A specific upregulated long noncoding RNA in colorectal cancer promotes cancer progression
Junshu Li, … , Lei Dai, Hongxin Deng
Junshu Li, … , Lei Dai, Hongxin Deng
Published May 26, 2022
Citation Information: JCI Insight. 2022;7(15):e158855. https://doi.org/10.1172/jci.insight.158855.
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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 6

SURC modulated CRC progression by regulating the expression of miR–185-5p.

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SURC modulated CRC progression by regulating the expression of miR–185-5...
(A) qPCR shows the expression of miR–185-5p in LoVo and SW620 cells (n = 3; **P < 0.01). (B) The FISH assay shows the expression of miR–185-5p in s.c. tumor tissue of SW620 cells. Scale bar: 100 μm. Analysis of miR–185-5p positive cells in each frame (n = 3; **P < 0.01). (C) Correlations between the SURC levels and the miR–185-5p levels in patients with CRC of HXCRC cohort (n = 75) were determined by FISH staining. Scale bar: 200 μm. The r values and P values are from Pearson’s correlation analysis. (D) Lower expression of miR–185-5p was detected in CRC samples than in matched normal tissues from HXCRC cohort (n = 90), which was measured by FISH. (E) Kaplan-Meier plots of overall survival and (F) disease-free survival for CRC samples from HXCRC cohort (n = 140). (G) Cell viability (n = 5; **P < 0.01) and (H) colony formation (n = 3; **P < 0.01) were examined after administration with miR–185-5p inhibitor. (I) qPCR shows the expression of pri-miR–185-5p in LoVo and SW620 cells infected with lenti-shNC and lenti-shSURC (n = 3; **P < 0.01). (J) Levels of miR–185-5p and (K) pri-miR–185-5p were examined at different times after administration with actinomycin d in SW620 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, B, and G–K, unpaired 2-tailed Student’s t test for D, and Log-Rank test (Kaplan-Meier curves) for E and F.