MicroRNA miR-425 inhibits proliferation and migration of colorectal cancer HCC116 cells

2021 ◽  
Vol 71 (9) ◽  
Author(s):  
Huifang Zhou ◽  
Wen Liu ◽  
Haiyun Chen ◽  
Jiajia Ni ◽  
Zhi Zhang ◽  
...  
Keyword(s):  
Flow Cytometric Analysis ◽  
Negative Control ◽  
Colorectal Carcinogenesis ◽  
Medical Laboratory ◽  
Migration And Invasion ◽  
Flow Cytometric ◽  
And Migration ◽  
Sphere Formation ◽  
Hct116 Cells

Abstract Objective: To verify the role of miR-425 in colorectal carcinogenesis. Methods: We conducted sphere formation assay, wound-healing assay, transwell assay, MTT cell proliferation assay, flow cytometric analysis, reverse transcription qPCR, and Western blotting to analyse proliferation and invasion of HCT116 cells transfected with miR-425 mimics, miR-425 inhibitor, miR-425 mimic negative control, and miR-425 inhibitor negative control, respectively. The experimental protocol was approved by the Medical Ethics Committee of the First People’s Hospital in Kashi (approval number: 2018 Kuaishen No. (100)). All experiments were conducted during December 2016 to July 2017 at Xinjiang Dingju Medical Laboratory, China. Results: Our results showed that miR-425 expression in HCT116 cells after transfection was up-regulated, which inhibited sphere formation. Overexpression of miR-425 inhibited proliferation of HTC116 cells and induced their apoptosis, and inhibited HCC116 cell migration and invasion. Conclusion: Overexpression of miR-425 could inhibited sphere formation, the migration and invasion of HCT116 cells through inhibiting proliferation and promoting apoptosis. Keywords: apoptosis; colonic carcinoma; microRNA; proliferation Continuous....

scholarly journals Elevated FOXC2 Expression Promotes Invasion of HCC Cell Lines and is Associated with Poor Prognosis in Hepatocellular Carcinoma

2017 ◽  
Vol 44 (1) ◽  
pp. 99-109 ◽  
Author(s):  
Fang Yang ◽  
Lizhi Lv ◽  
Kun Zhang ◽  
Qiucheng Cai ◽  
Jianyong Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Flow Cytometric Analysis ◽  
Vital Role ◽  
Migration And Invasion ◽  
Flow Cytometric ◽  
Kaplan Meier ◽  
Proliferation Assays ◽  
The Relationship

Background/Aims: Increasing evidence has indicated that Forkhead box protein C2 (FOXC2) plays an important role in carcinogenesis. However, the expression and the role of FOXC2 in hepatocellular carcinoma (HCC) have not been extensively studied. Methods: FOXC2 expression was analyzed by quantitative real-time polymerase chain reaction, Western blot analysis and immunohistochemistry in HCC tissue and cells. The relationship between FOXC2 expression and patient clinical significance and survival were assessed by Pearson’s correlation and Kaplan-Meier analysis, respectively. Cell proliferation assays, colony formation assays, flow cytometric analysis and Transwell assays were employed to measure the effects of FOXC2 on HCC cells in vitro. Results: The expression of FOXC2 was increased in HCC tissue, and high FOXC2 expression was associated with worse patient survival. Knockdown of FOXC2 inhibited HCC cell growth, migration, and invasion in vitro, as well as tumor growth. Furthermore, we found that activation of AKT-mediated MMP-2 and MMP-9 was involved in FOXC2 promoting an aggressive phenotype. Conclusions: Taken together, these findings demonstrate that FOXC2 is upregulated in HCC tissue and is associated with tumor size, vascular invasion and advanced TNM stage. Further investigation suggested that FOXC2 may play a vital role in promoting proliferation and invasion in HCC and serves as a novel therapeutic target in HCC.

scholarly journals Pyr3 Induces Apoptosis and Inhibits Migration in Human Glioblastoma Cells

