scholarly journals The LncRNA XIST Promotes Colorectal Cancer Cell Growth Through Regulating miR-497-5p/FOXK1 Axis

2020 ◽  
Author(s):  
Nan Wang ◽  
Jia-Xing He ◽  
Guo-Zhan Jia ◽  
Ke Wang ◽  
Shuai Zhou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Xist Expression ◽  
Cancer Cell Growth ◽  
Down Regulation ◽  
Lncrna Xist ◽  
And Migration

Abstract Background: Recently, accumulated numbers of studies have reported that long noncoding RNAs (lncRNAs) process an important role in tumorigenesis. As a new member found in lncRNAs, the role of lncRNA XIST (XIST) in colorectal cancer (CRC) was still elusive. The objective of this study was conducted to characterize a novel regulatory network involving XIST in CRC cells. Methods: The mRNAs of XIST, miR-497-5p, and forkhead box k1 (FOXK1) in CRC cells and tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). And the proliferation and apoptosis of CRC cells were determined using cell counting kit-8 assay and flow cytometry. Moreover, we also detected the cell migration and invasion using Transwell assays. The relationships between XIST, miR-497-5p, and FOXK1 were predicted and then the dual-luciferase reporter assay was used to their relationships. The protein level of FOXK1 was quantitated using western blot. Results: In CRC tissues and cell lines, XIST expression was up-regulated, in which also existed miR-497-5p down-regulation and FOXK1 up-regulation. XIST knockdown suppressed CRC cell proliferation and migration as well as its invasion. Moreover, blocking the XIST expression could inhibit CRC tumor growth in vivo and the effects were antagonized by loss of miR-497-5p. miR-497-5p was identified as a sponge of XIST and also targeted FOXK1 in CRC cells. Besides, XIST silencing-mediated inhibitory activity against CRC progression reversed miR-497-5p down-regulation or FOXK1 up-regulation. Conclusion: In conclusion, XIST promotes the malignancy of colon cancer cells partly by competitively binding to miR-497-5p, which then led to increased FOXK1 expression. We conclude that targeting XIST may be a possible treatment for colon cancer.

scholarly journals The lncRNA XIST promotes colorectal cancer cell growth through regulating the miR-497-5p/FOXK1 axis

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Nan Wang ◽  
Jia-Xing He ◽  
Guo-Zhan Jia ◽  
Ke Wang ◽  
Shuai Zhou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cancer Cell Growth ◽  
Forkhead Box ◽  
Proliferation And Apoptosis ◽  
Lncrna Xist

Abstract Background Recent studies suggest that long noncoding RNAs (lncRNAs) play an important role in tumorigenesis. As a newly identified lncRNA, the role of XIST in colorectal cancer (CRC) has not been established. Here, we sought to characterize the role of XIST and its associated regulatory network in CRC cells. Methods Expression of XIST mRNA, miR-497-5p, and forkhead box k1 (FOXK1) in CRC cells and tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). Proliferation and apoptosis of CRC cells were determined using the CCK-8 cell counting assay and flow cytometry. The rate of cell migration and invasion was determined using a transwell assay. The relationships between XIST, miR-497-5p, and FOXK1 were predicted and confirmed using a dual-luciferase reporter assay. Expression of FOXK1 protein was quantified by Western blot. Results XIST and FOXK1 expression were significantly upregulated in CRC tissues and cell lines, while miR-497-5p expression was downregulated. XIST knockdown significantly suppressed CRC cell proliferation, migration, and invasion. Silencing of XIST also reversed the downregulation of miR-497-5p and upregulation of FOXK1. Moreover, blocking XIST expression was shown to inhibit CRC tumor growth in vivo and the effects were antagonized by the loss of miR-497-5p. miR-497-5p was shown to act as a sponge of XIST and also targeted FOXK1 in CRC cells. Conclusions XIST was shown to promote the malignancy of CRC cells by competitively binding to miR-497-5p, resulting in an increase in FOXK1 expression. These results suggest that targeting of XIST may represent a possible treatment for CRC.

scholarly journals The lncRNA XIST promotes colorectal cancer cell growth through regulating the miR-497-5p/FOXK1 axis

2020 ◽  
Author(s):  
Nan Wang ◽  
Jia-Xing He ◽  
Guo-Zhan Jia ◽  
Ke Wang ◽  
Shuai Zhou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cancer Cell Growth ◽  
Forkhead Box ◽  
Proliferation And Apoptosis ◽  
Lncrna Xist

