scholarly journals Circ_DOCK1 regulates USP11 through miR-132-3p to control colorectal cancer progression

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Weitong Zhang ◽  
Zhenfen Wang ◽  
Guohao Cai ◽  
Ping Huang
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Western Blotting ◽  
Cancer Progression ◽  
Colorectal Cancer Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Colorectal Cancer Progression

Abstract Background Circular RNAs (circRNAs) take part in colorectal cancer malignancies. CircRNA dedicator of cytokinesis 1 (circ_DOCK1) is involved in colorectal cancer progression, but the mechanism underlying this circRNA that takes part in colorectal cancer development remains largely undetermined. Methods Tumor and normal para-cancerous tissues were collected from 42 colorectal cancer patients. Human colorectal cancer cell lines (HCT116 and SW480) were used for the experiments in vitro. Circ_DOCK1, microRNA (miR)-132-3p, and ubiquitin-specific protease 11 (USP11) levels were measured through quantitative real-time polymerase chain reaction and Western blotting. Cell growth, metastasis, and apoptosis were investigated via colony formation, 5-ethynyl-2′-deoxyuridine (EdU) staining, MTT, flow cytometry, Western blotting, and transwell analyses. The target association was evaluated via dual-luciferase reporter analysis, RNA pull-down, and immunoprecipitation (RIP). Xenograft assay was performed using HCT116 cells. USP11 and Ki67 levels in tumor tissues were detected via immunohistochemistry. Results Circ_DOCK1 expression was enhanced in colorectal cancer tissues and cells. Silencing circ_DOCK1 repressed cell growth, migration, and invasion, and facilitated apoptosis. Circ_DOCK1 sponged miR-132-3p, and miR-132-3p silence mitigated the effect of circ_DOCK1 interference on cell growth, metastasis, and apoptosis. MiR-132-3p targeted USP11, and circ_DOCK1 could regulate USP11 level by miR-132-3p. MiR-132-3p suppressed cell growth, metastasis, and apoptosis, and USP11 attenuated these effects. Knockdown of circ_DOCK1 decreased colorectal cancer cell xenograft tumor growth. Conclusion Circ_DOCK1 interference suppressed cell growth and metastasis, and increased apoptosis of colorectal cancer via decreasing USP11 by increasing miR-132-3p.

Long Non-Coding RNA-Colon Cancer Associated Transcript 1 Down-Regulation Inhibits Cell Proliferation and Promotes Apoptosis in Colorectal Cancer Through Enhancing miR-152 Expression

2020 ◽  
Vol 10 (12) ◽  
pp. 1766-1772
Author(s):  
Jindong Li ◽  
Xi Wang ◽  
Xin Huang ◽  
Na Li ◽  
Ya Ling ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Viability ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Biological Effects ◽  
Colorectal Cancer Cell ◽  
Luciferase Reporter ◽  
Pcr Analysis ◽  
Cancer Tissue ◽  
Colorectal Cancer Progression

Colorectal cancer is a common malignant cancer that is characterized by high mortality rate. CCAT1 is a type of newly discovered lncRNA. This research was conducted to study the role of CCAT1 in colorectal cancer. The findings showed that there was significant up-regulation of CCAT1 expression in colorectal cancer. Then, online bioinformatic database and dual-luciferase reporter assay to prove CCAT1 and miR-152 have direct binding sites. Many researches demonstrated that miR-152 played a crucial role in development of colorectal cancer. Therefore, we then explored the relationship between CCAT1 and miR-152 in colorectal cancer. qRT-PCR analysis showed that miR-152 was lowly expressed in cancer tissue and cells. We then explored the effect of CCAT1 and miR-152 on the biological effects of colorectal cancer cells. MiR-152 up-regulation significantly reduced colorectal cancer cell viability and enhanced apoptosis. Furthermore, CCAT1-shRNA inhibited colorectal cancer cell viability and enhanced cell apoptosis were significantly eliminated by miR-152 inhibitor. Combined with all results, CCAT1/miR-152 axis was related to colorectal cancer progression regulation, which might be used as new therapeutic targets for colorectal cancer treatment.

