Digman, M. A. | Search bioRxiv

bioRxiv2018

Collagen stiffness modulates MDA-MB231 cell metabolism through adhesion-mediated contractility

O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=148 SRC=\"FIGDIR/small/272948_fig1A.gif\" ALT=\"Figure 1A\">\nView larger version (39K):\norg.highwire.dtl.DTLVardef@1529bb0org.highwire.dtl.DTLVardef@6b656borg.highwire.dtl.DTLVardef@cf7c05org.highwire.dtl.DTLVardef@1d76412_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOAbstract Figure:C_FLOATNO Increasing collagen stiffness causes a shift in highly invasive MDA-MB231 cancer cells from glycolysis to oxidative phosphorylation. Glioma U251MG cells show an opposite trend and MCF10A non-tumorigenic cells have little change in metabolism signatures in response to substrates stiffness.\n\nC_FIG

cancer biology↗

bioRxiv2017

Restoring p53 Function and Silencing REV3L Suppresses the Cancerous Metabolic Phenotype in Cisplatin Treated Human Non-Small Lung Carcinoma Cells

Lung cancer is one of the deadliest cancers in the world accounting for over one-quarter of all cancer-related deaths, but in many cases, the cancer can develop a resistance to the cisplatin-based chemotherapies. It is well known that cancer cells exhibit the Warburg effect and some studies have suggested that cancer cell metabolism may be linked to cisplatin resistance. In this study, the effects of tumor suppressor protein p53 and translesional synthesis protein REV3L are studied to relate DNA damage signaling and repair to cellular metabolism by using the fluorescence lifetime of the metabolic coenzyme NADH. It was found that simultaneously restoring function to p53 and silencing REV3L suppressed the cancerous metabolic phenotype and resulted in the greatest amount of cancer cell death. This study demonstrates a previously unrecognized relationship between p53 and REV3L in cellular metabolism and may lead to improvements in chemotherapy treatment plans that reduce cisplatin resistance in cancer cells.

cancer biology↗