Harini, Lakshminarasimhan; Karthikeyan, B.; Viswanathan, Thimma Mohan; Kumar, Nachimuthu Senthil; Sundar, Krishnan; Kathiresan, Thandavarayan

doi:10.1007/978-3-030-77795-1_8

Cited by 2 publications

(1 citation statement)

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“…Hence, 2 to 6 µg of nanocarrier were adopted for loading of guanidine and guanidine-curcumin in these experiments [ 45 ]. In the cytotoxicity assay, 30 µM of curcumin induced 50% of cell death in MCF-7 [ 19 , 46 ] and the IC 50 values of free guanidine, Gu-HMSNAP, and GuC-HMSNAP were 40, 35, and 25 µM, respectively, at 24 h ( Figure 7 a). Therefore, cell death induced by guanidine alone and by guanidine–curcumin complex were directly correlated in a dose- and time-dependent manner.…”

Section: Resultsmentioning

confidence: 99%

Guanidine–Curcumin Complex-Loaded Amine-Functionalised Hollow Mesoporous Silica Nanoparticles for Breast Cancer Therapy

Viswanathan

Chitradevi

Zochedh

et al. 2022

Cancers

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The current study focuses on developing a tumour-targeted functionalised nanocarrier that wraps hollow mesoporous silica nanoparticles. The guanidine carbonate and curcumin are immobilised on the surface of 3-aminopropyl-triethoxy silane (APTES)-decorated hollow mesoporous silica nanoparticles (HMSNP), as confirmed through XPS and NMR analysis. XPS analysis demonstrates that the shape of the hysteresis loops is modified and that pore volume and pore diameter are consequently decreased compared to control. Guanidine (85%) and guanidine–curcumin complex (90%) were successfully encapsulated in HMSNAP and showed a 90% effective and sustained release at pH 7.4 for up to 72 h. Acridine orange/ethidium bromide dual staining determined that GuC-HMNSAP induced more late apoptosis and necrosis at 48 and 72 h compared with Gu-HMNSAP-treated cells. Molecular investigation of guanidine-mediated apoptosis was analysed using western blotting. It was found that cleaved caspases, c-PARP, and GSK-3β (Ser9) had increased activity in MCF-7 cells. GuC-HMSNAP increased the activity of phosphorylation of oncogenic proteins such as Akt (Ser473), c-Raf (Ser249), PDK1 (Ser241), PTEN (Ser380), and GSK-3β (Ser9), thus inducing cell death in MCF-7 cells. Altogether, our findings confirm that GuC-HMNSAP induces cell death by precisely associating with tumour-suppressing proteins, which may lead to new therapeutic approaches for breast cancer therapy.

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Section: Resultsmentioning

confidence: 99%