Dataset Information

Fasting, FDFT1 expression and colorectal cancer

ABSTRACT: First, lentivirus-mediated overexpression of FDFT1 and lentivirus-mediated knockdown of FDFT1 were performed in CT26 cells. Then control CT26 cells, FDFT1 overexpressing CT26 cells and FDFT1 knockdown CT26 cells were cultured under normal medium or fasting mimic medium. Fasting mimic medium was done by incubating cells in glucose-free DMEM (Gibco, USA) supplemented with 0.5g/L glucose and 1% FBS for 48h. So we have 6 groups: control CT26 cells, FDFT1 overexpressing CT26 cells, FDFT1 knockdown CT26 cells, control CT26 cells-under fasting mimic medium, FDFT1 overexpressing CT26 cells- under fasting mimic medium, FDFT1 knockdown CT26 cells- under fasting mimic medium.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Colon

DISEASE(S): Colon Cancer

SUBMITTER: Xiao Zhen

LAB HEAD: Meilin Weng

PROVIDER: PXD012029 | Pride | 2020-03-19

REPOSITORIES: Pride

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Publications

Fasting inhibits aerobic glycolysis and proliferation in colorectal cancer via the Fdft1-mediated AKT/mTOR/HIF1α pathway suppression.

Weng Mei-Lin ML Chen Wan-Kun WK Chen Xiang-Yuan XY Lu Hong H Sun Zhi-Rong ZR Yu Qi Q Sun Peng-Fei PF Xu Ya-Jun YJ Zhu Min-Min MM Jiang Nan N Zhang Jin J Zhang Jian-Ping JP Song Yuan-Lin YL Ma Duan D Zhang Xiao-Ping XP Miao Chang-Hong CH Miao Chang-Hong CH

Nature communications 20200420 1

Evidence suggests that fasting exerts extensive antitumor effects in various cancers, including colorectal cancer (CRC). However, the mechanism behind this response is unclear. We investigate the effect of fasting on glucose metabolism and malignancy in CRC. We find that fasting upregulates the expression of a cholesterogenic gene, Farnesyl-Diphosphate Farnesyltransferase 1 (FDFT1), during the inhibition of CRC cell aerobic glycolysis and proliferation. In addition, the downregulation of FDFT1 i ...[more]

PMID: 32313017

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Project description:Selenium has cancer preventive activity that is mediated, in part, through selenoproteins. The role of the 15 kDa selenoprotein (Sep15) in colon cancer was assessed by preparing and using mouse colon CT26 cells stably transfected with shRNA constructs targeting Sep15. Metabolic 75Se-labeling and Northern and Western blot analyses revealed that more than 90% of Sep15 was knocked down. Growth of the resulting Sep15-deficient CT26 cells was reduced (p<0.01) and cells formed significantly (p<0.001) fewer colonies in soft agar compared to control CT26 cells. Whereas most (14/15) BALB/c mice injected with control cells developed tumors, few (3/30) mice injected with Sep15 knockdown cells developed tumors (p<0.0001). The ability to form pulmonary metastases had similar results. Mice injected with the plasmid-transfected control cells had >250 lung metastases/mouse; however, mice injected with the Sep15 knockdown cells only had 7.8 +/- 5.4 metastases. To investigate molecular targets affected by Sep15 status, gene expression patterns between control and knockdown CT26 cells were compared. Ingenuity Pathways Analysis was used to analyze the 1045 genes that were significantly (p<0.001) affected by Sep15 deficiency. The highest scored biological functions were cancer and cellular growth and proliferation. Consistent with these observations, subsequent analyses revealed a G2/M cell cycle arrest in Sep15 CT26 knockdown cells. In contrast, to CT26 cells Sep15 knockdown in Lewis Lung Carcinoma (LLC1) cells did not affect anchorage-dependent or M-bM-^@M-^Sindependent cell growth. These data suggest tissue specificity in the cancer protective effects of Sep15 knockdown, which are mediated, at least in part, by influencing the cell cycle. mRNA was isolated from plasmid-transfected control and shSep15 knockdown CT26 cells (three replicates of each). Microarray analysis was performed on Affymetrix Mouse 430_2 gene chips. Three arrays were analyzed from different mRNA samples for each construct.

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