2018 ◽  
Vol 48 (4) ◽  
pp. 1694-1702 ◽  
Author(s):  
Hsin-Han Chang ◽  
Yu-Chen Cheng ◽  
Wen-Chiuan Tsai ◽  
Min-Jen Tsao ◽  
Ying Chen
Keyword(s):  
Membrane Potential ◽  
Tumor Growth ◽  
Western Blotting ◽  
Flow Cytometric Analysis ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Mitochondria Membrane Potential ◽  
Flow Cytometric ◽  
And Migration

Background/Aims: Glioblastoma, also known as glioblastoma multiforme (GBM), is a fast-growing type of tumor that is the most aggressive brain malignancy in adults. According to GEO profile analysis, patients with high transient receptor potential canonical 3 (TRPC3) expression have poor survival rates. The aim of this study is to evaluate the effects of Ethyl-1-(4-(2,3,3-trichloroacrylamide)phenyl)-5-(trifluoromethyl)-1H-pyrazole-4-carboxylate (Pyr3), a selective TRPC3 channel blocker, on the proliferation and migration of human glioblastoma cells. Methods: We first analyzed the TRPC3 mRNA expression in Gene Expression Omnibus (GEO) database. Then, TRPC3 protein expression was analyzed by Western blotting in three human GBM cell lines. The survival rate was measured by sulforhodamine B. JC1 staining was used to analyze the mitochondria membrane potential by flow cytometric analysis. Besides, the migration and invasion were evaluated by wound healing and Transwell assays. Annexin V and 7-aminoactinomycin D staining was used to monitor the apoptosis by flow cytometric analysis. The expression of apoptotic-related and migration-related proteins after Pyr3 treatment was detected by Western blotting. In addition, an orthotropic xenograft mouse model was used to assay the effect of Pyr3 in the in vivo study. Results: Basis on the results of bioinformatics study, glioma patients with higher TRPC3 expression had a shorter survival time than those with lower TRPC3 expression. GBM cell proliferation was decreased by Pyr3 treatment. The migration and invasion abilities of glioma cells were also inhibited via focal adhesion kinase and myosin light chain dephosphorization after Pyr3 treatment. Moreover, Pyr3 induced caspase-dependent apoptosis and mitochondria membrane potential imbalance in the GBM cells. In a xenograft animal model, Pyr3 in combination with temozolomide (TMZ) inhibited GBM tumor growth. Conclusion: Pyr3 inhibited GBM tumor growth in vitro and in vivo. Pyr3-TMZ combination therapy could be used to treat glioblastoma in the future.

scholarly journals Long intergenic non-coding RNA 1939 inhibits proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154

2019 ◽  
Author(s):  
Rongyuan Zhang ◽  
Yuhua Huang ◽  
Baocai Xu ◽  
Chuan Lv ◽  
Jianquan Hou ◽  
...  
Keyword(s):  
Flow Cytometric Analysis ◽  
Cell Counting ◽  
Regulation Mechanism ◽  
Human Renal Cell Carcinoma ◽  
Flow Cytometric ◽  
Non Coding Rna ◽  
And Migration ◽  
Induced Apoptosis ◽  
Proliferation And Migration

Abstract Background: Renal carcinoma (RCC) is widely accepted as a malignant tumor of urinary system. Long intergenic non-coding RNA 1939 (LINC01939) is a novel lncRNA which was found to be down-regulated in RCC. Thus, we set out to explore the effect and regulation mechanism of LINC01939 in RCC. Methods: LINC01939 and miR-154 in RCC tissues and cell lines were detected using qRT-PCR assay. Cell counting kit-8 (CCK-8) assays was exploited to examine cell viability. Flow cytometric analysis was conducted to examine apoptosis. Cell mobility was valued through wound healing assays. Western blotting was applied for examination of proteins related to proliferation, apoptosis, migration and Wnt/β-catenin/Notch. Results: LINC01939 was down-regulated in RCC tissues. LINC01939 overexpression impeded proliferation and migration, and induced apoptosis. Further study found that the overexpression of LINC01939 strongly suppressed miR-154 expression. Then, the inhibiting effect of overexpressed LINC01939 on proliferation and mobility and the promoting role of LINC01939 in apoptosis were abolished by the combination of miR-154 mimic. Finally, we found that the overexpressed LINC01939 inactivated Wnt/β-catenin and Notch through suppressing miR-154. Conclusion: The up-regulation of LINC01939 inhibited proliferation and migration of RCC cells by down-regulating miR-154.

