Silencing Circ_0005075 Inhibits the Invasion and Migration of Colon Cancer Cells and Induces Apoptosis

2021 ◽  
Vol 11 (3) ◽  
pp. 426-432
Author(s):  
Xiancheng Kong ◽  
Hao Zhang ◽  
Jianping Huang ◽  
Liang Yan ◽  
Li Sha ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Mirna Regulation ◽  
Migration Ability ◽  
Vimentin Expression ◽  
Sw620 Cell ◽  
Invasion And Migration ◽  
Sw620 Cells ◽  
And Migration ◽  
E Cadherin

Colon cancer is a common malignancy of the digestive tract, mostly occurring at the junction of the rectum and colon. It easily invades multiple internal organs and tissues, causing systemic injury and mortality to patients. The occurrence and development of colon cancer involve multiple genes and multiple factors. It is greatly significant to identify oncogenes and tumor suppressor genes that influence the development of colon cancer and to study their mechanism of action for colon cancer diagnosis and treatment. Furthermore, circRNA are involved in the development of several types of tumors by affecting miRNA regulation on target gene expression. In the present study, circ_0005075 siRNA and circ_0005075 siRNA + mir-335 inhibitor were transfected into colon cancer SW620 cells, and circ_0005075 gene expression was significantly decreased after transfecting circ_0005075 siRNA into SW620 cells. Silencing circ_0005075 expression significantly inhibited SW620 cell proliferation, invasion, and migration, and promoted apoptosis, downregulated PCNA and vimentin expression, and upregulated E-cadherin and cleaved caspase3 expression. After circ_0005075 siRNA + mir-335 was transfected, it inhibited circ_0005075 and mir-335 expression, which significantly affected the vigor, invasion and migration ability, apoptosis rate of SW620 cells, as well as PCNA, E-cadherin, vimentin, and cleaved caspase3 expression. Therefore, the present study demonstrated that circ_0005075 silencing inhibited the proliferation, invasion, and migration of SW620 cells and promoted apoptosis by upregulating mir-335 expression.

Bone Morphogenetic Protein 1 Targeting COL1A1 and COL1A2 to Regulate the Epithelial-Mesenchymal Transition Process of Colon Cancer SW620 Cells

2020 ◽  
Vol 20 (3) ◽  
pp. 1366-1374 ◽  
Author(s):  
Xijia Zhu ◽  
Xishun Luo ◽  
Shiyu Jiang ◽  
Haipeng Wang
Keyword(s):  
Colon Cancer ◽  
Cell Viability ◽  
Epithelial Mesenchymal Transition ◽  
Malignant Tumors ◽  
Beta Catenin ◽  
Migration Ability ◽  
Sw620 Cell ◽  
Mesenchymal Transition ◽  
Sw620 Cells ◽  
And Migration

Epithelial-mesenchymal transition (EMT) is an important factor in promoting the metastasis of colon cancer, which leads to clinical incurability. It has been found that bone morphogenetic proteins (BMPs) are closely related to EMT and the prognoses of most malignant tumors, including colon cancer tumors. However, the effects and mechanisms of BMP1 on the EMT of colon cancer are not yet clear. To explore the effects and mechanisms of BMP1 on the EMT of colon cancer, a BMP1 overexpression plasmid vector was used to interfere with SW620 cells and real-time fluorescence quantitative RNA and western blotting were used to detect the effects of BMP1 on the transcription and translation of COL1A1 and COL1A2 genes, as well as EMT-related genes, including beta-catenin, vimentin, and E-cadherin (E-Cad) genes in SW620 cells. MTT assay and Transwell techniques were used to detect the effects of BMP1 on the proliferation and migration of SW620 cells. The results demonstrate that BMP1 expression in SW620 cells is significantly lower than that in HCoEpiC cells, which promotes the expression of COL1A1 and COL1A2. Additionally, the expression of genes related to EMT, including beta-catenin and vimentin, increased, whereas E-Cad expression decreased. This difference was significant, which led to an increase in cell viability and the number of migrating cells in SW620 cells. Based on the overexpression of BMP1, the expression of COL1A1 and COL1A2 in SW620 was inhibited, which inhibited the process of EMT. Specifically, vimentin expression decreased, and E-Cad and beta-catenin expression increased. Additionally, SW620 cell viability decreased and migration ability decreased. Therefore, it can be concluded that the absence of BMP1 promotes the expression of COL1A and COL1A2 in colon cancer and promotes the process of EMT. Increasing the expression of BMP1 can inhibit the process of EMT in colon cancer, thereby inhibiting the migration of tumors.

