Epigallocatechin3gallate and simvastatin inhibit myeloma cancer cells proliferation by apoptosis and cell cycle arrest upregulation.

Khalifa, Eman; Ramadan, Lamiaa Mohamed Mahmoud; shabana, El shaimaa; Ghanem, Reham A.; El beltagy, Nanis Salah El metwally; Nouh, Walaa E.; Abuelnader, Eman Hamed Mohamed

doi:10.21608/ejchem.2025.339837.10900

	Epigallocatechin3gallate and simvastatin inhibit myeloma cancer cells proliferation by apoptosis and cell cycle arrest upregulation.
Egyptian Journal of Chemistry
Articles in Press, Accepted Manuscript, Available Online from 22 April 2025
Document Type: Original Article
DOI: 10.21608/ejchem.2025.339837.10900
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Authors
Eman Khalifa ¹; Lamiaa Mohamed Mahmoud Ramadan ²; El shaimaa shabana ³; Reham A. Ghanem ⁴; Nanis Salah El metwally El beltagy ⁵; Walaa E. Nouh ⁶; Eman Hamed Mohamed Abuelnader ⁷
¹Medical laboratories department, Faculty of applied health science technology, Nile Valley University, Fayoum, Egypt.
²Lamiaa M. Ramadan Department of Biochemistry, Biotechnology Research Institute, National Research Centre.
³fellow of biochemistry genetic unit children hospital faculty of medicine mansoura university
⁴Oral biology department, faculty of oral and dental medicine, Delta university for science and technology, Gamasa, Egypt
⁵Fellow of microbiology/Medical Analysis,Mansoura University Children’s Hospital Faculty of Medicine
⁶Mansoura University Children's Hospital, Faculty of Medicine, Mansoura University, Mansoura, Egypt
⁷Fellow of biochemistry/Medical Analysis, Mansoura University Children’s Hospital, Faculty of Medicine
Abstract
Abstract Myeloma cancer (MC) is the second most common hematologic malignancy. It represents a clonal disorder of plasma B-cells arising in the bone marrow. Despite the wide advance in treatment options over recent years, the disease remains incurable. The current study was designed to evaluate Epigallocatechin3gallate (ECG) and simvastatin (SVN) anticancer effect on MC cells. MC cells were divided into the control, MC+ECG, MC+SVN, and MC+ECG+SVN groups. MC cells proliferation in all groups was evaluated using cell morphological status, qRT-PCR was used to analyze apoptotic gene expression, the cell cycle was examined using flowcytometry, and biochemical analysis of oxidative and antioxidant mediators was determined. The doses of ECG (100µmol/L) and SVN (0.1µmol/L) induced cytotoxicity in about 60% of myeloma cells. ECG induced apoptotic genes upregulation (P53, poly (ADP-ribose) polymerase 1 (PARP-1), B-cell leukemia/lymphoma 2 (Bcl-2)-associated protein x (Bax), and caspase-3), and anti-apoptotic gene downregulation (Bcl-2). Moreover, the current regimens have a potent effect on cancer cell growth through G2/M arrest, as observed Graphical abstract figure. The current regimens induced oxidative stress downregulation and antioxidant enzymes activity upregulation. In conclusion, both ECG and/or simvastatin caused MC cell toxicity. Nevertheless, the synergistic influence of ECG and simvastatin possesses a more potent consequence on minimizing the resistance of tumor cell and killing tumor cells.
Keywords
Keywords: Myeloma cancer cells; ECG; Simvastatin; apoptosis; cell cycle


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