Upregulated long non-coding RNA SBF2-AS1 promotes proliferation in esophageal squamous cell carcinoma | Zendy

Rui Chen | Zendy; Wenjia Xia | Zendy; Xiaoxiao Wang | Zendy; Mantang Qiu | Zendy; Rong Yin | Zendy; Siwei Wang | Zendy; Xiaoxiang Xi | Zendy; Jie Wang | Zendy; Youtao Xu | Zendy; Gaochao Dong | Zendy; Lin Xu | Zendy; Wei De | Zendy

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Upregulated long non-coding RNA SBF2-AS1 promotes proliferation in esophageal squamous cell carcinoma

Author(s) -

Rui Chen,

Wenjia Xia,

Xiaoxiao Wang,

Mantang Qiu,

Rong Yin,

Siwei Wang,

Xiaoxiang Xi,

Jie Wang,

Youtao Xu,

Gaochao Dong,

Lin Xu,

Wei De

Publication year - 2018

Publication title -

oncology letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.766

H-Index - 54

eISSN - 1792-1082

pISSN - 1792-1074

DOI - 10.3892/ol.2018.7968

Subject(s) - downregulation and upregulation , cell cycle , molecular medicine , cancer research , oncogene , gene silencing , cell , cell growth , apoptosis , biology , cancer , long non coding rna , medicine , gene , genetics , biochemistry

Esophageal cancer is one of the most common types of malignant tumors located within the digestive system, with >50% of esophageal cancer cases worldwide occurring in China. Recent studies have demonstrated that long non-coding RNAs (lncRNAs) are frequently dysregulated in cancer; however, few lncRNAs have been characterized in esophageal squamous cell carcinoma (ESCC). In the present study, a novel lncRNA, SET-binding factor 2 (SBF2) antisense RNA1 (SBF2-AS1) was exhibited in ESCC. Expression levels of SBF2-AS1 in ESCC and adjacent non-cancerous tissues were detected using the reverse transcription-quantitative polymerase chain reaction. SBF2-AS1 was knocked down, and proliferation, migration, invasion, apoptosis and the cell cycle were examined in ESCC cells. Results identified that SBF2-AS1 was significantly upregulated in ESCC compared with adjacent non-cancerous tissues (fold increase, 8.82; P=0.023). The SBF2-AS1 expression level was significantly increased in patients who had a smoking (9.927 vs. 4.507; P=0.030) and/or drinking (10.938 vs. 4.232; P=0.032) history. Patients with a large tumor size exhibited increased SBF2-AS1 expression (≥4 vs. <4 cm, 14.898 vs. 5.435; P=0.018). Patients with advanced ESCC exhibited increased upregulation of SBF2-AS1 [tumor-node-metastasis (TNM) I-II vs. TNM III-IV, 1.302 vs. 15.475; P<0.01]. SBF2-AS1 was also silenced using small interfering RNA. Cell proliferative and invasive ability were significantly inhibited (P<0.05) following SBF2-AS1 silencing, the cell cycle was arrested in the G 2 phase; however, there was no significant difference in the proportion of apoptotic cells. Gene Set Enrichment Analysis revealed that genes associated with cell cycle biological processes, including the cancer suppressor gene cyclin-dependent kinase 1A (CDKN1A), were significantly associated with SBF2-AS1 in ESCC tissues. Further validation confirmed that CDKN1A expression levels were increased in ECA-109 cells following SBF2-AS1 silencing. The results of the present study demonstrate that SBF2-AS1 is significantly upregulated in ESCC, and that silencing of SBF2-AS1 inhibits the proliferative and invasive ability of ESCC cells. SBF2-AS1 may be a novel biomarker and therefore a potential therapeutic target for ESCC.

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