Long Noncoding RNA Myocardial Infarction-Associated Transcript as a Cancer Promoting Factor in Colon Cancer Development

2019 ◽  
Vol 9 (5) ◽  
pp. 655-661
Author(s):  
Wang Zhi ◽  
Jiang Zongdan ◽  
Zhang Yushu ◽  
Xu Xiaojun ◽  
Zhang Zhenyu
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cell Number ◽  
Cyclin D3 ◽  
Sw620 Cell ◽  
Invasion And Migration ◽  
Cancer Tissues

Objection: The study aimed to explain the effects and mechanisms of long noncoding RNA (lncRNA) MIAT in development of colon cancer. Methods: The adjacent and cancer tissues which were collected from 30 cases colon cancer patients were evaluated pathology by HE staining and lncRNA MIAT expression by ISH assay. In the vitro study, SW620 cells were divided into NC, siRNA-control and siMIAT groups. Measuring cell proliferation, apoptosis, cell cycle, invasion and migration by CCK-8, flow cytometry, transwell and wound healing, and evaluating the relative proteins expressions by WB assay. Results: Compared with adjacent normal tissues, the lncRNA MIAT was significantly up-regulation in colon cancer tissues (P < 0.001). By cell experiment, with lncRNA MIAT knockdown, the cell proliferation was significantly depressed (P < 0.001) via significantly improving cell apoptosis and keeping the cell in the G1 phase (P < 0.001, respectively); the invasion SW620 cell number and wound healing rate were significantly suppressed (P < 0.001, respectively). The relative proteins (CDK2, Cyclin D3 and MMP-9) expressions of siMIAT group were significantly down-regulation compared with those of NC group (P < 0.001, respectively). Conclusion: Our study found that lncRNA MIAT expression is closely associated with colon cancer and may be one of key roles in progression and metastasis in colon cancer.

scholarly journals MiR-144 inhibits growth and metastasis in colon cancer by down-regulating SMAD4

2019 ◽  
Vol 39 (3) ◽  
Author(s):  
Shihou Sheng ◽  
Lin Xie ◽  
Yuanyu Wu ◽  
Meng Ding ◽  
Tao Zhang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Scratch Test ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Cancer Breast ◽  
Smad4 Expression ◽  
Sw620 Cells ◽  
And Migration ◽  
Cancer Tissues

Abstract MicroRNAs (MiRs) are thought to display regulator action in tumor suppression and oncogenesis. miR-144 plays an important role in the development of various cancers, such as colorectal cancer, breast cancer, and lung cancer, by targetting different molecules potentially involved in many signaling pathways. SMAD4 is a common signaling during tumor progression, and it can inhibit cell proliferation and promote cell motility in most epithelial cells. The present study focused on the effect of miR-144 and SMAD4 on colon cancer in order to find the novel gene therapy target for the treatment of colon cancer. Quantitative real-time polymerase chain reaction was used to assess the expression level of miR-144 in colon cancer tissues and SW620 cells. MTT assay, scratch test, and transwell assay were used to evaluate cell proliferation, migration, and invasion, respectively. Moreover, luciferase assays were utilized to identify the predictive effect of miR-144 on SMAD4. Western blotting was performed to determine the relative expression of protein related to SMAD4. We found miR-144 level was significantly lower in colon cancer tissues and SW620 cells. Moreover, SMAD4 level, both in mRNA and protein, was obviously elevated in colon cancer tissues. Further, miR-144 mimics treatment inhibited cells proliferation, invasion, and migration. Fluorescence intensity of miR-144 mimics group in wild type cells was decreased. MiR-144 mimics repressed the SMAD4 expression both in mRNA and protein. These findings about miR-144/SMAD4 pair provide a novel therapeutic method for colon cancer patients.

C-Myc-activated long noncoding RNA CCAT1 promotes colon cancer cell proliferation and invasion

Tumor Biology ◽  
2014 ◽  
Vol 35 (12) ◽  
pp. 12181-12188 ◽  
Author(s):  
Xiaolu He ◽  
Xueming Tan ◽  
Xiang Wang ◽  
Heiying Jin ◽  
Li Liu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Colon Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Proliferation And Invasion

Effect of Targeting Leucine-Zipper-Like Transcription Regulator 1 Gene on Colon Cancer Cells

2021 ◽  
Vol 11 (8) ◽  
pp. 1588-1594
Author(s):  
Xuemin Song ◽  
Dongming Luo ◽  
Qian Zhong ◽  
Ke Wei ◽  
Yangyang Tang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Real Time ◽  
Real Time Pcr ◽  
Leucine Zipper ◽  
Clinicopathological Characteristics ◽  
Control Group ◽  
Sw620 Cell ◽  
Cancer Tissues ◽  
Proliferation And Invasion

LZTR1 is associated with several diseases, including liver cancer, childhood cancer, and schwannomas. However, LZTR1’s role in colon cancer and its mechanism of action have not been reported. The colon cancer tissues and adjacent tissues were collected to measure the expression of LZTR1 by Real time PCR. Colon cancer SW620 cell lines were cultured and randomly divided into control group and LZTR1 group followed by analysis of LZTR1 expression by real time PCR, cell proliferation by MTT assay, Caspase3 activity, Bcl-2 and Bax level by Real time PCR, cell invasion by Transwell chamber; NF-κB/VEGF expression by Western blot. LZTR1 expression was significantly reduced in colon cancer tissues compared to adjacent tissues (P <0.05) and negatively correlated with colon cancer TNM stage, tumor size, and lymph node metastasis, and positively associated with tumor differentiation (P <0.05). LZTR1 plasmid transfection into SW620 cells can significantly up-regulate LZTR1, inhibit tumor cell proliferation and invasion, increase Caspase 3 activity and Bax level, downregulate Bcl-2, NF-κB and VEGF (P <0.05). LZTR1 expression is reduced in colon cancer tissues, which is related to its clinicopathological characteristics. Up-regulation of LZTR1 can regulate apoptosis and inhibit tumor proliferation and invasion by regulating NF-κB/VEGF signaling pathway.

