Abstract
Reprogrammed metabolism is an important hallmark of cancer cells. Pyruvate kinase (PK) is one of the major rate-limiting enzymes in glucose metabolism. The M2 isoform of PK (PKM2), is considered to be an important marker of metabolic reprogramming and one of the key enzymes. Recently, through the continuous development of genome-wide analysis and functional studies, accumulating evidence has demonstrated that long non-coding RNAs (LncRNAs) play vital regulatory roles in cancer progression by acting as either potential oncogenes or tumor suppressors. Furthermore, several studies have shown that up-regulation of PKM2 in cancer tissues is associated with LncRNAs expression and patient survival. Thus, scientists have begun to unveil the mechanism of LncRNA-associated PKM2 in cancer metabolic progression. Based on these novel findings, in this mini-review, we summarize the detailed molecular mechanisms of LncRNA related to PKM2 in cancer metabolism. We expect that this work will promote a better understanding of the molecular mechanisms of PKM2, and provide a profound potential for targeting PKM2 to treat tumors.
Highlights
In the field of tumor research, much attention has recently been paid to the metabolic reprogramming of tumor cells
The overexpression of lincRNA-p21 in DU145 and LNCaP cells reduced the level of M2 isoform of PK (PKM2), confirming that lincRNA-p21 is a negative regulator of PKM2. These results demonstrate that the regulatory mechanism of PKM2 mediated by Long intergenic non-coding RNA (LincRNA)-p21 depends on the PTEN/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) cascade [65]
PKM2 has been shown to have a critical role in cancer cell metabolism
Summary
In the field of tumor research, much attention has recently been paid to the metabolic reprogramming of tumor cells. Xin et al [52] reported that HULC activates the PI3K/AKT/mTOR pathway in human liver cancer by inhibiting the expression of PTEN, depending on autophagy.
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