scholarly journals LncRNA CRNDE Promoted Colorectal Cancer Cells Reisitance To Paclitaxel Through Wnt/β-Catenin Signaling Pathway

2021 ◽  
Author(s):  
Rui Ma ◽  
Chuan-yang Yu ◽  
Xiang Tao ◽  
Zhi Yang ◽  
Qi Huang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Signaling Pathway ◽  
Colorectal Neoplasia ◽  
Cancer Treatments ◽  
Sw620 Cell ◽  
Invasion And Migration ◽  
Over Expression ◽  
Colorectal Cancer Cells ◽  
Sw620 Cells ◽  
And Migration

Abstract Background The lncRNA colorectal neoplasia differentially expressed (lncRNA CRNDE) is commonly over-expressed in different human cancers and involved in different biological functions. Paclitaxel(PTX) is a tricyclic diterpenoid compound which often used as a natural anticancer drugs in cancer treatments. Although there have many research reports about the mechanisms of LncRNA involved in PTX treatment, there are no any research about lncRNA CRNDE and PTX resistance in colorectal cancer. The purpose of this study is to investigate the mechanisims of LncRNA CRNDE involving PTX resistance in colorectal cancer. Results We constructed lncRNA CRNDE over-expression vector and transfected it into SW620 cell. CCK8, Transwell experiments proved that over-expression of lnc CRNDE increased SW620 cells proliferation and invasion, while the si-CRNDE group was significantly decreased. over-expression CRNDE can significantly up-regulate β-catenin, c-myc, APC and Axin2 expression and affect the expression of cyclinD1 and CDK4 after treated with PTX. Conclusion lncRNA CRNDE promotes CRCs proliferation, invasion and migration. Over-expression of LncRNA CRNDE enhanced the reisitance of CRC to PTX through inhibition of Wnt/ β-catenin signaling pathway.

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.

LncRNA CEACAMP8 Regulates the Proliferation, Invasion and Migration of Trophoblast Cells

2019 ◽  
Vol 9 (9) ◽  
pp. 1215-1221
Author(s):  
Li Jie ◽  
Zhangcai Zheng ◽  
Liping Liu ◽  
Yali Liu ◽  
Zhaoyan Meng ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Flow Cytometry Analysis ◽  
Trophoblast Cells ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Qpcr Analysis ◽  
And Migration ◽  
E Cadherin

Preeclampsia (PE) is an idiopathic hypertension syndrome occurring after 20 weeks of gestation. Reports showed that lncRNAs expression was abnormal in preeclampsia. We aimed to investigate the role of lncRNA CEACAMP8 in the proliferation, invasion and migration of trophoblast cells to improve the preeclampsia. The cell transfection effects were determined by RT-qPCR analysis. The proliferation, invasion and migration of HTR-8/SVneo cells were detected by CCK-8 assay, transwell assay and wound healing assay. The flow cytometry analysis analyzed the cell cycle. Moreover, the expression of CDK2, cyclinD1, P21, MMP2, MMP9, E-cadherin, b-catenin and vimentin was determined by the western blot analysis. Consequently, CEACAMP8 inhibition promoted the proliferation, invasion and migration of HTR-8/SVneo cells and kept most of the cells in the S phase. The expression of proteins related to the proliferation, invasion and migration of HTR-8/SVneo cells were also changed in accordance with the increase of proliferation, invasion and migration of HTR-8/SVneo cells. In addition, lncRNA CEACAMP8 inhibition decreased the expression of E-cadherin and b-catenin, and increased the vimentin expression to promote the epithelial-mesenchymal transition. And, CEACAMP8 overexpression could reverse the above changes. This study indicated that CEACAMP8 inhibition promoted the proliferation, invasion and migration of HTR-8/SVneo cells and lncRNA CEACAMP8 overexpression reversed.

Melatonin down-regulates microRNA-10a and decreases invasion and migration of triple-negative breast cancer cells

2019 ◽  
Vol 2 (2) ◽  
pp. 86-99
Author(s):  
Jessica Gisleine de Oliveira ◽  
Jéssica Helena de Mora Marques ◽  
Jéssica Zani Lacerda ◽  
Lívia Carvalho Ferreira ◽  
Marcelo Mafra Campos Coelho ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Viability ◽  
Cancer Metastasis ◽  
Gene Expression Regulation ◽  
Mirna Sequence ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
E Cadherin

