<p>SNHG8 is upregulated in esophageal squamous cell carcinoma and directly sponges microRNA-411 to increase oncogenicity by upregulating KPNA2</p>

Abstract

Background: The long noncoding RNA, small nucleolar RNA host gene 8 (SNHG8), is upregulated in multiple human cancer types. However, whether SNHG8 is aberrantly expressed in esophageal squamous cell carcinoma (ESCC) and its biological functions have yet to be elucidated. Thus, we aimed to determine the expression status of SNHG8 in ESCC, explore the effects of SNHG8 on the oncogenicity of ESCC, and investigate the potential underlying mechanisms. Methods: SNHG8 expression in ESCC tissues and cell lines was determined via reversetranscription quantitative polymerase chain reaction. The actions of SNHG8 on the malignant characteristics of ESCC were explored using CCK-8 assay, flow-cytometric analysis, Transwell migration and invasion assays, and tumor xenografts in nude mice. Results: SNHG8 expression was significantly higher in ESCC tissues and cell lines. High SNHG8 expression was revealed to closely correlate with primary tumor invasion depth, lymph node metastases, TNM stage, and worse overall survival among patients with ESCC. Functional investigation showed that ablation of SNHG8 notably restricted ESCC cell proliferation, migration, and invasion while inducing apoptosis in vitro and hindered tumor growth in vivo. In the meantime, SNHG8 acted as a molecular sponge of microRNA-411 (miR-411) in ESCC. Furthermore, miR-411 exerted a tumor-suppressive effect on ESCC cells, and karyopherin alpha 2 (KPNA2) turned out to be a direct target gene of miR-411. Restoring KPNA2 expression neutralized the inhibitory effects of miR-411 overexpression on the malignant behaviors of ESCC cells. Moreover, silencing of miR-411 abrogated the influence of SNHG8 downregulation in ESCC cells. Conclusion: SNHG8 may play oncogenic roles in the malignancy of ESCC by sponging miR-411 to increase KPNA2 expression. The SNHG8-miR-411-KPNA2 pathway may be a novel target for the treatment of patients with ESCC and offer potential biomarkers for the diagnosis and prognosis of ESCC.

Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

“…Long non-coding RNA UCA1 can up-regulates PTP1B to enhance cell proliferation through sequestering miR-206 in breast cancer [38]. SNHG8 plays oncogenic roles in the malignancy of esophageal squamous cell carcinoma by sponging miR-411, thus increasing KPNA2 expression [39]. In this study, we identified two miRNAs (let-7b and miR-1266) binding with HOST2 and demonstrated a negative correlation between HOST2 expression and let-7b/miR-1266 in TNBC samples.…”

<p>Long Noncoding RNA <em>ZFPM2-AS1</em> Enhances the Malignancy of Cervical Cancer by Functioning as a Molecular Sponge of microRNA-511-3p and Consequently Increasing FGFR2 Expression</p>

“…The apoptosis of transfected cells was evaluated by menas of flow-cytometric analysis. 30 After cultivation for 48 h, transfected cells were harvested using trypsin without EDTA and rinsed with precooled phosphate-buffered saline, followed by quantification of apoptotic cells using the Annexin V-Fluorescein Isothiocyanate (FITC) Apoptosis Detection Kit (BioLegend, San Diego, CA, USA). Namely, the transfected cells were resuspended in 100 μL of Annexin-V-binding buffer prior to double staining with 5 µL of Annexin V-FITC and 5 µL of the propidium iodide solution.…”

Analyses of DNA methylation involved in the activation of nuclear karyopherin alpha 2 leading to the progression and prognostic significance across human breast cancer

“…KPNA2, an adaptor protein for nuclear receptor importin-β, mediates numerous nuclear translocations of macromolecules by classical nuclear localization singal through the nuclear pore complex [25][26][27].…”