Galangin-Loaded Chitosan Nanoparticles Inhibit Lung Cancer Cell Proliferation Via Cell Cycle Arrest and Cyclin-Dependent Kinase Modulation

被引:0
作者
Bepari, Asmatanzeem [1 ]
Niazi, Shaik Kalimulla [2 ]
Khaled, Yomna [3 ]
Shaikh, Mujeeb Ahmed [4 ]
Shaikh, Farha M. [4 ]
Al-Zharani, Mohammed [5 ]
Nasr, Fahd A. [5 ]
Chandrashekhar, Sarala [6 ]
Bepari, Uzma [6 ]
Altamimi, Hanan Nasser [7 ]
机构
[1] Princess Nourah Bint Abdulrahman Univ, Coll Med, Dept Basic Hlth Sci, Riyadh 11671, Saudi Arabia
[2] Riyadh Elm Univ, Dept Preparatory Hlth Sci, Riyadh 13244, Saudi Arabia
[3] Princess Nourah Bint Abdulrahman Univ, Coll Med, Dept Internal Med, Riyadh 11671, Saudi Arabia
[4] AlMaarefa Univ, Coll Med, Dept Basic Med Sci, Riyadh 13713, Saudi Arabia
[5] Imam Mohammad Ibn Saud Islamic Univ IMSIU, Coll Sci, Dept Biol, Riyadh 11623, Saudi Arabia
[6] Cauvery Heart & Multispecial Hosp, Dept Obstret & Gynaecol, Mysuru 570029, India
[7] Prince Sattam Bin Abdulaziz Univ, Coll Appl Med Sci, Dept Med Lab, Al Kharj 11942, Saudi Arabia
关键词
Galangin; Chitosan nanoaprticles; Cyclin-dependent kinases; Proliferation; Lung cancer; D1; APOPTOSIS;
D O I
10.1007/s10904-025-03901-6
中图分类号
O63 [高分子化学(高聚物)];
学科分类号
070305 ; 080501 ; 081704 ;
摘要
Lung carcinoma, which is among the primary causes of cancer-related mortality globally, emphasizes the critical need for more effective and focused treatment strategies. The production, properties, and anticancer properties of galangin-loaded chitosan composites (GLG-CSNCs) targeting A549 lung carcinoma cells were examined in this work. The synthesised GLG-CSNCS were then exposed to A549 lung cancer cells for 24 h to assess their cytotoxicity using the MTT assay; mitochondrial damage was analyzed using MitoTracker staining, and cell cycle progression was analyzed by flow cytometry. Furthermore, apoptosis-related molecules, cyclins, and cell cycle-regulated proteins were all analyzed using Western blot analysis. GLG-CSNCs were found to have an average particle size of 121.5 nm. In lung cancer cells, GLG-CSNC treatment resulted in considerable cytotoxicity and mitochondrial damage. Western blot tests also confirmed that key cyclin-dependent kinases (Cyclin D1, CDK4) and their regulatory cyclins were reduced, whereas the CDK inhibitor p21 was elevated. These findings suggest that GLG-CSNCs effectively halt the cell cycle's G1 phase, which stops cancer cells from proliferating. Overall, our study demonstrates that by causing G1 phase arrest of the cell cycle and modifying cyclin-dependent kinase, GLG-CSNCs have potential as a new, biocompatible nanotherapeutic element employed in the treatment of lung malignancy.
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页数:16
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