The Protective Role of Inhibition of Keratin on Rheumatoid Arthritis

2019 ◽  
Vol 9 (6) ◽  
pp. 797-803
Author(s):  
Yan Zhao ◽  
Lanxiu Yang ◽  
Jihong Pan ◽  
Huan Zhang ◽  
Guodong Sun ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Flow Cytometric Analysis ◽  
Protective Role ◽  
Invasion And Migration ◽  
Flow Cytometric ◽  
Migratory Capacity ◽  
Synovial Tissues ◽  
And Migration ◽  
Fibroblast Like Synoviocytes

Objective: Rheumatoid arthritis (RA) is a common inflammatory disease. Studies showed that keratin type II cuticular Hb4 (KRT84) was highly expressed in the synovial membrane of patients with RA. However, the function and mechanism of KRT84 in RA is still unclear. Methods: In this study, we isolated fibroblast-like synoviocytes (FLS) from the mixed knee joint synovial tissues from five patients with RA and the cells were treated with KRT84 siRNA. After transfection of 24 h and 36 h, the knockdown efficiency and expression of relevant genes was detected by RT-PCR. MTT assay, transwell assay, wound scratch assays, flow cytometric analysis and ELISA were used to assess cell proliferation, invasive and migratory capacity. Results: We found that the invasion and migration of RAFLS were significantly decreased after transfection of KRT84 siRNA. ELISA showed a remarkably decrease in TNF-α secretion after KRT84 knockdown. We also explore stimulatory factors for high expression of KRT84 in RA. The inhibitors of ERK, STAT3 and NF-κ B pathways were employed. Our results showed that the expression of KRT84 in RAFLS was evidently increased after treatment with ERK and STAT3 pathway inhibitor. Conclusions: These results imply a protective role of KRT84 knockdown on RA and lay a foundation for further studies on the pathogenetic mechanisms of RA.

scholarly journals Formation of Autoimmune Lesions Is Independent of Antibiotic Treatment in NOD Mice

2021 ◽  
Vol 22 (6) ◽  
pp. 3239
Author(s):  
 Mami Sato ◽  
Rieko Arakaki ◽  
Hiroaki Tawara ◽  
Takaaki Tsunematsu ◽  
Naozumi Ishimaru
Keyword(s):  
Intestinal Microbiota ◽  
Flow Cytometric Analysis ◽  
Nod Mice ◽  
Antibiotic Administration ◽  
T And B Cells ◽  
Spleen Cells ◽  
Flow Cytometric ◽  
Enteral Microbiota ◽  
The Relationship

The relationship between autoimmunity and changes in intestinal microbiota is not yet fully understood. In this study, the role of intestinal microbiota in the onset and progression of autoimmune lesions in non-obese diabetic (NOD) mice was evaluated by administering antibiotics to alter their intestinal microenvironment. Flow cytometric analysis of spleen cells showed that antibiotic administration did not change the proportion or number of T and B cells in NOD mice, and pathological analysis demonstrated that autoimmune lesions in the salivary glands and in the pancreas were also not affected by antibiotic administration. These results suggest that the onset and progression of autoimmunity may be independent of enteral microbiota changes. Our findings may be useful for determining the appropriate use of antibiotics in patients with autoimmune diseases who are prescribed drugs to maintain systemic immune function.

scholarly journals Mechanism of LIN28B in Trophoblastic Villous Cells of Unexplained Recurrent Abortion

2021 ◽  
Author(s):  
QiaoYao Huang ◽  
YanRu Niu ◽  
LiJun Song ◽  
JinZhi Huang ◽  
Chenxi Wang ◽  
...  
Keyword(s):  
Negative Control ◽  
Cellular Level ◽  
Cellular Migration ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Akt Phosphorylation ◽  
Real Time Quantitative Pcr ◽  
Villous Trophoblast