Abstract Background: Recent studies suggest that long noncoding RNAs (lncRNAs) play an important role in tumorigenesis. As a newly identified lncRNA, the role of XIST in colorectal cancer (CRC) has not been established. Here, we sought to characterize the role of XIST and its associated regulatory network in CRC cells. Methods: Expression of XIST mRNA, miR-497-5p, and forkhead box k1 (FOXK1) in CRC cells and tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). Proliferation and apoptosis of CRC cells were determined using the CCK-8 cell counting assay and flow cytometry. The rate of cell migration and invasion was determined using a transwell assay. The relationships between XIST, miR-497-5p, and FOXK1 were predicted and confirmed using a dual-luciferase reporter assay. Expression of FOXK1 protein was quantified by Western blot. Results: XIST and FOXK1 expression were significantly upregulated in CRC tissues and cell lines, while miR-497-5p expression was downregulated. XIST knockdown significantly suppressed CRC cell proliferation, migration, and invasion. Silencing of XIST also reversed the downregulation of miR-497-5p and upregulation of FOXK1. Moreover, blocking XIST expression was shown to inhibit CRC tumor growth in vivo and the effects were antagonized by the loss of miR-497-5p. miR-497-5p was shown to act as a sponge of XIST and also targeted FOXK1 in CRC cells.Conclusion: XIST was shown to promote the malignancy of CRC cells by competitively binding to miR-497-5p, resulting in an increase in FOXK1 expression. These results suggest that targeting of XIST may represent a possible treatment for colon cancer.

scholarly journals The lncRNA XIST promotes colorectal cancer cell growth through regulating the miR-497-5p/FOXK1 axis

2020 ◽  
Author(s):  
Nan Wang ◽  
Jia-Xing He ◽  
Guo-Zhan Jia ◽  
Ke Wang ◽  
Shuai Zhou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cancer Cell Growth ◽  
Forkhead Box ◽  
Proliferation And Apoptosis ◽  
Lncrna Xist

Abstract Background: Recent studies suggest that long noncoding RNAs (lncRNAs) play an important role in tumorigenesis. As a newly identified lncRNA, the role of XIST in colorectal cancer (CRC) has not been established. Here, we sought to characterize the role of XIST and its associated regulatory network in CRC cells.Methods: Expression of XIST mRNA, miR-497-5p, and forkhead box k1 (FOXK1) in CRC cells and tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). Proliferation and apoptosis of CRC cells were determined using the CCK-8 cell counting assay and flow cytometry. The rate of cell migration and invasion was determined using a transwell assay. The relationships between XIST, miR-497-5p, and FOXK1 were predicted based on these results, and confirmed using a dual-luciferase reporter assay. Expression of FOXK1 protein was quantified by Western blot.Results: XIST and FOXK1 expression were significantly upregulated in CRC tissues and cell lines, while miR-497-5p expression was downregulated. XIST knockdown significantly suppressed CRC cell proliferation, migration, and invasion. Silencing of XIST also reversed the downregulation of miR-497-5p and upregulation of FOXK1. Moreover, blocking XIST expression was shown to inhibit CRC tumor growth in vivo and the effects were antagonized by the loss of miR-497-5p. miR-497-5p was shown to act as a sponge of XIST and also targeted FOXK1 in CRC cells.Conclusion: XIST was shown to promote the malignancy of CRC cells by competitively binding to miR-497-5p, resulting in an increase in FOXK1 expression. These results suggest that targeting of XIST may represent a possible treatment for colon cancer.

scholarly journals MiR-301a Promotes Colorectal Cancer Cell Growth and Invasion by Directly Targeting SOCS6

2015 ◽  
Vol 35 (1) ◽  
pp. 227-236 ◽  
Author(s):  
Yantian Fang ◽  
Bo Sun ◽  
Jianbin Xiang ◽  
Zongyou Chen
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cytokine Signaling ◽  
Loss Of Function ◽  
Cancer Cell Growth ◽  
Invasion And Migration ◽  
And Migration

Background/Aims: Colorectal cancer (CRC) is one of the most common malignancies worldwide, and microRNAs play a crucial role in CRC biology. The purpose of this study was to investigate the exact functions and potential mechanisms of action of miR-301a in CRC. Methods: Quantitative real-time PCR was conducted to assess the expression of miR-301a. Cell proliferation was detected using MTT and colony formation assay, and cell invasion and migration were evaluated using Transwell assay. Luciferase reporter assay was used to identify the direct regulation of suppressor of cytokine signaling 6 (SOCS6) by miR-301a. Results: We first confirmed the upregulation of miR-301a in CRC tissues and cell lines. Gain-of-function and loss-of-function studies in the human CRC cell lines, SW480 and SW620, showed that miR-301a acts as an oncogene by increasing cell proliferation, migration and invasion as well as tumor growth. Furthermore, SOCS6 was identified as a target gene of miR-301a. Reintroduction of SOCS6 partially abrogated miR-301a-induced cell proliferation, migration and invasion. Conclusion: These data suggest that miR-301a promotes CRC progression by directly downregulating SOCS6 expression, and miR-301a may represent a novel biomarker for the prevention and treatment of CRC.

