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. 2019 Nov 12;39(11):BSR20192453. doi: 10.1042/BSR20192453

Figure 2. LncRNAs regulate PKM2 expression to inhibit cancer cell metabolism via PTEN and PI3K/AKT/mTOR signal pathway.

Figure 2

(A) MEG3 promotes β-catenin degradation through a PTEN-dependent ubiquitin–proteasome system. Thus, MEG3 inhibits β-catenin activity through PKM2 reduction and PTEN increase. (B) LincRNA-p21 is a negative regulator of PKM2. The regulatory mechanism of PKM2 mediated by LincRNA-p21 depends on the PTEN/AKT/mTOR cascade. (C) When HULC is overexpressed, HULC increases autophagy by increasing the expression of LC3I and LC3II. At the same time, HULC enhances the interaction between LC3 and ATG3. Thus, HULC inhibits PTEN through enhancing the cellular autophagy by increasing ubiquitin–proteasome dependent LC3II. The result is activation of the AKT-PI3K-mTOR pathway to inhibit tumor cell growth and metabolism when PTEN is reduced, based on inhibition of PTEN in liver cancer cells. Strikingly, HULC reduced the expression of PTEN, β-catenin and increased the expression of PKM2 in hematoma cells.