Abstract
ABSTRACTThe role of long non-coding RNAs (lncRNAs) in acute myeloid leukemia (AML) is becoming increasingly questioned. Previous studies have reported that the lncRNA small nucleolar RNA host gene 1 (SNHG1) is involved in multiple human malignant tumors, while its expression and role in AML is still unexplored. Here, we show that SNHG1 is highly expressed in AML specimens from non-M3 patients, as well as AML cell lines. Meanwhile, upregulation of SNHG1 is correlated with poor prognosis. Notably, SNHG1 facilitates the proliferation and inhibits the apoptosis of AML cells in vitro. Consistent with these findings, knockdown of SNHG1 significantly inhibits AML progression in an immunodeficient mouse model. Mechanistically, we found that an anti-tumor microRNA-101 (miR-101) is upregulated and its target genes are downregulated in AML cells after SNHG1 knockdown. Further investigations display that SNHG1 can serve as a competing endogenous RNA to inhibit miR-101. In conclusion, our data indicate that SNHG1 plays an important role in facilitating AML progression at least in part by negatively regulating miR-101, and provides a new target for treating AML.
Highlights
Acute myeloid leukemia (AML) is a type of hematologic malignant disease characterized by abnormal proliferation of primitive and juvenile myeloid cells in bone marrow (BM) and peripheral blood (PB), and significant suppression of normal hematopoiesis (Burnett and Venditti, 2006; Marcucci et al, 2011; Thomas and Majeti, 2017)
small nucleolar RNA host gene 1 (SNHG1) is highly expressed in AML specimens and cell lines and upregulation of SNHG1 is correlated with poor prognosis To evaluate whether SNHG1 is implicated in AML, we first collected the BM specimens from AML patients and healthy controls
We observed that the expression of SNHG1 is high in AML cell lines (MOLM-13, HL-60 and THP-1) (Fig. 1B), suggesting that SNHG1 may play a critical role in AML pathogenesis
Summary
Acute myeloid leukemia (AML) is a type of hematologic malignant disease characterized by abnormal proliferation of primitive and juvenile myeloid cells in bone marrow (BM) and peripheral blood (PB), and significant suppression of normal hematopoiesis (Burnett and Venditti, 2006; Marcucci et al, 2011; Thomas and Majeti, 2017). AML is well known for its high incidence, recurrence and death rates (Kadia et al, 2016). Many strategies, such as chemotherapy, supportive therapy and hematopoietic stem cell (HSC) transplantation, have been applied to treat AML, the prognosis of this disease is still poor (Burnett et al, 2011; Marcucci et al, 2011). LncRNAs have been getting more and more attention due to their role in promoting the development and progression of many kinds of malignant tumors, including leukemia (Ma et al, 2018; Quinn and Chang, 2016). The underlying function, molecular mechanism and clinical significance of lncRNAs in AML have not been fully uncovered
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