RETRACTED: Knockdown of long noncoding RNA HOTAIR inhibits cell growth of human lymphoma cells by upregulation of miR-148b (Retracted article. See vol. 122, 2021)

Lymphoma is a common cause of cancer worldwide with an increasing incidence in recent years. A large number of studies have shown that HOX transcript antisense intergenic RNA (HOTAIR) exerts as an oncogene in various neoplasms. However, the function of HOTAIR in lymphoma still remains unclear. The present study aimed to investigate the function of HOTAIR in lymphoma and its underlying mechanisms. The expressions of HOTAIR, miR-148b, and BMI1 in lymphoma samples and cells (AHH-1, Raji, and U937) were quantified by quantitative reverse polymerase chain reaction (qRT-PCR). Cell viability was measured by trypan blue assay. The efficiency of transfection was verified by qRT-PCR or Western blot analysis. Apoptotic cells and cell cycle progression were both detected by flow cytometry assay. Furthermore, Western blot analysis was performed to assess the expression of mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) pathway-related core factors. We found that HOTAIR knockdown reduced cell viability but increased apoptotic cells and inhibited cell cycle progression in Raji and U937 cells. miR-148b expression was upregulated by HOTAIR inhibition. Meanwhile, miR-148b inhibitor abolished the modulation of HOTAIR silence on cell growth, as evidenced by increased cell viability, reduced apoptotic cells, and decreased the rate of G1 phase cells. Furthermore, miR-148b negatively regulated the expression of BMI1 by targeting its 3 '-untranslated region (3 '-UTR), and BMI1 overexpression blocked the effect of miR-148b mimic on cell growth. In addition, BMI1 promoted the activation of MAPK and ERK in Raji and U937 cells. In conclusion, the present study demonstrated that HOTAIR knockdown inhibited the cell growth and promoted apoptosis of lymphoma cells via upregulation of miR-148b and miR-148b further regulated the expression of BMI1 via MAPK and ERK signaling pathways.