Verapamil-induced autophagy-like process in colon adenocarcinoma COLO 205 cells; the ultrastructural studies

التفاصيل البيبلوغرافية
العنوان: Verapamil-induced autophagy-like process in colon adenocarcinoma COLO 205 cells; the ultrastructural studies
المؤلفون: Barbara Gajkowska, Beata Pająk, Elżbieta Kania, Arkadiusz Orzechowski
المصدر: Pharmacological Reports. 64:991-996
بيانات النشر: Springer Science and Business Media LLC, 2012.
سنة النشر: 2012
مصطلحات موضوعية: Pathology, medicine.medical_specialty, Programmed cell death, Necrosis, Cell, Apoptosis, Adenocarcinoma, Biology, Cell Line, Tumor, Autophagy, medicine, Humans, Pharmacology, Cell Membrane, General Medicine, medicine.disease, Chromatin, medicine.anatomical_structure, Verapamil, Cell culture, Colonic Neoplasms, Cancer cell, Cancer research, medicine.symptom, medicine.drug
الوصف: Background Verapamil (Ver) is a well known, worldwide used drug to correct cardiac arrhythmias. The main Ver target is the L-type calcium channel. Modulation of calcium homeostasis vaulted Ver into use in medical applications. Methods To examine COLO 205 cells morphology after Ver treatment, an electron microscopy technique was used. Results This study shows ultrastructural evidence that Ver initiates autophagy-like process in human colon adenocarcinoma COLO 205 cells. TEM photographs revealed the presence of differently developed autophagic vacuoles in response to Ver administration. Furthermore, extensive ultrastructural cell alterations confirmed that cancer cells died via necrosis or apoptosis, as demonstrated by ruptured plasma membrane or condensed chromatin, respectively. Conclusion It is the evidence that apoptosis resistant COLO 205 cells are overruled by autophagy-like process. Autophagy-like cell death could be a promising venue to delete cancer cells. Ver appears to be a new potentially effective anticancer compound.
تدمد: 1734-1140
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1baabcfabd8d87fac0745464e3c5ceb4
https://doi.org/10.1016/s1734-1140(12)70896-4
حقوق: CLOSED
رقم الأكسشن: edsair.doi.dedup.....1baabcfabd8d87fac0745464e3c5ceb4
قاعدة البيانات: OpenAIRE