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. 2019 Apr 12;11:3171–3185. doi: 10.2147/CMAR.S195424

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© 2019 Gao et al.

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SLC5A1-regulated cancer cell growth is dependent on AMPK/mTOR signaling. (A) Immunoblotting analysis of phosphorylated-AMPK and mTOR with cell lysates from Panc-2 with or without SLC5A1 blockade and cultured with 0.5 mmol/L-glucose. Protein expression of phosphorylated-AMPK was increased while phosphorylated-MTOR was decreased in SLC5A1 blockade cells. (B) Pretreatment with compound C (1 μM) recovered the viability of SLC5A1 knockdown pancreatic cancer cells. (C) Compound C diminished the prolonged G0/G1 arrest induced in SLC5A1 knockdown Panc-1 and Panc-2 cells. (D) Compound C recovered the clonogenic survival in SLC5A1 knockdown Panc-1 and Panc-2 cells. *P<0.05.