[KMT2A Activates Akt/mTOR Signaling Pathway Through LncRNA-HOTAIR to Influence the Biological Behavior of AML Cells].

Objective: To investigate the expression of lysine methyltransferase 2A (KMT2A) in acute myeloid leukemia (AML) cells and its molecular mechanism affecting the proliferation of AML cells.

Methods: Co-immunoprecipitation assay was used to detect the binding of KMT2A to long non-coding RNA-HOX transcript antisense RNA (lncRNA-HOTAIR). AML cell proliferation was detected by 5-ethynyl-2'-deoxyuridine (EdU) assay.

Results: The PCR amplification signal of KMT2A group was significantly stronger than that of the negative control group and IgG group (P<0.01). Compared with the negative control group and KMT2A-OE + lncRNA-HOTAIR-KD group, the ratio of EdU cells in both KMT2A-OE group and lncRNA-HOTAIR-OE group significantly increased (P<0.01). Compared with negative control group, the ratio of EDU cells in KMT2A-KD group and lncRNA-HOTAIR-KD group significantly decreased (P<0.01), the expression levels of p-Akt and p-mTOR in both KMT2A-OE group and lncRNA-HOTAIR-OE group significantly increased (P<0.01).

Conclusion: KMT2A can interact with lncRNA-HOTAIR to promote the activation of Akt/mTOR signaling pathway, thus promoting the proliferation of AML cells.