Articles written in Journal of Biosciences
Volume 46 All articles Published: 3 February 2021 Article ID 0004 Article
The silence of lncRNA small nucleolar RNA host gene 16 (SNHG16) suppressed acute lymphoblastic leukemia(ALL) cell proliferation and migration, whereas its role in acute myeloid leukemia (AML) still lacksclarity. This study showed that SNHG16 was upregulated in AML patients and cells. And SNHG16 overexpressionremarkably enhanced the proliferation and migration capacities of HL60 and AML-193 cells, whileSNHG16 knockdown acted the opposite way. Subsequently, we revealed that SNHG16 directly bound toCELF2 (CUGBP Elav-like family member 2) protein, and caused CELF2 mRNA unstably and proteinsreducing. CELF2 was decreased both in AML patients and cells. CELF2 overexpression or interferenceweakened the effect of overexpressing or silencing SNHG16 on proliferation and migration. Moreover, thetransfection of pcDNA-CELF2 elevated PTEN (phosphatase and tensin homolog) activity and hindered thephosphoinositide 3-kinase (PI3K)/AKT signaling. And SNHG16 reduced PTEN activity and promoted thePI3K/AKT pathway activation by restraining CELF2. Furthermore, GDC-0941 (a specific inhibitor of thePI3K/AKT pathway) impeded the effect of SNHG16 increase, and bpV(pic) (a specific PTEN inhibitor)declined the effect of SNHG16 decrease on cell proliferation and migration. Taken together, the present studyindicated that SNHG16 promoted proliferation and migration of AML cells via PTEN/PI3K/AKT axis throughsuppressing CELF2 protein.
Volume 46, 2020
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