A specific upregulated long noncoding RNA in colorectal cancer promotes cancer progression
Junshu Li, Yanhong Ji, Na Chen, Huiling Wang, Chao Fang, Xiaonan Yin, Zhiyuan Jiang, Zhexu Dong, Dan Zhu, Jiamei Fu, Wencheng Zhou, Ruiyi Jiang, Ling He, Zhang Hantao, Gang Shi, Lin Cheng, Xiaolan Su, Lei Dai, Hongxin Deng
Junshu Li, Yanhong Ji, Na Chen, Huiling Wang, Chao Fang, Xiaonan Yin, Zhiyuan Jiang, Zhexu Dong, Dan Zhu, Jiamei Fu, Wencheng Zhou, Ruiyi Jiang, Ling He, Zhang Hantao, Gang Shi, Lin Cheng, Xiaolan Su, Lei Dai, Hongxin Deng
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Research Article Cell biology Gastroenterology

A specific upregulated long noncoding RNA in colorectal cancer promotes cancer progression

Abstract

Long noncoding RNA (lncRNA) plays a crucial role in the pathogenesis of various diseases, including colorectal cancer (CRC). The gene mutations of adenomatous polyposis coli (APC) were found in most patients with CRC. They function as important inducers of tumorigenesis. Based on our microarray results, we identified a specific upregulated lncRNA in CRC (SURC). Further analysis showed that high SURC expression correlated with poorer disease-free survival and overall survival in patients with CRC. Furthermore, we found that mutated APC genes can promote the transcription of SURC by reducing the degradation of β-catenin protein in CRC. Functional assays revealed that knockdown of SURC impaired CRC cell proliferation, colony formation, cell cycle, and tumor growth. Additionally, SURC promotes CCND2 expression by inhibiting the expression of miR–185-5p in CRC cells. In conclusion, we demonstrate that SURC is a specific upregulated lncRNA in CRC and the SURC/miR–185-5p/CCND2 axis may be targetable for CRC diagnosis and therapy.

Authors

Junshu Li, Yanhong Ji, Na Chen, Huiling Wang, Chao Fang, Xiaonan Yin, Zhiyuan Jiang, Zhexu Dong, Dan Zhu, Jiamei Fu, Wencheng Zhou, Ruiyi Jiang, Ling He, Zhang Hantao, Gang Shi, Lin Cheng, Xiaolan Su, Lei Dai, Hongxin Deng

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Figure 4

SURC promotes cell proliferation and tumor growth in vivo and in vitro.

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SURC promotes cell proliferation and tumor growth in vivo and in vitro. ...
(A) SW620 and LoVo cells were transfected with shNC or shSURC and detected by qPCR (n = 3; **P < 0.01). (B) Detection of SURC expression in s.c. tumors by FISH. Scale bar: 100 μm. Analysis of SURC positive cells in each frame (n = 3; **P < 0.01). (C–F) Tumor volume and tumor weight were measured in SW620 and LoVo tumors and compared among groups (n = 6; **P < 0.01). (G) CCK8 assay shows relative cell growth at 0, 24, 48, and 72 hours (n = 5; **P < 0.01). (H) The colony formation pictures of SW620 and LoVo cells infected with shNC and shSURC. A total of 3 biologically independent experiments were performed (n = 3; **P < 0.01). (I) RKO cells were infected with lenti-SURC and detected by qPCR (n = 3; **P < 0.01). (J) FISH staining shows SURC expression of xenograft tumors from mice injected s.c. with control or SURC-overexpressing RKO cells. Scale bar: 100 μm. Analysis of SURC positive cells in each frame (n = 3; **P < 0.01). (K and L) Tumor volume and tumor weight were measured in RKO tumors among various groups (n = 5; *P < 0.05, **P < 0.01). (M) CCK8 assay shows relative cell proliferation at 0, 24, 48, and 72 hours in RKO cells (n = 5; **P < 0.01). (N) Effects of SURC overexpression on colony formation in RKO cells (n = 3; **P < 0.01). Data are shown as the mean ± SEM. Statistical differences were calculated using 1-way ANOVA and Dunnett’s multiple-comparison test for A–H and unpaired 2-tailed Student’s t test for I–N. Ctrl, Control.