Breast cancer metastasis is one of the main factors associated with high mortality rates among patients. MicroRNAs (miRNAs) play an important role in gene expression regulation, and are associated with the metastatic process in breast cancer. Melatonin, a hormone secreted mainly in the pineal gland, has several oncostatic effects. The aim of this study was to investigate the action of melatonin in the modulation of miRNA-10a-5p and its association with metastatic mechanisms. We have evaluated the effects of melatonin on cell viability in MDA-MB-468 cell line after 24 hours of treatment. MDA-MB-468 and MDA-MB-231 cells were either transfected with inhibitor of miR-10a, or received a scrambled miRNA sequence as a negative control, then these cells were treated with or without melatonin. Gene expression of miR-10a was verified by real-time PCR. Invasion and migration assay using matrigel inserts were performed. The protein expression was analyzed by western blotting to quantify the epithelial-mesenchymal transition (EMT) markers (E-cadherin, claudin 7, and vimentin) and proliferation marker (PIK3CA). Our results showed that melatonin (1 mM) significantly decreased cell viability, and also affected miR-10a expression, which suppressed cell invasion and migration. Melatonin reduced vimentin and claudin 7 protein expressions, and increased E-cadherin. In contrast, inhibition of miR-10a reduced vimentin and did not modulate claudin 7 and E-cadherin. In conclusion, we demonstrated the effectiveness of melatonin in decreasing miR-10a, affecting invasion and migration, and proteins involved with the EMT process, which supports its potential role in the regulation of metastasis.  

Mechanisms Underlying the Altered Proliferation, Invasion and Migration of Endometrial Carcinoma Cells via Small Interfering RNA Specific Snail-1 Transcription Factor in HEC-1A Cells

2019 ◽  
Author(s):  
Jun Jiang ◽  
Jianfen Wang ◽  
Yong Shen ◽  
Xuelu Jiang
Keyword(s):  
Transcription Factor ◽  
Endometrial Carcinoma ◽  
Epithelial To Mesenchymal Transition ◽  
Migration Ability ◽  
Small Interference Rna ◽  
Mesenchymal Transition ◽  
Migration Assay ◽  
Invasion And Migration ◽  
And Migration ◽  
E Cadherin

Snail-1 is a transcription factor that play a role in the regulation of invasion, and metastasis of malignant cells via modulation of the epithelial-to-mesenchymal transition (EMT) process. Here in the current investigation, we knocked down the expression of Snail-1 through small interference RNA (siRNA) in Endometrial carcinoma (EC) associating cell line, namely HEC-1A, and then assessed the migration and proliferation of the transfected cells. We exerted Snail-1 specific siRNA to transfect the HEC-1A cells. Using quantitative Real-time PCR, the mRNA expression levels of Snail-1, MMP-9, Vimentin, and E-cadherin as well as expression level of miR-34a were measured. In addition, western blotting was carried out to determine the protein level of Snail-1. Using MTT and migration assay, the ability of transfected HEC-1A cells in proliferation and migration was evaluated. Snail-1 mRNA and protein expressions were decreased after transfection of HEC-1A cells. As well transfection caused decreased expression of MMP-9 and vimentin, while the expressions of E-cadherin and miR-34a were increased. Transfection of HEC-1A cells resulted in promoted apoptosis rate and reduced migration ability. EMT of EC tumor cells is partially under the impression of Snail-1, which alters the apoptosis and metastasis of these cells. As a consequence, silencing Snail-1 by siRNA may suggest a potentially promising tool in the EC therapy.

miRNA-200a Regulating Proliferation, Migration, and Infiltration of Tongue Squamous Cell Carcinoma Cells by Targeting DEK Proto-Oncogene

2021 ◽  
Vol 11 (3) ◽  
pp. 492-499
Author(s):  
Jiajie Ouyang ◽  
Chao Hu ◽  
Xueyang Zhang ◽  
Qianqi Wu
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tongue Squamous Cell Carcinoma ◽  
Luciferase Reporter ◽  
Migration Ability ◽  
Vimentin Expression ◽  
And Migration ◽  
E Cadherin

Tongue squamous cell carcinoma (TSCC) is the most frequently occurring oral cancer and is characterized by high proliferation and metastasis rates. Incomplete understanding of the pathogenesis of TSCC coupled with frequent tongue movement increases the difficulty of therapy. Additionally, TSCC is prone to recurrence and metastasis after treatment. Thus, exploring mechanisms of proliferation, migration, and infiltration of TSCC cancer cells is essential for reducing morbidity and mortality. Transfection of miRNA-200a mimics into SCC15 cells showed that miRNA-200a expression decreased significantly, and DEK expression significantly increased. Transfection of miRNA-200a mimics (miRNA-200a group), negative control mimics (miRNA-NC group), empty vector (miRNA-200a + pcDNA3.1 group), and miRNA-200a mimics and DEK overexpression vector (miRNA-200a + DEK group) into SCC15 cells respectively indicates that overexpression of miRNA-200a substantially inhibits SCC15 cell proliferation, infiltration and migration, decreases PCNA and Vimentin expression, and promotes E-cadherin expression. miRNA-200a + DEK transfection induced greater cell proliferation, infiltration and migration, much higher PCNA and Vimentin expression, and significantly lower E-cadherin expression. Luciferase reporter gene detection of overexpressed DEK or DEK expression after inhibiting miRNA-200a expression indicated a targeting association between miRNA-200a and DEK. miRNA-200a inhibits proliferation, infiltration and migration ability of TSCC by targeting DEK and may represent a novel means for clinical intervention in TSCC. miRNA-200a inhibits proliferation, invasion, and migration of TSCC by targeting DEK.