scholarly journals Exosome-transmitted circCOG2 promotes colorectal cancer progression via miR-1305/TGF-β2/SMAD3 pathway

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Lei Gao ◽  
Xiaolong Tang ◽  
Qingsi He ◽  
Guorui Sun ◽  
Chao Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Metastatic Potential ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Colorectal Cancer Progression ◽  
Dual Luciferase Reporter Assay

AbstractCircular RNAs (circRNA) are abundantly present in the exosome. Yet, the role of exosome-transmitted circRNA in colorectal cancer (CRC) remains unclear. In this study, we examined the function and mechanism of circCOG2 in CRC. We analyzed the expression of circCOG2 in CRC tissues, plasmas, and exosomes by qRT-PCR. The function of circCOG2 was evaluated by CCK-8, clone formation, transwell and wound healing assay, and using an in vivo study; while its mechanism was analyzed using a dual luciferase reporter assay, RNA pull-down assay, Western blot, and rescue experiments. We found that circCOG2 was increased in CRC tissues, plasmas, and exosomes. Upregulated circCOG2 promoted CRC proliferation, migration, and invasion through the miR-1305/TGF-β2/SMAD3 pathway, and this effect could be transmitted from CRC cells with the high metastatic potential to CRC cells with low metastatic potential by exosomes. Our results revealed that circCOG2 is correlated with poor prognosis and may be used as a therapeutic target for CRC.

scholarly journals Circ_0003266 sponges miR-503-5p to suppress colorectal cancer progression via regulating PDCD4 expression

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Caihong Wen ◽  
Xiaoqing Feng ◽  
Honggang Yuan ◽  
Yong Gong ◽  
Guangsheng Wang
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Progression ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Pdcd4 Expression ◽  
Novel Target

Abstract Background Circular RNAs (circRNAs) feature prominently in tumor progression. However, the biological function and molecular mechanism of circ_0003266 in colorectal cancer (CRC) require further investigation. Methods Circ_0003266 expression in 46 pairs CRC tissues / adjacent tissues, and CRC cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR); after circ_0003266 was overexpressed or knocked down in CRC cells, cell proliferation, apoptosis, migration, and invasion were evaluated by the cell counting kit-8 (CCK-8), flow cytometry, and Transwell assays, respectively; the interaction among circ_0003266, miR-503-5p, and programmed cell death 4 (PDCD4) was confirmed using bioinformatics analysis and dual-luciferase reporter assay; PDCD4 protein expression in CRC cells was quantified using Western blot. Results Circ_0003266 was significantly lowly expressed in CRC tissues and cell lines. Circ_0003266 overexpression markedly repressed CRC cell proliferation, migration, and invasion, and accelerated the cell apoptosis, but its overexpression promoted the malignant phenotypes of CRC cells. PDCD4 was a direct target of miR-503-5p and circ_0003266 promoted PDCD4 expression by competitively sponging miR-503-5p. Conclusion Circ_0003266 suppresses the CRC progression via sponging miR-503-5p and regulating PDCD4 expressions, which suggests that circ_0003266 may serve as a novel target for the treatment of CRC.

Circ_0000218 plays a carcinogenic role in colorectal cancer progression by regulating miR-139-3p/RAB1A axis

2019 ◽  
Vol 167 (1) ◽  
pp. 55-65 ◽  
Author(s):  
Fu-Lai Pei ◽  
Ming-Zheng Cao ◽  
Yue-Feng Li
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Rna Immunoprecipitation ◽  
Proliferation And Metastasis ◽  
Polymerase Chain ◽  
Local Lymph Node ◽  
Colorectal Cancer Progression

