Cellular Proliferation

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The relationship between cellular proliferation and energy metabolism is investigated using cancer Hela cells. Tumor cells need to generate an ample amount of ATP(Adenosine triphosphate)in order to synthesis bioactive compounds like lipids, proteins, and nucleotides for rapid cell proliferation[1]. The generation of this ATP is vital for cell division and other basic function to the regulation of cell volume, solute concentration, and cellular architecture[2][3][4]. ATP’s role in the basic function in the cells makes the cell cycle sensitive to changes in availability of mitochondrion derived ATP[5]. In fact, ATP levels differ at various stages of the cell cycle[5]. Additionally reports have shown that cells fail to transition between different stages of the cell cycle under diminished levels of ATP[2]. It is confirmed that interfering with the mitochondrial Oxidative Phosphorylation(OxsPhos) pathway would cause cell cycle arrest since the majority of ATP is produced through OsxPhos pathway[6]. Additionally reports have shown that there is a low energy cell cycle checkpoint that monitors the energy capability before committing to another round of cell division[7].

References

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  1. ^ Weinberg, Frank; Chandel, Navdeep S. (2009). "Mitochondrial Metabolism and Cancer". Annals of the New York Academy of Sciences. 1177 (1): 66–73. doi:10.1111/j.1749-6632.2009.05039.x. ISSN 0077-8923.
  2. ^ Pedersen, Peter L. (1994). "ATP Synthase: The machine that makes ATP". Current Biology. 4 (12): 1138–1141. doi:10.1016/S0960-9822(00)00257-8. ISSN 0960-9822.
  3. ^ Pattappa, Girish; Heywood, Hannah K.; de Bruijn, Joost D.; Lee, David A. (2011). "The metabolism of human mesenchymal stem cells during proliferation and differentiation". Journal of Cellular Physiology. 226 (10): 2562–2570. doi:10.1002/jcp.22605. ISSN 0021-9541.
  4. ^ Agarwal, Bhawana (2011). "A role for anions in ATP synthesis and its molecular mechanistic interpretation". Journal of Bioenergetics and Biomembranes. 43 (3): 299–310. doi:10.1007/s10863-011-9358-3. ISSN 0145-479X.
  5. ^ a b Sweet, S.; Singh, G. (1999). "Changes in mitochondrial mass, membrane potential, and cellular adenosine triphosphate content during the cell cycle of human leukemic (HL-60) cells". Journal of Cellular Physiology. 180 (1): 91–96. doi:10.1002/(SICI)1097-4652(199907)180:1<91::AID-JCP10>3.0.CO;2-6. ISSN 0021-9541.
  6. ^ Moreno-Sánchez, Rafael; Rodríguez-Enríquez, Sara; Marín-Hernández, Alvaro; Saavedra, Emma (2007). "Energy metabolism in tumor cells". FEBS Journal. 274 (6): 1393–1418. doi:10.1111/j.1742-4658.2007.05686.x. ISSN 1742-464X.
  7. ^ McBride, Heidi M.; Neuspiel, Margaret; Wasiak, Sylwia (2006). "Mitochondria: More Than Just a Powerhouse". Current Biology. 16 (14): R551–R560. doi:10.1016/j.cub.2006.06.054. ISSN 0960-9822.

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/PlantABCTransporterSandbox

  1. ^ Sekine, K.; Takubo, K.; Kikuchi, R.; Nishimoto, M.; Kitagawa, M.; Abe, F.; Nishikawa, K.; Tsuruo, T.; Naito, M. (2008). "Small Molecules Destabilize cIAP1 by Activating Auto-ubiquitylation". Journal of Biological Chemistry. 283 (14): 8961–8968. doi:10.1074/jbc.M709525200. ISSN 0021-9258.{{cite journal}}: CS1 maint: unflagged free DOI (link)