Version 1
: Received: 19 September 2024 / Approved: 20 September 2024 / Online: 23 September 2024 (08:45:31 CEST)
How to cite:
Negrea, G. G.; Balacescu, L.; Sesarman, A.; Banciu, M. Under Normoxia Simvastatin Shifts Lipid Metabolism of B16.F10 Melanoma Cells to Support Their Aggressiveness. Preprints2024, 2024091655. https://doi.org/10.20944/preprints202409.1655.v1
Negrea, G. G.; Balacescu, L.; Sesarman, A.; Banciu, M. Under Normoxia Simvastatin Shifts Lipid Metabolism of B16.F10 Melanoma Cells to Support Their Aggressiveness. Preprints 2024, 2024091655. https://doi.org/10.20944/preprints202409.1655.v1
Negrea, G. G.; Balacescu, L.; Sesarman, A.; Banciu, M. Under Normoxia Simvastatin Shifts Lipid Metabolism of B16.F10 Melanoma Cells to Support Their Aggressiveness. Preprints2024, 2024091655. https://doi.org/10.20944/preprints202409.1655.v1
APA Style
Negrea, G. G., Balacescu, L., Sesarman, A., & Banciu, M. (2024). Under Normoxia Simvastatin Shifts Lipid Metabolism of B16.F10 Melanoma Cells to Support Their Aggressiveness. Preprints. https://doi.org/10.20944/preprints202409.1655.v1
Chicago/Turabian Style
Negrea, G. G., Alina Sesarman and Manuela Banciu. 2024 "Under Normoxia Simvastatin Shifts Lipid Metabolism of B16.F10 Melanoma Cells to Support Their Aggressiveness" Preprints. https://doi.org/10.20944/preprints202409.1655.v1
Abstract
Our previous studies demonstrated a tight connection between simvastatin (SIM) inhibition of B16.F10 murine melanoma cell proliferation in vivo and in vitro and strong suppression of the subunit α of hypoxia inducible factor 1 (HIF-1) (HIF-1 α) production in these cancer cells. Since the translation of HIF-1α is modulated by signaling pathways coordinated by Akt, SIM effects on the link between these two regulatory factors and cancer cell metabolism under normoxia was investigated, which to our knowledge have never been described before. To achieve the proposed aim, SIM effects on cell metabolism were analysed at mRNA (via RNA-seq and RT-qPCR) as well as protein level (via western blot and catalytic activity of the key enzymes) Our data suggested that SIM might orientate glucose transport and metabolism to ensure replenishment of tricarboxylic acid (TCA) cycle activity. Moreover, it seems that SIM enhanced biosynthetic role of TCA over its energy role to further support synthesis of lipid-derived signaling molecules. Thus, under normoxia SIM treatment orientated lipid metabolism to stimulate isoprenoid and prostaglandin synthesis which might favor melanoma cell survival and aggressiveness.
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