scholarly journals LncRNA XIST promotes liver cancer progression by acting as a molecular sponge of miR-200b-3p to regulate ZEB1/2 expression

2021 ◽  
Vol 49 (5) ◽  
pp. 030006052110162
Author(s):  
Lili Liu ◽  
Hua Jiang ◽  
Hongming Pan ◽  
Xiuming Zhu
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Xist Expression ◽  
Lncrna Xist

Objective To evaluate the predictive value of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) for survival, and determine the involvement of miRNA(miR)-200b-3p and zinc finger E-box-binding homeobox (ZEB) 1/2 in the pro-tumor effect of lncRNA XIST in liver cancer. Methods We evaluated lncRNA XIST expression in liver cancer tissues and cell lines by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and analyzed the correlation between its expression and overall survival of liver cancer patients by Kaplan–Meier analysis. Its effects on cell proliferation, migration, and invasion were analyzed by Cell-Counting Kit-8 and Transwell assays. The association between lncRNA XIST and miR-200b-3p, and the effects of lncRNA XIST on ZEB1/2 expression were explored using luciferase reporter assays, real-time PCR, and western blotting. Results The lncRNA XIST was significantly upregulated in liver cancer, and increased lncRNA XIST expression was associated with a poor prognosis. The lncRNA XIST promoted liver cancer cell proliferation, migration, and invasion in vitro, and acted as a molecular sponge for miR-200b-3p, and also regulated the expression of ZEB1/2 via miR-200b-3p. Conclusion The lncRNA XIST is an oncogenic lncRNA that promotes liver cancer metastasis, and its pro-metastatic phenotype can be partially attributed to the lncRNA XIST/miR-200b-3p/ZEB1/2 signaling axis.

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.

scholarly journals CircHMGCS1 is upregulated in colorectal cancer and promotes proliferation of colorectal cancer cells by targeting microRNA-503-5p

2019 ◽  
Vol 17 ◽  
pp. 205873921986955 ◽  
Author(s):  
Jingqing Dong ◽  
Jun Li ◽  
Jihui Luo ◽  
Weiqiang Wu
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Quantitative Polymerase Chain Reaction ◽  
Clinical Parameter ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Apoptosis Pathway ◽  
Colorectal Cancer Cells ◽  
And Migration ◽  
Related Proteins

This study aims to explore the regulatory mechanism of circHMGCS1/microRNA-503-5p (miR-503-5p) axis during colorectal cancer (CRC) development and progression. Real-time quantitative polymerase chain reaction (RT-qPCR) was applied to evaluate the expression of circHMGCS1 and miR-503-5p in CRC samples and their adjacent non-tumor specimen. Then, cell proliferation and cell apoptosis and migration and invasion of circHMGCS1-knocked down cells were further detected, using cell counting kit-8 (CCK-8), flow cytometry, Transwell assay, and western blotting assays. CircHMGCS1 was found to be significantly upregulated in CRC, and its high expression was closely correlated with the poor clinical parameter. In addition, the knockdown of circHMGCS1 could significantly inhibit CRC cells’ growth promoting apoptosis, as suggested by the expression of apoptosis pathway-related proteins, which changed consistently. Furthermore, miR-503-5p inhibitors were able to reverse the suppression of cell proliferation induced by silencing circHMGCS1. Therefore, circHMGCS1 might serve as a promising bio-marker and treatment target for CRC.

scholarly journals miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Mingli Suo ◽  
Yanfei Sun ◽  
Hailan Yang ◽  
Jing Ji ◽  
Yinfang He ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Cell Invasion ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Trophoblast Cells ◽  
Down Regulation ◽  
Invasion And Migration ◽  
Potential Biomarker ◽  
And Migration

Abstract Preeclampsia (PE), a common obstetrical disorder, is characterized by impaired migration and invasion abilities of trophoblastic cells. MicroRNA-183-5p (miR-183) was reported to regulate cell migration and invasion in various types of human cancers; however, its role in the pathogenesis of PE remains elusive. Herein, we investigated the role of miR-183 in HTR-8/SVneo trophoblast cells invasion and migration and explored the underlying mechanism. Our results showed that miR-183 was significantly up-regulated in placental tissues from pregnant women compared with that in normal pregnant women. Overexpression of miR-183 inhibited proliferation, migration and invasion, as well as induced apoptosis in HTR-8/SVneo cells. Otherwise, down-regulation of miR-183 achieved the opposite effects. Bioinformatics prediction and luciferase reporter assay confirmed that matrix metalloproteinase-9 (MMP-9) is a target of miR-183. In addition, MMP-9 expression was significantly down-regulated, and inversely correlated with the miR-183 level in placental tissues from pregnant women with severe PE. Down-regulation of MMP-9 suppressed the trophoblast cell invasion and migration, whereas overexpression of MMP-9 promoted cell invasion and migration in HTR-8/SVneo cells. More importantly, up-regulation of MMP-9 reversed the inhibitory effects of miR-183 on cell invasion and migration in trophoblast cells. Collectively, our findings suggested that miR-183 may play critical roles in the pathogenesis of PE and serve as a potential biomarker for severe PE.

