High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer

Liu, Jun-Jie; Qiu, Mantang; Xia, Wenjia; Liu, Chao; Xu, Youtao; Wang, Jie; Leng, Xuechun; Su, Heng; Zhu, Rong; Zhao, Ming; Ji, Fengqing; Xu, Lin; Xu, Kan; Yin, Rong

doi:10.1186/s13046-016-0352-9

Cited by 77 publications

(71 citation statements)

References 35 publications

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“…Nuclear and cytoplasmic fraction data also demonstrated that SBF2-AS1 was distributed in the nucleus and cytoplasm, which indicates that SBF2-AS1 may serve multiple functions at the transcriptional and post-transcriptional levels. According to our previous study (19), SBF2-AS1 may also transcriptionally downregulate the expression of CDKN1A via SUZ12 binding within the nucleus, as confirmed by the present study. CDKN1A, a cyclin-dependent kinase inhibitor, serves an important role in cell cycle arrest, and is therefore regarded as a tumor suppressor gene (40).…”

Section: Discussionsupporting

confidence: 71%

“…Evidence indicates that SBF2-AS1 may function as an oncogenic gene in ESCC. In previous studies, it was reported that SBF2-AS2 was able to bind to suppressor of zeste 12 homolog (SUZ12), a core component of PRC2 (19,(37)(38)(39). The enrichment of SUZ12 subsequently induces the inhibition of trimethylation of histone 3 Lys 27 in the promoter region of CDKN1A, and therefore downregulates the expression of CDKN1A (19).…”

Section: Discussionmentioning

confidence: 99%

“…SBF2-AS1, located at the 11p15.1 locus, is a 2,708-nt antisense RNA to SBF2. A previous study identified that SBF2-AS1 was able to bind with PRC2 and guided PRC2 to the promoter of CDKN1A and therefore decreased CDKN1A expression (19). However, the exact role of SBF2-AS1 in ESCC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

“…In a previous study, the novel lncRNA SET-binding factor 2 (SBF2) antisense RNA1 (SBF2-AS1) was identified and was demonstrated to be upregulated in non-small cell lung cancer (NSCLC), and was also able to promote proliferation of NSCLC cells (19). SBF2-AS1, located at the 11p15.1 locus, is a 2,708-nt antisense RNA to SBF2.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2018

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Abstract. 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. IntroductionHuman esophageal cancer (EC) is the third most common digestive system malignancy worldwide, and is associated with a high mortality rate (1). EC is also one of the most common malignant tumors in China, ranking third and Abbreviations: ESCC, esophageal squamous cell carcinoma; EA, esopha geal adenocarcinoma; ncRNA, non-coding RNA; lncRNA, long non-coding RNA; SBF2-AS1, SET-binding factor 2 antisense RNA 1; CCK-8, Cell Counting Kit-8; PRC2, Polycomb repressive complex 2; CDKN1A, cyclin-dependent kinase inhibitor 1A

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Section: Discussionsupporting

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2018

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“…In addition, the lncRNA ANRIL has been found to be significantly upregulated in NSCLC tissues, and its expression promotes cell proliferation and inhibits cell apoptosis in vitro and in vivo [22] . Moreover, HOTAIR, MALAT1 and SBF2-AS1 have been shown to exert oncogenic functions in NSCLC [23][24][25] . However, even in light of these discoveries, other NSCLC-related lncRNAs and their modulatory effects have not yet been identified.…”

Section: Discussionmentioning

confidence: 99%

The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer

Zhang

Hou

et al. 2017

Acta Pharmacol Sin

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Long non-coding RNAs (lncRNAs) are associated with the occurrence, development and prognoses of non-small cell lung cancer (NSCLC). In the present study, we investigated the functional mechanisms of the lncRNA XIST in two human NSCLC cell lines, A549 and NCI-H1299. In all the 5 NSCLC cell lines (NL9980, NCI-H1299, NCI-H460, SPC-A-1 and A549) tested, the expression levels of XIST were significantly elevated, as compared with those in normal human bronchial epithelial cell line BEAS-2B. In A549 and NCI-H1299 cells, knockdown of XIST by siRNA significantly inhibited the cell proliferation, migration and invasion, and promoted cell apoptosis. Furthermore, XIST knockdown elevated the expression of E-cadherin, and suppressed the expression of Bcl-2. Moreover, knockdown of XIST significantly suppressed the tumor growth in NSCLC A549 xenograft mouse model. Bioinformatic analysis and luciferase reporter assays revealed that XIST was negatively regulated by miR-449a. We further identified reciprocal repression between XIST and miR449a, which eventually influenced the expression of Bcl-2: XIST functioned as a miRNA sponge of miR-449a, which was a negative regulator of Bcl-2. These data show that expression of the lncRNA XIST is associated with an increased growth rate and metastatic potential in NSCLC A549 and NCI-H1299 cells partially through miR-449a, and suggest that XIST may be a potential prognostic factor and therapeutic target for patients with NSCLC.

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The expression and role of SUZ12 in lung adenocarcinoma

Hu,

Zhong

2024

Cancer Medicine

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BackgroundSUZ12 is one of the core members of the polycomb repressive complex 2 (PRC2), but its expression and role in lung adenocarcinoma (LUAD) are unclear. We aimed to explore the expression, prognosis, biological functions and roles of SUZ12 in LUAD.MethodsThe expression of SUZ12 was detected by immunohistochemical staining, qRT‐PCR, and western blotting in LUAD tissues and cells. The biological functions and molecular mechanisms of SUZ12 were characterized by a range of in vitro and in vivo experiments.ResultsSUZ12 was overexpressed in LUAD tissues, and high SUZ12 expression was correlated with worse clinicopathological features and a poorer prognosis. Knockdown of SUZ12 significantly inhibited cell growth, colony formation, invasion, and migration, and induced apoptosis and G1/S phase arrest, while overexpression of SUZ12 had the opposite effects. Knockdown of SUZ12 decreased the tumorigenic capacity of A549 cells in vivo. The expression of key signaling molecules related to the cell cycle, apoptosis, migration, and immunity were altered by the knockdown or overexpression of SUZ12. SUZ12 can directly bind to the Bax promoter region, EZH2 and H3K27me3 levels dependents on SUZ12. The expression levels of SUZ12 and Bax were negatively correlated in LUAD tissues.ConclusionsSUZ12 is a new oncogene related to the poor prognosis of LUAD. SUZ12 regulates LUAD progression by regulating the expression of related signaling molecules, and as a part of the PRC2 complex, it may bind to the Bax promoter to silence Bax expression.

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High expression of long non-coding RNA SBF2-AS1 promotes proliferation in non-small cell lung cancer

Cited by 77 publications

References 35 publications

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

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

The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer

The expression and role of SUZ12 in lung adenocarcinoma

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