lncRNA Metallothionein 1J Pseudogene Positively Regulate miRNA-383 to Suppress Osteosarcoma Biological Activities via Wnt Pathway

2019 ◽  
Vol 9 (8) ◽  
pp. 1073-1080
Author(s):  
Wei Liu ◽  
Bin Wang ◽  
Shaojing Ju
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Wnt Pathway ◽  
Biological Activities ◽  
Mg63 Cell ◽  
Cell Number ◽  
Osteosarcoma Cell ◽  
Wound Healing Assay ◽  
Primary Bone Tumor ◽  
Invasion And Migration

Background: Osteosarcoma is a type of primary bone tumor that usually occurs in the metaphyseal region of long bones. It has been unclear lncRNA MT1JP in osteosarcoma development. Material and Methods: The MG63 cell were respectively MT1JP, miRNA-383 and miRNA-383 inhibitor. Measuring the cell proliferation, apoptosis and cell cycle by MTT and flow cytometry and evaluation the MG63 cell invasion and migration by transwell and wound healing assay in difference groups. The relative proteins (Wnt, β-catenin, Cyclin D1, MMP-2 and MMP-9) were measured by Western blot (WB) assay. By luciferase target assay, analysis the correlation between miRNA-383 and Wnt in MG63 cell. Results: Compared with WT group, the cell proliferation rate of pcDNAMT1JP and miRNA-383 groups were significantly down-regulation with cell apoptosis rates and G1 phase rates were significantly increased (P < 0.01, respectively). By transwell and wound healing assay, the invasion cell number and wound healing rate of pcDNA-MT1JP and miRNA-383 groups were significantly depressed (P < 0.01, respectively). By WB assay, Wnt, β-catenin, c-Myc, MMP-2 and MMP-9 proteins expressions of pcDNA-MT1JP and miRNA-383 groups were significantly suppressed compared with those of WT group (P < 0.01, respectively). By luciferase target assay, Wnt was the targeted gene of miRNA-383 in MG63 cell. Conclusion: MT1JP could suppress osteosarcoma cell lines MG63 cell biological activities via stimulating miRNA-383 and depressing Wnt pathway.

scholarly journals INHBA promotes the proliferation, migration and invasion of colon cancer cells through the upregulation of VCAN

2021 ◽  
Vol 49 (6) ◽  
pp. 030006052110149
Author(s):  
Jia Guo ◽  
Yuan Liu
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Counting ◽  
Migration And Invasion ◽  
High Morbidity ◽  
Colon Cancer Cells ◽  
Invasion And Migration ◽  
And Migration ◽  
Cancer Tissues

Objective Colon cancer has high morbidity and mortality rates, and proliferation, invasion and migration play an important role in colon cancer progression. Here, the effects of inhibin subunit beta A (INHBA) on cell proliferation, invasion and migration were investigated. Methods The UALCAN database was used to assess INHBA expression in colon cancer tissues and predict the survival of patients with high and low INHBA expression. The relevant proteins were detected by RT-qPCR and western blot. Cell transfection was performed to overexpress or inhibit INHBA and versican (VCAN). The high correlation between INHBA and VCAN found through LinkedOmics and StarBase databases was verified by immunoprecipitation assays. Cell proliferation was detected by cell counting kit-8 and colony formation assays. Wound healing and Transwell assays were used to assess migration and invasion. Results INHBA expression was upregulated in colon cancer tissues and cells. INHBA inhibition impaired the proliferation, migration and invasion of these cells. In addition, we confirmed the correlation between INHBA and VCAN in colon cancer cells. Finally, we found that INHBA interference inhibited the aggressive behavior of colon cancer cells by downregulating VCAN. Conclusion INHBA promotes the proliferation, migration and invasion of colon cancer cells through the upregulation of VCAN.

Long Non-Coding RNA F11-Antisense 1 (F11-AS1) Suppresses Ovarian Cancer Biological Activity by Regulating Phosphatase and Tensin Homolog Deleted on Chromosome Ten (PTEN)

2021 ◽  
Vol 11 (9) ◽  
pp. 1752-1759
Author(s):  
Fang Song ◽  
Fengshuang Li
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Biological Activity ◽  
Cell Apoptosis ◽  
Mrna Level ◽  
Cell Number ◽  
Skov3 Cell ◽  
Down Regulation ◽  
Invasion And Migration

Aim: To discuss F11-AS1’s effects and mechanisms in ovarian cancer development. Methods: Evaluating F11-AS1 expression by ISH assay and F11-AS1 mRNA level in difference cell lines by RT-qPCR assay. Using MTT, flow cytometry, transwell and wound healing assay to evaluate SKOV3 cell proliferation, cell apoptosis, invasion and migration. And using WB assay to measure PTEN, p-PI3K, AKT, P53 and MMP-9 proteins expressions. Results: F11-AS1 was significantly down-regulation with stage increasing in cancer tissues (P <0.01, respectively). With F11-AS1 transfection, the SKOV3 cell proliferation rate was significantly depressed with cell apoptosis and G1 phase rate significantly increasing (P <0.001, respectively). And then, invasion cell number and wound healing rate of lncRNA group which transfected with F11-AS1 significantly down-regulation (P <0.001). By WB assay, PTEN and P53 proteins expressions significantly up-regulation and p-PI3K, AKT and MMP-9 proteins expressions were significantly down-regulation (P <0.001). Conclusion: F11-AS1 depresses ovarian cancer biological activity by regulating PTEN by vitro study.

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