scholarly journals The Novel Long Noncoding RNA TUSC7 Inhibits Proliferation by Sponging MiR-211 in Colorectal Cancer

2017 ◽  
Vol 41 (2) ◽  
pp. 635-644 ◽  
Author(s):  
Jian Xu ◽  
Rui Zhang ◽  
Jian Zhao
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Proliferation Rate ◽  
Expression Level ◽  
The Novel ◽  
Cell Proliferation Rate ◽  
Potential Tumor Suppressor

Background/Aims: The novel long noncoding RNA (lncRNA) tumor suppressor candidate 7 (TUSC7) has been reported as a potential tumor suppressor, while the functional role of TUSC7 is still unknown in colorectal cancer (CRC). Here, we characterized TUSC7 expression profile in CRC patients and investigated its biological function and potential molecular mechanism. Methods: RNA isolation, qRT-PCR, cell counter kit-8 assay, cell cycle assay, EdU assay, and western blot were performed. Statistical analyses were performed using SPSS 18.0 software and p value < 0.05 was considered as statistically significant. Results: In a cohort of CRC patients, we found TUSC7 was significantly downregulated in CRC tissues compared with adjacent non-tumor tissues (P < 0.01). Patients with high expression of TUSC7 had better survival than those with low expression of TUSC7 (HR = 0.342, 95% CI: 0.120-0.972, P = 0.044). Cell count kit 8 and EdU assays showed that ectopic expression of TUSC7 in HCT116 and SW480 cells significantly inhibited cell proliferation rate. After silence of TUSC7 with small interfering RNA, cell proliferation rate increased. Flow cytometry analyses revealed cycles were arrested at G1 phase after TUSC7 overexpression. We found there were 2 binding sites of miR-211-3p within the sequence of TUSC7 and TUSC7 expression level was negatively correlated with miR-211-3p. TUSC7 overexpression increased the expression level of CDK6, which is a downstream target of miR-211-3p, in both RNA and protein level. Furthermore, luciferase reporter assay indicated that TUSC7 could sponge miR-211-3p. Conclusion: To summary, we demonstrated that TUSC7 is a potential tumor suppressor in CRC, and TUSC7 could inhibit CRC cell proliferation by completely sponging miR-211-3p.

scholarly journals Long noncoding RNA BLACAT1 indicates a poor prognosis of colorectal cancer and affects cell proliferation by epigenetically silencing of p15

2017 ◽  
Vol 8 (3) ◽  
pp. e2665-e2665 ◽  
Author(s):  
Jun Su ◽  
Erbao Zhang ◽  
Liang Han ◽  
Dandan Yin ◽  
Zhili Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Poor Prognosis

Long noncoding RNA THOR is highly expressed in colorectal cancer and predicts a poor prognosis

2020 ◽  
Vol 16 (25) ◽  
pp. 1911-1920
Author(s):  
Feifei Chu ◽  
Yuanbo Cui ◽  
Kunkun Li ◽  
Xingguo Xiao ◽  
Li Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Prognostic Biomarker ◽  
Cell Counting ◽  
Tumor Node Metastasis ◽  
Tumor Node Metastasis Stage

Aim: Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. This study aimed to investigate the role of long noncoding RNA THOR in CRC. Materials & methods: The expression of THOR in 103 cases of CRC tissues and four CRC cell lines was examined by quantitative real-time PCR. Cell counting kit-8 and colony formation assays were applied to detect cell proliferation, and flow cytometry was used for testing cell cycle and apoptosis of CRC. Results: We found that THOR was highly expressed in CRC and correlated with tumor node metastasis stage, histological subtype, tumor size and differentiation and survival in CRC patients. Meanwhile, knockdown of THOR significantly suppressed cell proliferation and cell cycle of CRC, whereas promoted cell apoptosis. Conclusion: Our findings suggest that THOR is an oncogenic long noncoding RNA in CRC and a potential prognostic biomarker for this cancer.

scholarly journals Epigenetic Regulation of the lncRNA MEG3 and Its Target c-MET in Pancreatic Neuroendocrine Tumors

2015 ◽  
Vol 29 (2) ◽  
pp. 224-237 ◽  
Author(s):  
Sita D. Modali ◽  
Vaishali I. Parekh ◽  
Electron Kebebew ◽  
Sunita K. Agarwal
Keyword(s):  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Neuroendocrine Tumors ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Growth Factor Receptor ◽  
Pancreatic Neuroendocrine Tumors ◽  
Suppressor Activity ◽  
Tumor Suppressor Activity ◽  
Insulinoma Cells

Abstract Biallelic inactivation of MEN1 encoding menin in pancreatic neuroendocrine tumors (PNETs) associated with the multiple endocrine neoplasia type 1 (MEN1) syndrome is well established, but how menin loss/inactivation initiates tumorigenesis is not well understood. We show that menin activates the long noncoding RNA maternally expressed gene 3 (Meg3) by histone-H3 lysine-4 trimethylation and CpG hypomethylation at the Meg3 promoter CRE site, to allow binding of the transcription factor cAMP response element-binding protein. We found that Meg3 has tumor-suppressor activity in PNET cells because the overexpression of Meg3 in MIN6 cells (insulin-secreting mouse PNET cell line) blocked cell proliferation and delayed cell cycle progression. Gene expression microarray analysis showed that Meg3 overexpression in MIN6 mouse insulinoma cells down-regulated the expression of the protooncogene c-Met (hepatocyte growth factor receptor), and these cells showed significantly reduced cell migration/invasion. Compared with normal islets, mouse or human MEN1-associated PNETs expressed less MEG3 and more c-MET. Therefore, a tumor-suppressor long noncoding RNA (MEG3) and suppressed protooncogene (c-MET) combination could elicit menin's tumor-suppressor activity. Interestingly, MEG3 and c-MET expression was also altered in human sporadic insulinomas (insulin secreting PNETs) with hypermethylation at the MEG3 promoter CRE-site coinciding with reduced MEG3 expression. These data provide insights into the β-cell proliferation mechanisms that could retain their functional status. Furthermore, in MIN6 mouse insulinoma cells, DNA-demethylating drugs blocked cell proliferation and activated Meg3 expression. Our data suggest that the epigenetic activation of lncRNA MEG3 and/or inactivation of c-MET could be therapeutic for treating PNETs and insulinomas.

scholarly journals Long noncoding RNA ZEB1-AS1 acts as a Sponge of miR-141-3p to Inhibit Cell Proliferation in Colorectal Cancer

2020 ◽  
Vol 17 (11) ◽  
pp. 1589-1597
Author(s):  
Guanghai Wu ◽  
Mei Xue ◽  
Yongjie Zhao ◽  
Youkui Han ◽  
Chao Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Inhibit Cell Proliferation
Sign in / Sign up

Export Citation Format

Share Document