Background: The tumor suppressor protein p53 is a most promising target for the development of anticancer drugs. Allicin (diallylthiosulfinate) is one of the most active components of garlic (Alliium sativum L.) and possesses a variety of health-promoting properties with pharmacological applications. However, whether allicin plays an anti-cancer role against breast cancer cells through the induction of p53-mediated apoptosis remains unknown.
Methods And Results: In this study, we investigate the anti-breast cancer effect of allicin in vitro by using MCF-7 and MD-MBA-231 cells. We found that allicin reduces cell viability, induces apoptosis and cell cycle arrest in both cells. Allicin activated p53 and caspase 3 expressions in both cells but produced different effects on the expression of p53-related biomarkers. In MDA-MB-231 cells, allicin up-regulated the mRNA and protein expression of A1BG and THBS1 while down-regulated the expression of TPM4. Conversely, the mRNA and protein expression of A1BG, THBS1 and TPM4 were all reduced in MCF-7 cells. Hence, allicin induces cell cycle arrest and apoptosis in breast cancer cells through p53 activation but it effects on the expression of p53-related biomarkers were dependent upon the specific type of breast cancer involved.
Conclusions: These findings suggest that allicin induces apoptosis and regulates biomarker expression in breast cancer cell lines through modulating the p53 signaling pathway. Furthermore, our results promote the utility of allicin as compound for further studies as an anticancer drug targeting p53.
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http://dx.doi.org/10.1007/s11033-021-06722-1 | DOI Listing |
Cancer Causes Control
December 2024
Department of Clinical Nutrition, the First Affiliated Hospital of Anhui Medical University, 218 Jixi Road, Hefei, 230022, Anhui, China.
Breast cancer is the leading cause of cancer-related death and the most common cancer among women worldwide. It is crucial to identify potentially modifiable risk factors to intervene and prevent breast cancer effectively. Sleep factors have emerged as a potentially novel risk factor for female breast cancer.
View Article and Find Full Text PDFDaru
December 2024
Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Objective(s): Some forms of breast cancer such as triple-negative phenotype, are serious challenge because of high metastatic cases, high mortality and resistance to conventional therapy motivated the search for alternative treatment approaches. Nanomaterials are promising candidates and suitable alternatives for improving tumor and cancer cell treatments.
Materials And Methods: Biosynthesis of ZnO NPs by help of Berberis integerrima fruit extract, has been done.
J Med Chem
December 2024
Department of Medicinal Chemistry, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
Rearranged during transfection (RET) kinase is a validated therapeutic target for various cancers characterized by RET alterations. Although two selective RET inhibitors, selpercatinib and pralsetinib, have been approved by the FDA, acquired resistance through solvent-front mutations has been identified rapidly. Developing proteolysis targeting chimera (PROTAC) targeting RET mutations offers a promising strategy to combat drug resistance.
View Article and Find Full Text PDFACS Biomater Sci Eng
December 2024
Future Industries Institute, University of South Australia, Mawson Lakes, South Australia 5095, Australia.
Polymer based nanoformulations offer substantial prospects for efficacious chemotherapy delivery. Here, we developed a pH-responsive polymeric nanoparticle based on acidosis-triggered breakdown of boronic ester linkers. A biocompatible hyaluronic acid (HA) matrix served as a substrate for carrying a doxorubicin (DOX) prodrug which also possesses natural affinity for CD44 cells.
View Article and Find Full Text PDFACS Nano
December 2024
The Fifth Affiliated Hospital, Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, the School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou 511436, China.
Tumor-specific cytotoxic T cell immunity is critically dependent on effective antigen presentation and sustained signal transduction. However, this immune response is frequently compromised by the inherently low immunogenicity of breast cancer and the deficiency in major histocompatibility complex class I (MHC-I) expression. Herein, a chimeric peptide-engineered stoichiometric polyprodrug (PDPP) is fabricated to potentiate the cytotoxic T cell response, characterized by a high drug loading capacity and precise stoichiometric drug ratio, of which the immunogenic cell death (ICD) inducer of protoporphyrin IX (PpIX) and the epigenetic drug of decitabine (DAC) are condensed into a polyprodrug called PpIX-DAC.
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