Repository logoGCRIS
  • English
  • Türkçe
  • Русский
Log In
New user? Click here to register. Have you forgotten your password?
Home
Communities
Browse GCRIS
Entities
Overview
GCRIS Guide
  1. Home
  2. Browse by Author

Browsing by Author "Vakifahmetoglu, Cekdar"

Filter results by typing the first few letters
Now showing 1 - 2 of 2
  • Results Per Page
  • Sort Options
  • Loading...
    Thumbnail Image
    Article
    Enhanced Doxorubicin Cytotoxicity on Breast Cancer Spheroids by Aptamer Targeted Co-Delivery With Hyaluronidase
    (Wiley, 2025) Kavruk, Murat; Demirel, Dide Su; Bonyadi, Farzaneh; Guner, Buket Cakmak; Dursun, Ali Dogan; Vakifahmetoglu, Cekdar; Ozalp, Veli Cengiz
    Breast cancer is one of the most prevalent solid tumors in women and can be classified into subtypes based on molecular characteristics, such as hormone receptor status and HER2 expression. Aptamers, highly specific affinity molecules, are extensively studied for targeted drug delivery using nanocarriers to enhance anti-cancer efficacy. This study focused on HER2-responsive co-delivery of doxorubicin and hyaluronidase via aptamer-gated mesoporous silica nanoparticles to improve therapeutic outcomes in solid tumors. SK-BR-3 spheroids are employed as a model for resistant tumor environments in solid tumors. Previous research is shown that conjugating cytotoxic drugs with nanoparticles or cells enhances drug penetration into tumor spheroids. In this work, doxorubicin is loaded into mesoporous silica nanoparticles and capped with HER2-specific aptamers, while the particle surface is functionalized with hyaluronidase. This dual-functionalized nanocarrier system achieves an approximate to 8.5-fold increase in cytotoxicity compared to aptamer-targeted delivery lacking hyaluronidase. The enhanced effect is attributed to hyaluronidase-mediated loosening of the spheroid structure, facilitating nanoparticle penetration and localized release of doxorubicin at high concentrations on HER2-positive cells.
  • Loading...
    Thumbnail Image
    Article
    Citation - WoS: 3
    Citation - Scopus: 2
    Targeted Multidrug Delivery Systems To Kill Antibiotic-Resistant Staphylococcus Aureus
    (Elsevier, 2023) Ozalp, Veli Cengiz; Ucak, Samet; Dursun, Ali D.; Sudagidan, Mert; Icin, Oyku; Vakifahmetoglu, Cekdar; Gurlo, Aleksander
    Different ordered mesoporous silica (OMS) nanoparticles, ranging from regular COK-12 to COK-12 modified in terms of pore shape and size, have been employed as standard drug carriers for the controlled adsorption and release of drug molecules in comparison to well-known OMS SBA-15 and MCM-41. The cytotoxicity analysis demonstrated that regular COK-12 particles were less harmful to mammalian cultured cells, causing lower apoptosis induction than modified COK-12, MCM-41, and SBA-15 particles.Thus, regular COK-12 was further used to prepare a dual antibiotic-loaded drug delivery material, followed by surface functionalization with Staphylococcus aureus-specific aptamers for targeting. The results demonstrated that the joint loading of lysozyme and vancomycin in regular COK-12 improved the ability of the antibiotic treatments to kill methicillin-resistant Staphylococcus strains via aptamer targeting. The minimum inhibitory concentration (MIC) values decreased 4.1-fold and 12-fold compared to the non-targeted use of the antimicrobial agents in homogeneous solutions for vancomycin and lysozyme, respectively, clearly demonstrating the high potential of COK-12 to be used as a carrier in multidrug therapy.
Repository logo
Collections
  • Scopus Collection
  • WoS Collection
  • TrDizin Collection
  • PubMed Collection
Entities
  • Research Outputs
  • Organizations
  • Researchers
  • Projects
  • Awards
  • Equipments
  • Events
About
  • Contact
  • GCRIS
  • Research Ecosystems
  • Feedback
  • OAI-PMH
OpenAIRE Logo
OpenDOAR Logo
Jisc Open Policy Finder Logo
Harman Logo
Base Logo
OAI Logo
Handle System Logo
ROAR Logo
ROARMAP Logo
Google Scholar Logo

Log in to GCRIS Dashboard

Powered by Research Ecosystems

  • Privacy policy
  • End User Agreement
  • Feedback