Abstract Accumulating researches have confirmed that circRNA abnormal expression plays a prominent role in the progression of colorectal cancer (CRC). The role of circ_0000218 in CRC and its potential mechanism are not clear. In this study, real-time polymerase chain reaction (RT-PCR) was employed to measure the circ_0000218, miR-139-3p and RAB1A mRNA expression in CRC tissues and cells. Immunohistochemistry and western blot were conducted to determine the RAB1A expression in CRC tissues and cells, respectively. Colony formation assay and BrdU method were employed to monitor the effect of circ_0000218 on cell proliferation. Transwell assay was adopted to detect cell migration and invasion. Dual luciferase reporter assay and RNA immunoprecipitation assay were adopted to confirm the targeting relationship between circ_0000218 and miR-139-3p, miR-139-3p and RAB1A. We demonstrated that circ_0000218 was notably upregulated in CRC tissues and cell lines, and its high expression level was markedly linked to the increase of T staging and local lymph node metastasis. Circ_0000218 overexpression enhanced the proliferation and metastasis of CRC cells while knocking down circ_0000218 caused the opposite effects. We also observed that miR-139-3p was negatively regulated by circ_0000218, while RAB1A was positively regulated by it. Collectively, this study suggested that circ_0000218 upregulated RAB1A and promoted CRC proliferation and metastasis via sponging miR-139-3p.

scholarly journals Long noncoding RNA MAPKAPK5-AS1 promotes colorectal cancer progression by cis-regulating the nearby gene MK5 and acting as a let-7f-1-3p sponge

2020 ◽  
Author(s):  
Ting Yang ◽  
Wei-Cong Chen ◽  
Pei-Cong Shi ◽  
Man-Ru Liu ◽  
Tao Jiang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Noncoding Rna ◽  
Vital Role ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Colorectal Cancer Progression ◽  
Molecular Therapeutic

Abstract Background: Long noncoding RNAs (lncRNAs) are considered critical regulators in cancers; however, the clinical significance and mechanisms of MAPKAPK5-AS1 (hereinafter referred to as MK5-AS1) in colorectal cancer (CRC) remain mostly unknown.Methods: In this study, quantitative real-time PCR (qPCR) and western blotting were utilized to detect the levels of MK5-AS1, let-7f-1-3p and MK5 (MAPK activated protein kinase 5) in CRC tissues and cell lines. The biological functions of MK5-AS1, let-7f-1-3p and MK5 in CRC cells were explored using Cell Counting Kit-8 (CCK8), colony formation and transwell assays. The potential mechanisms of MK5-AS1 were evaluated by RNA pull-down, RNA immunoprecipitation (RIP), dual luciferase reporter assay, chromatin immunoprecipitation (CHIP) and bioinformatics analysis. The effects of MK5-AS1 and MK5 on CRC were investigated by a xenotransplantation model. Results: We confirmed that MK5-AS1 was significantly increased in CRC tissues. Knockdown of MK5-AS1 suppressed cell migration and invasion in vitro and inhibited lung metastasis in mice. Mechanistically, MK5-AS1 regulated SNAI1 expression by sponging let-7f-1-3p and cis-regulated the adjacent gene MK5. Moreover, MK5-AS1 recruited RBM4 and eIF4A1 to promote the translation of MK5. Our study verified that MK5 promoted the phosphorylation of c-Jun, which activated the transcription of SNAI1 by directly binding to its promoter. Conclusions: MK5-AS1 cis-regulated the nearby gene MK5 and acted as a let-7f-1-3p sponge, playing a vital role in CRC tumorigenesis. This study could provide novel insights into molecular therapeutic targets of CRC.

scholarly journals LINC01224 promotes colorectal cancer progression through targeting miR-485-5p/MYO6 axis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jingfeng Gu ◽  
Liang Dong ◽  
Yun Wang ◽  
Wenjia Nie ◽  
Wencong Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Binding Interaction ◽  
Tissue Samples ◽  
Rna Immunoprecipitation ◽  
Colorectal Cancer Progression ◽  
Transcription Factor Yy1

