Abstract
The aberrant expression and dysfunction of long non‐coding RNAs (lncRNAs) have been identified as critical factors governing the initiation and progression of different human cancers, including diffuse large B‐cell lymphoma (DLBCL). LncRNA small nucleolar RNA host gene 16 (SNHG16) has been recognized as a tumour‐promoting factor in various types of cancer. However, the biological role of SNHG16 and its underlying mechanism are still unknown in DLBCL. Here we disclosed that SNHG16 was overexpressed in DLBCL tissues and the derived cell lines. SNHG16 knockdown significantly suppressed cell proliferation and cell cycle progression, and it induced apoptosis of DLBCL cells in vitro. Furthermore, silencing of SNHG16 markedly repressed in vivo growth of OCI‐LY7 cells. Mechanistically, SNHG16 directly interacted with miR‐497‐5p by acting as a competing endogenous RNA (ceRNA) and inversely regulated the abundance of miR‐497‐5p in DLBCL cells. Moreover, the proto‐oncogene proviral integration site for Moloney murine leukaemia virus 1 (PIM1) was identified as a novel direct target of miR‐497‐5p. SNHG16 overexpression rescued miR‐497‐5p‐induced down‐regulation of PIM1 in DLBCL cells. Importantly, restoration of PIM1 expression reversed SNHG16 knockdown‐induced inhibition of proliferation, G0/G1 phase arrest and apoptosis of OCI‐LY7 cells. Our study suggests that the SNHG16/miR‐497‐5p/PIM1 axis may provide promising therapeutic targets for DLBCL progression.
Highlights
Diffuse large B‐cell lymphoma (DLBCL) is the most common sub‐ type of non‐Hodgkin's lymphoma
Many long non‐coding RNAs (lncRNAs) have been shown to function in cancers by acting as competing endogenous RNAs, celebrated as microRNA ‘sponges’ or a miRNA ‘decoy’, which competitively bind to miRNA via the base complementary and thereby increase the abundance of miRNA targets.[17,18]
LncRNA MALAT‐1 contributes to proliferation and cell cycle progression, and it represses apoptosis of DLBCL cells.[41]
Summary
Diffuse large B‐cell lymphoma (DLBCL) is the most common sub‐ type of non‐Hodgkin's lymphoma. Long non‐coding RNAs (lncRNAs), which are defined as RNA se‐ quence >200 nucleotides in length with no or feeble protein‐coding potential, are critical regulators of physiological and pathological processes including human cancer.[7] Accumulating studies provide evidence to support the close correlation of the dysregulation of lncRNAs with carcinogenesis, tumour metastasis and therapeutic resistance.[8,9,10,11,12,13] Mechanistically, lncRNAs modulate biological pro‐ cesses via interacting with other cellular macromolecules, including DNA, RNA and protein, at the transcriptional or post‐transcriptional level.[14,15,16] Recently, many lncRNAs have been shown to function in cancers by acting as competing endogenous RNAs (ceRNAs), celebrated as microRNA (miRNA) ‘sponges’ or a miRNA ‘decoy’, which competitively bind to miRNA via the base complementary and thereby increase the abundance of miRNA targets.[17,18] LncRNA small nucleolar RNA host gene 16 (SNHG16) has been widely investigated in human solid neoplasias.[19,20,21,22,23] Functionally, SNHG16 promotes cell proliferation, cell cycle progression, migration, invasion and che‐ motherapy resistance, and it inhibits apoptosis in most human can‐ cers.[19,20,21,22,23] In contrast, SNHG16 functions as a tumour suppressor in acute lymphoblastic leukaemia (ALL) via repressing cell proliferation and invasion by sponging miR‐124‐3p.24. In vitro and in vivo experiments were performed to investigate the biological role of SNHG16 and its potential molecular mechanism in DLBCL
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