Long non-coding RNA LINC00115 contributes to the progression of colorectal cancer by targeting miR-489-3p via PI3K/AKT/mTOR pathway

2020 ◽  
Author(s):  
Weiyu Feng ◽  
Baodong Li ◽  
Jinbang Wang ◽  
Huiliang Zhang ◽  
Yonggang Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Molecular Mechanisms ◽  
Biological Effects ◽  
Inverse Correlation ◽  
Mtor Signaling ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Regulatory Relationship ◽  
Tissue Samples

Abstract Background Long noncoding RNAs (lncRNAs) are tumor-related regulators and have been found to be involved in the underlying molecular mechanisms of colorectal cancer (CRC). However, the role of lncRNA LINC00115 during CRC progression is not entirely elucidated. Methods The expression of LINC00115 was analyzed in paired CRC tissue samples and its clinical significance was evaluated. The biological effects on CRC cells proliferation, apoptosis, migration, invasion and PI3K/AKT/mTOR signaling were assessed by Cell Counting Kit-8 assay, Transwell assay, flow cytometry analysis and Western blot, respectively. The regulatory relationship between LINC00115 and miR-489-3p was determined by dual-luciferase reporter assays. Results LINC00115 was significantly overexpressed in CRC and its overexpression predicted poor outcome of the patients. Downregulation of LINC00115 markedly inhibited CRC cell proliferation, increased cell apoptosis, and suppressed cell migration and invasion. Moreover, downregulation of LINC00115 led to the inactivation of PI3K/AKT/mTOR signaling. Bioinformatics analysis identified miR-489-3p as a candidate target of LINC00115. Furthermore, we revealed an inverse correlation between LINC00115 and miR-489-3p in CRC tissues. miR-489-3p might directly target LINC00115 and downregulation of miR-489-3p could rescue the biological effects induced by the absence of LINC0015. Conclusion LINC00115 serves as an excellent oncogene of CRC metastasis, the deeper understanding of LINC00115/miR-489-3p axis might provide potential therapeutic targets for CRC metastasis.

LncRNA Phosphoglucomutase 5-Antisense RNA 1 Modulation Affects the Proliferation and Metastasis Capabilities via Upregulating miR-484 Expression in Colorectal Cancer Cells

2021 ◽  
Vol 11 (1) ◽  
pp. 176-184
Author(s):  
Yongsheng Zhou ◽  
Jijin Wu ◽  
Shushan Yin
Keyword(s):  
Colorectal Cancer ◽  
Cell Viability ◽  
Antisense Rna ◽  
Cell Counting ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Down Regulation ◽  
Colorectal Cancer Cells ◽  
Proliferation And Metastasis ◽  
Hct116 Cells

Background: LncRNA emerges to be helpful in the diagnosis and treatment of colorectal cancer (CRC). We intended to uncover the underlying modulatory pathway of lncRNA PGM5-AS1 in CRC cells. Materials and Methods: The prediction of target of PGM5-AS1 was by informatics and verified by dual luciferase assay. Transcription levels of PGM5-AS1 and miR-484 were determined by qPCR. Cell viability was measured by cell counting kit (CCK)-8. Migration rate was assessed by wound healing assay and invasion by Transwell. Cell growth was evaluated by colony formation assay. Results: PGM5-AS1 was up-regulated in CRC tissue and cell lines while its down-regulation contributed to the decreasing of cell viability, growth, migration and invasion capabilities of SW480 and HCT116 cells. Moreover, miR-484 was the target of PGM5-AS1. In addition, the down-regulation of PGM5-AS1 partially restored the elevated cell viability, growth, migration and invasion capacities following the inhibition of miR-484 expression in SW480 and HCT116 cells. Conclusions: The loss of miR-484 expression in CRC might be involved in the promotion and metastasis of CRC, the consequence which could be the result of the overexpression of PGM5-AS1. Hence, the down-regulation of PGM5-AS1 could be a therapeutic target in the prevention or intervention of CRC.

Sign in / Sign up

Export Citation Format

Share Document