Abstract Background Long noncoding RNAs (lncRNAs) are related to colorectal cancer (CRC) development. However, the role and mechanism of lncRNA LINC01224 in CRC development are largely unknown. Methods LINC01224, Yin Yang 1 (YY1), microRNA (miR)-485-5p, and myosins of class VI (MYO6) levels were examined using quantitative reverse transcription polymerase chain reaction and western blotting. Functional analyses were processed through CCK-8, colony formation, flow cytometry, transwell, and xenograft analyses. Dual-luciferase reporter, chromatin immunoprecipitation (ChIP), RNA immunoprecipitation, and pull-down assays were conducted to analyze the binding interaction. Results LINC01224 abundance was elevated in CRC tissue samples and cell lines. Elevated LINC01224 might indicate the lower 5-year overall survival in 52 CRC patients. LINC01224 was upregulated via the transcription factor YY1. LINC01224 knockdown restrained CRC cell proliferation, migration, and invasion and increased apoptosis. MiR-485-5p was sponged by LINC01224, and miR-485-5p downregulation relieved the influence of LINC01224 interference on CRC progression. MYO6 was targeted via miR-485-5p and regulated via LINC01224/miR-485-5p axis. MiR-485-5p overexpression suppressed CRC cell proliferation, migration, and invasion and facilitated apoptosis. MYO6 upregulation mitigated the role of miR-485-5p. LINC01224 knockdown decreased xenograft tumor growth. Conclusion YY1-induced LINC01224 regulates CRC development via modulating miR-485-5p/MYO6 axis.

scholarly journals Long Noncoding RNA LINC00857 Promotes Proliferation, Migration, and Invasion of Colorectal Cancer Cell through miR-1306/Vimentin Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Na Chang ◽  
Yayun Cui ◽  
Xue Liang ◽  
Dan Han ◽  
Xiaomin Zheng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cell ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Colorectal Cancer Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
The Novel ◽  
Tissue Samples ◽  
Mesenchymal Transition

Colorectal cancer is a commonly diagnosed cancer and the leading cause of cancer-related death which still increasing in many countries. The lack of biomarkers for early detection and clinic treatment results in high morbidity and mortality. The novel role of long noncoding RNA LINC00857 on cell proliferation migration and invasion was explored in this article. The expression level of LINC00857 in colorectal cancer tissue samples and cells was determined notably higher than normal tissue samples and cells. Silence LINC00857 can significantly inhibit colorectal cancer cell viability and metastasis in vitro. Moreover, LINC00857 depletion caused cell accumulation in the G0/G1 phase. In addition, we recognized the novel LINC00857–miR-1306–vimentin axis and demonstrated it by dual-luciferase reporter assay. And this signaling axis could be considered as the target for colorectal cancer treatment. In conclusion, LINC00857 can promote colorectal cancer progress by sponging miR-1306 and upregulate vimentin to accelerate the epithelial-mesenchymal transition process.

scholarly journals Circular RNA 100146 Promotes Colorectal Cancer Progression by miR-149/HMGA2 Axis

2020 ◽  
Author(s):  
Kunpeng Liu ◽  
Yuhua Mou ◽  
Xiufang Shi ◽  
Tingkun Liu ◽  
Zhanfeng Chen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Xenograft Model ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Western Blot Assay

Aim: Colorectal cancer (CRC) has developed into the third leading reason of cancer-associated death worldwide. Studies has confirmed that circular RNAs (circRNAs) sponge microRNAs (miRNAs) to regulate the function of downstream genes. This study aimed to expound the underlying mechanism of circRNA 100146 in CRC. Methods: The expression of circRNA 100146, miR-149 and high mobility group A2 (HMGA2) was detected by quantitative real time PCR (RT-qPCR). A series of bio-functional effects (cell viability, apoptosis, migration/invasion) were evaluated by methyl thiazolyl tetrazolium (MTT), flow cytometry, transwell. Protein level was measured by Western blot assay. The xenograft model was established for in vivo experiments. The interactions among circRNA 100146, miR-149 and HMGA2 were evaluated by dual-luciferase reporter assay, RNA immunoprecipitation assays, or RNA pulldown assay. Results: CircRNA 100146 was upregulated in CRC tissues and cells. CircRNA 100146 knockdown inhibited cell proliferation, promoted apoptosis and suppressed migration and invasion in vitro, and impeded tumor growth in vivo. Also, miR-149 was negalitively regulated by circRNA 100146, and targeted to HMGA2 and mediated its expression. Moreover, miR-149 interference abrogated the activities of silenced circRNA 100146 in proliferation, apoptosis, migration and invasion. Furthermore, HMGA2 overexpression abated the effects above caused by circRNA 100146 silencing, while the mutant on miR-149 binding sites in HMGA2 3’UTR lead to it losing this ability. Conclusion: CircRNA 100146 knockdown repressed proliferation, enhanced apoptosis and hindered migration and invasion in SW620 and SW480 cells through targeting miR-149/HMGA2 axis.

