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Background: Our study aims to investigate the effect of colon cancer-associated transcript-1 (CCAT-1) on colon cancer cells' activity and metabolism under different glucose environments and .
Methods: The levels of proliferation, migration, glucose, lactic acid, glucose metabolism-related enzymes, apoptosis genes, epithelial-mesenchymal transition (EMT) marker proteins, and PI3K/Akt/C-MYC pathway in -silenced SW620 cells cultured with different glucose levels were tested. Twenty BALB/C nude mice with hyperglycemia or normal blood sugar were transplanted with -silenced SW620 cells, blood glucose levels, lactic acid, insulin, and volume of transplanted tumor cells, the expression of EMT marker proteins, and PI3K/Akt/C-MYC pathway was detected.
Results: The levels of proliferation, migration, glucose, lactic acid, LDH-A, PKM2, and HK2 decreased, apoptosis increased in SW620 cells cultured with low glucose or silenced (P<0.05); levels of E-cadherin and ZO-1 significantly increased, and levels of N-cadherin, vimentin, and p-Akt decreased in CCAT-1-silenced SW620 cells cultured with high glucose (P<0.05). Hyperglycemic nude mice transplanted with CCAT-1-silenced colon cancer cells showed decreased tumor volume, blood glucose, lactic acid, insulin, P-AKT, and P-C-MYC than EV group (P<0.05).
Conclusions: can enhance glucose metabolism and proliferation and migration of colon cancer cells by upregulating the expression of glycolysis enzymes, inhibiting apoptosis, activating the Akt/C-MYC pathway, and promoting EMT expression.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7807285 | PMC |
| http://dx.doi.org/10.21037/jgo-20-474 | DOI Listing |
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