Abstract Background: LIN28B plays an important role in early embryonic development, but its role in villous trophoblast implantation and differentiation remains unknown. To verify the role of LIN28B in trophoblastic villous tissue and cells from women with URSA(unexplained recurrent spontaneous abortion)and artificial termination of pregnancy (negative control, NC). Methods:The Lin28b gene and its protein expression level were detected with real-time quantitative PCR, Western immunoblotting analysis, and immunocytochemistry. The gene was also overexpressed in chorionic villous cell lines (HTR-8/SVneo and BeWo) to examine its effect on trophoblast function.Results: The expression of LIN28B mRNA and protein of URSA villi was lower than that in the NC group. At the cellular level, overexpression of LIN28B enhanced cellular migration, and invasion, and inhibited apoptosis. LIN28B may inhibit apoptosis by promoting Akt phosphorylation and by inhibiting Bad phosphorylation and Bcl-2 expression. In addition, LIN28B inhibited cell fusion and reduced cellular syncytia. Conclusions: LIN28B can inhibit cell proliferation, invasion and migration in vitro, and promote apoptosis and fusion. The low expression of LIN28B in URSA villous trophoblast cells may be one of the causes of abortion. The role of LIN28B in villous trophoblasts needs further study.

scholarly journals Does LIN28B gene dysregulation make women more likely to abort?

2021 ◽  
Author(s):  
QiaoYao Huang ◽  
YanRu Niu ◽  
LiJun Song ◽  
JinZhi Huang ◽  
Chenxi Wang ◽  
...  
Keyword(s):  
Negative Control ◽  
Cellular Level ◽  
Cellular Migration ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Akt Phosphorylation ◽  
Real Time Quantitative Pcr ◽  
Villous Trophoblast

Background: LIN28B plays an important role in early embryonic development, but its role in villous trophoblast implantation and differentiation remains unknown. To verify the role of LIN28B in trophoblastic villous tissue and cells from women with URSA(unexplained recurrent spontaneous abortion)and artificial termination of pregnancy (negative control, NC). Methods:The Lin28b gene and its protein expression level were detected with real-time quantitative PCR, Western immunoblotting analysis, and immunocytochemistry. The gene was also overexpressed in chorionic villous cell lines (HTR-8/SVneo and BeWo) to examine its effect on trophoblast function. Results: The expression of LIN28B mRNA and protein of URSA villi was lower than that in the NC group. At the cellular level, overexpression of LIN28B enhanced cellular migration, and invasion, and inhibited apoptosis. LIN28B may inhibit apoptosis by promoting Akt phosphorylation and by inhibiting Bad phosphorylation and Bcl-2 expression. In addition, LIN28B inhibited cell fusion and reduced cellular syncytia. Conclusions: LIN28B can inhibit cell invasion and migration in vitro, and promote apoptosis and fusion. The low expression of LIN28B in URSA villous trophoblast cells may be one of the causes of abortion. The role of LIN28B in villous trophoblasts needs further study.

scholarly journals Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Guosen Wang ◽  
Weiwei Sheng ◽  
Jingtong Tang ◽  
Xin Li ◽  
Jianping Zhou ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Migration And Invasion ◽  
Chemical Agent ◽  
Cell Migration And Invasion ◽  
Agent Treatment ◽  
Hct116 Cells

Abstract Serine-arginine protein kinase 2 (SRPK2) is aberrantly expressed in human malignancies including colorectal cancer (CRC). However, little is known about the molecular mechanisms, and the role of SRPK2 in chemosensitivity remains unexplored in CRC. We recently showed that SRPK2 promotes pancreatic cancer progression by down-regulating Numb and p53. Therefore, we investigated the cooperation between SRPK2, Numb and p53 in the cell migration, invasion and chemosensitivity of CRC in vitro. Here, we showed that SRPK2 expression was higher in CRC tumors than in nontumor tissues. SRPK2 expression was positively associated with clinicopathological characteristics of CRC patients, including tumor differentiation, T stage, N stage and UICC stage. Additionally, SRPK2 had no association with mutant p53 (mtp53) in SW480 and SW620 cells, but negatively regulated Numb and wild-type p53 (wtp53) in response to 5-fluorouracil or cisplatin treatment in HCT116 cells. Moreover, SRPK2, Numb and p53 coimmunoprecipitated into a triple complex with or without the treatment of 5-fluorouracil in HCT116 cells, and p53 knockdown reversed the up-regulation of wtp53 induced by SRPK2 silencing with chemical agent treatment. Furthermore, overexpression of SRPK2 increased cell migration and invasion and decreased chemosensitivity to 5-fluorouracil or cisplatin in HCT116 cells. Conversely, SRPK2 silencing decreased cell migration and invasion and increased chemosensitivity to 5-fluorouracil or cisplatin, yet these effects could be reversed by p53 knockdown under chemical agent treatment. These results thus reveal a novel role of SRPK2-Numb-p53 signaling in the progression of CRC and demonstrate that SRPK2 is a potential therapeutic target for CRC clinical therapy.