scholarly journals Long noncoding RNA MAPKAPK5-AS1 promotes colorectal cancer progression by cis-regulating the nearby gene MK5 and acting as a let-7f-1-3p sponge

2020 ◽  
Author(s):  
Ting Yang ◽  
Wei-Cong Chen ◽  
Pei-Cong Shi ◽  
Man-Ru Liu ◽  
Tao Jiang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Noncoding Rna ◽  
Vital Role ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Colorectal Cancer Progression ◽  
Molecular Therapeutic

Abstract Background: Long noncoding RNAs (lncRNAs) are considered critical regulators in cancers; however, the clinical significance and mechanisms of MAPKAPK5-AS1 (hereinafter referred to as MK5-AS1) in colorectal cancer (CRC) remain mostly unknown. Methods: In this study, quantitative real-time PCR ( qPCR ) and western blotting were utilized to detect the levels of MK5-AS1, let-7f-1-3p and MK5 (MAPK activated protein kinase 5) in CRC tissues and cell lines. The biological functions of MK5-AS1, let-7f-1-3p and MK5 in CRC cells were explored using Cell Counting Kit-8 ( CCK8 ), colony formation and transwell assays. The potential mechanisms of MK5-AS1 were evaluated by RNA pull-down, RNA immunoprecipitation ( RIP ), dual luciferase reporter assay, chromatin immunoprecipitation ( CHIP ) and bioinformatics analysis. The effects of MK5-AS1 and MK5 on CRC were investigated by a xenotransplantation model. Results : We confirmed that MK5-AS1 was significantly increased in CRC tissues. Knockdown of MK5-AS1 suppressed cell migration and invasion in vitro and inhibited lung metastasis in mice. Mechanistically, MK5-AS1 regulated SNAI1 expression by sponging let-7f-1-3p and cis -regulated the adjacent gene MK5. Moreover, MK5-AS1 recruited RBM4 and eIF4A1 to promote the translation of MK5. Our study verified that MK5 promoted the phosphorylation of c-Jun, which activated the transcription of SNAI1 by directly binding to its promoter. Conclusions : MK5-AS1 cis -regulated the nearby gene MK5 and acted as a let-7f-1-3p sponge, playing a vital role in CRC tumorigenesis. This study could provide novel insights into molecular therapeutic targets of CRC.

scholarly journals Decreased level of miR-1301 promotes colorectal cancer progression via activation of STAT3 pathway

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Fangfang Yang ◽  
Hua Wang ◽  
Bianbian Yan ◽  
Tong Li ◽  
Lulu Min ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Cancer Progression ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Aberrant Expression ◽  
Cell Migration And Invasion ◽  
Lovo Cells ◽  
Colorectal Cancer Progression

Abstract The molecular pathogenesis of colorectal cancer (CRC) has been widely investigated in recent years. Accumulating evidence has indicated that microRNA (miRNA) dysregulation participates in the processes of driving CRC initiation and progression. Aberrant expression of miR-1301 has been found in various tumor types. However, its role in CRC remains to be elucidated. In the present study, we identified miR-1301 was enriched in normal colorectal tissues and significantly down-regulated in CRC. Decreased level of miR-1301 strongly correlated with aggressive pathological characteristics, including advanced stage and metastasis. Bioinformatics and dual luciferase assay demonstrated that STAT3 is a direct target of miR-1301. Gain and loss-of-function assays showed that miR-1301 had no effect on cell proliferation. Overexpression of miR-1301 suppressed cell migration and invasion capacity of pSTA3-positive LoVo cells, but not pSTAT3-negative SW480 cells, while inhibition of miR-1301 consistently promoted cell migration and invasion in both cell lines. Additionally, miR-1301 inhibition restored the suppressed migration and invasion of STAT3- knockdown LoVo cells. MiR-1301 functioned as a tumor suppressor to modulate the IL6/STAT3 signaling pathway. In summary, this study highlights the significant role of miR- 1301/STAT3 axis in CRC metastasis.

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