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Fig. 3 | Journal of Translational Medicine

Fig. 3

From: UBE2T promotes autophagy via the p53/AMPK/mTOR signaling pathway in lung adenocarcinoma

Fig. 3

knockdown of UBE2T reduced autophagy by upregulating the expression of p53 and affecting its nuclear-cytoplasmic localization. A GSEA revealed the signaling pathways associated with UBE2T in NSCLC. B, C p53 expression levels were detected in UBE2T-deficient cells, UBE2T-overexpression cells, and the corresponding control cells via western blot analysis. D, F A549 cells infected with lentivirus-mediated shUBE2T were incubated in EBSS supplemented with or without pifithrin-a (PFT-a, 20 mM) for 8 h. After that, immunoblot analysis was performed with antibodies against LC3 and p62, separately. E, G The levels of nuclear p53 and cytoplasmic p53 in control cells and UBE2T deficient cells were examined after the separation of protein fractions using a cytoplasmic and nuclear extraction kit following the instruction. The effects of UBE2T on the AMPK/mTOR pathway were investigated. Cell lysis was subjected to western blot analysis with antibodies against p-AMPK, AMPK, p-mTOR, mTOR, and GAPDH. H, J UBE2T overexpression activated the AMPK/mTOR signaling pathway. I, K Silencing UBE2T inhibited the AMPK/mTOR signaling pathway. GAPDH was used as internal controls. All experiments were repeated at least three times. Protein bands were quantified using Image J. *P < 0.05, **P < 0.01, ***P < 0.001

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