scholarly journals Up-regulation of miRNA-148a inhibits proliferation, invasion, and migration while promoting apoptosis of cervical cancer cells by down-regulating RRS1

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Ying Zhang ◽  
Bingmei Sun ◽  
Lianbin Zhao ◽  
Zhengling Liu ◽  
Zonglan Xu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Hela Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Cervical Cancer Cells ◽  
And Migration

Abstract The purpose of the present study is to figure out the role of miRNA-148a (miR-148a) in growth, apoptosis, invasion, and migration of cervical cancer cells by binding to regulator of ribosome synthesis 1 (RRS1). Cervical cancer and adjacent normal tissues, as well as cervical cancer cell line Caski, HeLa, C-33A, and normal cervical epithelial cell line H8 were obtained to detect the expression of miR-148a and RRS1. Relationship between miR-148a and RRS1 expression with clinicopathological characteristics was assessed. The selected Caski and HeLa cells were then transfected with miR-148a mimics, miR-148a inhibitors or RRS1 siRNA to investigate the role of miR-148a and RRS1 on proliferation, apoptosis, colony formation, invasion, and migration abilities of cervical cancer cells. Bioinformatics information and dual luciferase reporter gene assay was for used to detect the targetting relationship between miR-148a and RRS1. Down-regulated miR-148a and up-regulated RRS1 were found in cervical cancer tissues and cells. Down-regulated miR-148a and up-regulated RRS1 are closely related with prognostic factors of cervical cancer. RRS1 was determined as a target gene of miR-148a and miR-148a inhibited RRS1 expression in cervical cancer cells. Up-regulation of miR-148a inhibited cell proliferation, migration, and invasion while promoting apoptosis in Caski and HeLa cells. Our study suggests that miR-148a down-regulates RRS1 expression, thereby inhibiting the proliferation, migration, and invasion while promoting cell apoptosis of cervical cancer cells.

scholarly journals Role of S100 Proteins in Colorectal Carcinogenesis

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Paula Moravkova ◽  
Darina Kohoutova ◽  
Stanislav Rejchrt ◽  
Jiri Cyrany ◽  
Jan Bures
Keyword(s):  
Calcium Binding ◽  
Colorectal Neoplasia ◽  
Serum Levels ◽  
S100 Proteins ◽  
Colorectal Carcinogenesis ◽  
Invasion And Migration ◽  
Common Cancer ◽  
The Family ◽  
And Migration

The family of S100 proteins represents 25 relatively small (9–13 kD) calcium binding proteins. These proteins possess a broad spectrum of important intracellular and extracellular functions. Colorectal cancer is the third most common cancer in men (after lung and prostate cancer) and the second most frequent cancer in women (after breast cancer) worldwide. S100 proteins are involved in the colorectal carcinogenesis through different mechanisms: they enable proliferation, invasion, and migration of the tumour cells; furthermore, S100 proteins increase angiogenesis and activate NF-κβsignaling pathway, which plays a key role in the molecular pathogenesis especially of colitis-associated carcinoma. The expression of S100 proteins in the cancerous tissue and serum levels of S100 proteins might be used as a precise diagnostic and prognostic marker in patients with suspected or already diagnosed colorectal neoplasia. Possibly, in the future, S100 proteins will be a therapeutic target for tailored anticancer therapy.

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