Epigenetic silencing of NDRG2 promotes colorectal cancer proliferation and invasion

2015 ◽  
Vol 31 (1) ◽  
pp. 164-171 ◽  
Author(s):  
Sung Noh Hong ◽  
Sung Jin Kim ◽  
Eun-Ran Kim ◽  
Dong Kyung Chang ◽  
Young-Ho Kim
Keyword(s):  
Colorectal Cancer ◽  
Epigenetic Silencing ◽  
Cancer Proliferation ◽  
Proliferation And Invasion

scholarly journals miR-125 inhibits colorectal cancer proliferation and invasion by targeting TAZ

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Meiyuan Yang ◽  
Xiaoli Tang ◽  
Zheng Wang ◽  
Xiaoqing Wu ◽  
Dong Tang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Underlying Mechanism ◽  
Cell Counting ◽  
Binding Motif ◽  
Cancer Proliferation ◽  
Qrt Pcr ◽  
Sirna Knockdown ◽  
Proliferation And Invasion ◽  
Hct116 Cells

Abstract Colorectal cancer (CRC) is the third most common malignant tumor worldwide and is a serious threat to human health. MicroRNAs (miRNAs) play a key role in oncogenesis and cancer progression. MiRNA-125 (miR-125) is an important miRNA that is dysregulated in several kinds of cancers. Thus, we investigated the expression and effects of miR-125 and Transcriptional co-activator with PDZ-binding motif (TAZ) for a better understanding of the underlying mechanism of tumor progression in CRC, which may provide an emerging biomarker for diagnosis and treatment of CRC. We measured the expression levels of miR-125 in CRC tissues, adjacent tissues, and cell lines (e.g. HCT116, SW480, FHC) by quantitative real-time polymerase chain reaction (qRT-PCR). The effect of miR-125 on proliferation and invasion in CRC cells was detected by Cell Counting Kit-8 (CCK-8), clone formation assay, and transwell assay. Western blotting and qRT-PCR were used to investigate the expression of TAZ after knocking down miR-125 in HCT116 cells or overexpressing miR-125 in SW480 cells. MiR-125 was significantly down-regulated in CRC compared with pericarcinomatous tissue from 18 patients. An miR-125 inhibitor promoted CRC cell proliferation and invasion, while miR-125 mimic had the opposite effect. Moreover, we found that TAZ was an miR-125 target and the siRNA knockdown of TAZ could reverse the effect of the miR-125 inhibitor on proliferation and invasion in HCT116 cells. The present study shows that miR-125 suppresses CRC proliferation and invasion by targeting TAZ.

scholarly journals The inhibitory role of miR‑485‑5p in colorectal cancer proliferation and invasion via targeting of CD147

2018 ◽  
Author(s):  
Yuqin Pan ◽  
Huiling Sun ◽  
Xiuxiu Hu ◽  
Bangshun He ◽  
Xiangxiang Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Proliferation ◽  
Inhibitory Role ◽  
Proliferation And Invasion

scholarly journals MicroRNA-320b promotes colorectal cancer proliferation and invasion by competing with its homologous microRNA-320a

2015 ◽  
Vol 356 (2) ◽  
pp. 669-675 ◽  
Author(s):  
Jiaojiao Zhou ◽  
Mengwen Zhang ◽  
Yanqing Huang ◽  
Lin Feng ◽  
Hailong Chen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Proliferation ◽  
Proliferation And Invasion

ZC3H13 suppresses colorectal cancer proliferation and invasion via inactivating Ras–ERK signaling

2018 ◽  
Vol 234 (6) ◽  
pp. 8899-8907 ◽  
Author(s):  
Dehua Zhu ◽  
Jianping Zhou ◽  
Jinbo Zhao ◽  
Guiyang Jiang ◽  
Xiupeng Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Erk Signaling ◽  
Cancer Proliferation ◽  
Proliferation And Invasion

scholarly journals Oncogenic lncRNA ZNF561-AS1 is essential for colorectal cancer proliferation and survival through regulation of miR-26a-3p/miR-128-5p-SRSF6 axis

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Zizhen Si ◽  
Lei Yu ◽  
Haoyu Jing ◽  
Lun Wu ◽  
Xidi Wang
Keyword(s):  
Colorectal Cancer ◽  
Rna Binding ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Cancer Proliferation ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background Long non-coding RNAs (lncRNA) are reported to influence colorectal cancer (CRC) progression. Currently, the functions of the lncRNA ZNF561 antisense RNA 1 (ZNF561-AS1) in CRC are unknown. Methods ZNF561-AS1 and SRSF6 expression in CRC patient samples and CRC cell lines was evaluated through TCGA database analysis, western blot along with real-time PCR. SRSF6 expression in CRC cells was also examined upon ZNF561-AS1 depletion or overexpression. Interaction between miR-26a-3p, miR-128-5p, ZNF561-AS1, and SRSF6 was examined by dual luciferase reporter assay, as well as RNA binding protein immunoprecipitation (RIP) assay. Small interfering RNA (siRNA) mediated knockdown experiments were performed to assess the role of ZNF561-AS1 and SRSF6 in the proliferative actives and apoptosis rate of CRC cells. A mouse xenograft model was employed to assess tumor growth upon ZNF561-AS1 knockdown and SRSF6 rescue. Results We find that ZNF561-AS1 and SRSF6 were upregulated in CRC patient tissues. ZNF561-AS1 expression was reduced in tissues from treated CRC patients but upregulated in CRC tissues from relapsed patients. SRSF6 expression was suppressed and enhanced by ZNF561-AS1 depletion and overexpression, respectively. Mechanistically, ZNF561-AS1 regulated SRSF6 expression by sponging miR-26a-3p and miR-128-5p. ZNF561-AS1-miR-26a-3p/miR-128-5p-SRSF6 axis was required for CRC proliferation and survival. ZNF561-AS1 knockdown suppressed CRC cell proliferation and triggered apoptosis. ZNF561-AS1 depletion suppressed the growth of tumors in a model of a nude mouse xenograft. Similar observations were made upon SRSF6 depletion. SRSF6 overexpression reversed the inhibitory activities of ZNF561-AS1 in vivo, as well as in vitro. Conclusion In summary, we find that ZNF561-AS1 promotes CRC progression via the miR-26a-3p/miR-128-5p-SRSF6 axis. This study reveals new perspectives into the role of ZNF561-AS1 in CRC.

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