scholarly journals Allicin depresses biological activities of pancreatic cancer cells by regulating miRNA-339-5p/ZNF-689 axis

2021 ◽  
Author(s):  
Zeqian Yu ◽  
Susu Zhao
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Biological Activities ◽  
Caspase 8 ◽  
Vimentin Expression ◽  
Invasion And Migration ◽  
And Migration ◽  
E Cadherin

IntroductionThe aim of this study was to discuss Allicin’s anti-tumor effects and relative in pancreatic cancer cell via vitro and vivo study.Material and methodsUsing PANC-1 and Hs766T cell as research cell lines in our study. The PANC-1 abd GS799T cell were respectively treated with difference concentrations of Allicin. In next step, the PANC-1 abd GS799T cell were transfected with si-miRNA-339-5p which knockdown miRNA-339-5p. The cells were treated with difference concentration of Allicin. Measuring cell proliferation, apoptosis, invasion and migration by MTT, EDU, flow cytometry, TUNEL, transwell and wound healing assay. Relative gene (miRNA-339-5p, ZNF-689, Caspase-3, Caspase-8, E-cadherin and Vimentin) and protein (ZNF-689, Caspase-3, Caspase-8, E-cadherin and Vimentin) expression were evaluated by RT-qPCR and WB assay.ResultsAllicin had effects to suppress PANC-1 and Hs766T cell biological activities including cell proliferation, invasion and migration with cell apoptosis significantly increasing, however, with si-miRNA-339-5p which inhibit miRNA-339-5p expression transfection, the cells biological activities enhancing with cell apoptosis depressing, Compared with NC group, miRNA-339-5p, Caspase-3, Caspase-8 and E-cadherin expression were significantly increased and ZNF-689 and Vimentin expression were significantly depressed in Allicin treated groups, however, with miRNA-339-5p inhibitor transfection, the Allicin’s effects significantly disappear.ConclusionsAllicin had anti-tumor effect to pancreatic cancer biological activities via regulation miRNA-339-5p/ZNF-689 axis in vitro study.

scholarly journals EMT Participates in the Regulation of Exosomes Secretion and Function in Esophageal Cancer Cells

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Chuangui Chen ◽  
Zhao Ma ◽  
Hongjing Jiang
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Promoting Effect ◽  
Migration Ability ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
And Function ◽  
Esophageal Cancer Cells

Epithelial-mesenchymal transition (EMT) is a key step in tumor invasion and distant metastasis. Abundant evidence has documented that exosomes can mediate EMT of tumor cells and endow them with the ability of invasion and migration. However, there are few studies focusing on whether EMT can reverse the secretion of exosomes. In this study, 2 esophageal cancer cells (FLO-1 and SK-GT-4) were selected to compare the migration ability and EMT activation, and to further analyze the secretion ability of exosomes of the 2 cell lines. According to the results, inhibited activation of EMT in FLO-1 cells with relatively high migration ability could effectively reduce the secretion of exosomes. Besides, in SK-GT-4 cells, EMT activation induced by TGF-β could promote the secretion of exosomes. FLO-1 cell derived exosomes exhibited a paracrine effect of promoting the migration of SK-GT-4 cells, and the use of EMT inhibitors could weaken this ability. Furthermore, inhibition of EMT could change the relative content of some miRNAs in exosomes, with a particularly significant downregulation in the expression of miR-196-5p, miR-21-5p and miR-194-5p. Significantly, artificial transfection of the 3 miRNAs into exosomes by electroporation resulted in the recovery of migration-promoting effect of exosomes. Subsequent experiments further revealed that the effect of EMT on these miRNAs could be explained by the intracellular transcription level or the specific sorting mechanism of exosomes. To sum up, our study undoubtedly reveals that EMT has a regulatory effect on exosomes in the quantity and contents in esophageal cancer cells. Significantly, findings in our study provide experimental evidence for the interaction of EMT with the secretion and sorting pathway of exosomes, and also give a new direction for the further study of tumor metastasis.

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