scholarly journals Indole-thiazolidinone conjugate inhibits nasopharyngeal carcinoma cell migration and invasion by targeting NF κB pathway

2021 ◽  
Vol 18 (3) ◽  
pp. 519-525
Author(s):  
Guoping Zhang ◽  
Sheng Zhang
Keyword(s):  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Matrix Metalloproteinase ◽  
Carcinoma Cells ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Nuclear Fraction ◽  
Invasion And Migration ◽  
Migration Potential ◽  
And Migration

Purpose: To investigate the effect of indole-thiazolidinone on metastasis in HK1 nasopharyngeal carcinoma cells. Methods: HK1 cell proliferation was determined colorimetrically using 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. Invasion and migration of HK1 cells were assessed using Matrigel™ chamber coated invasion and wound healing assays, respectively. Results: Indole-thiazolidinone suppressed proliferation of HK1 and NPC 039 NPC cell lines at 72 h. The degree of proliferation of HK1 cells on treatment with 0.25, 0.5, 1.0, 1.5, 2.0, 2.5 and 3.0 μM indolethiazolidinone was 99, 87, 71, 64, 49, 38 and 31 %, respectively. In HK1 cell cultures, migration potential was reduced to 58.32, 47.54, 28.91 and 17.65 %, on exposure to 1.5, 2.0, 2.5 and 3.0 μM indole-thiazolidinone, respectively. Incubation with 1.5, 2.0, 2.5 and 3.0 μM indole-thiazolidinone resulted in cell invasion values of 63.41, 49.37, 35.12 and 19.67 %, respectively. There was a marked decrease in the expressions of matrix metalloproteinase 2 and matrix metalloproteinase 9 in HK1 cells on treatment with indole-thiazolidinone (p < 0.05). In addition, indole-thiazolidinone treatment resulted in decrease in p65 and p50 in nuclear fraction. Treatment of HK1 and NPC 039 cells with indolethiazolidinone and henenalin synergistically decreased cell proliferation. Indole-thiazolidinone treatment caused significant decrease in tumor growth in mice (p < 0.05). Conclusion: Indole-thiazolidinone inhibits proliferation and metastasis in nasopharyngeal carcinoma cells. Therefore, it has potential for development as a therapeutic management of nasopharyngeal carcinoma in humans.

lncRNA FOXD2-AS1 affects trophoblast cell proliferation, invasion and migration through targeting miRNA

Zygote ◽  
2020 ◽  
Vol 28 (2) ◽  
pp. 131-138 ◽  
Author(s):  
Yulei Zhang ◽  
Xiaoqin Chen
Keyword(s):  
Cell Proliferation ◽  
Matrix Metalloproteinase ◽  
Trophoblast Cell ◽  
Matrix Metalloproteinase 2 ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Trophoblast Cells ◽  
Invasion And Migration ◽  
And Migration

SummaryThe abnormal expression of lncRNAs and miRNAs has been found in the placentas of patients with preeclampsia (PE). Therefore, we determined the role of lncRNA FOXD2-AS1/miR-3127 in trophoblast cells. The expression of lncRNA FOXD2-AS1 was detected by qRT-PCR. The proliferation, migration and invasion ability of trophoblast cells were evaluated using CCK-8, wound healing and transwell assays. The target gene of lncRNA FOXD2-AS1 was determined by StarBase and luciferase reporter assays. Western blotting was used to analyze the expression of matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9). The results showed that FOXD2-AS1 affected trophoblast cell viability in vitro, while the expression of miR-3127 was decreased. FOXD2-AS1 silencing decreased the promotion effects on trophoblast cell induced by miR-3127 inhibition. In addition, FOXD2-AS1 and miR-3127 presented the same effect on MMP2 and MMP9 levels. lncRNA FOXD2-AS1 modulated trophoblast cell proliferation, invasion and migration through downregulating miR-3127 expression. Therefore, lncRNA FOXD2-AS1 could act as a latent therapeutic marker in preeclampsia.

scholarly journals Down-regulation of SOX18 inhibits laryngeal carcinoma cell proliferation, migration, and invasion through JAK2/STAT3 signaling

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Yice Xu ◽  
Qingyuan Zhang ◽  
Jie Zhou ◽  
Zhaolong Li ◽  
Junyu Guo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Laryngeal Carcinoma ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Down Regulation ◽  
Invasion And Migration ◽  
Stat3 Signaling ◽  
And Migration

AbstractLaryngeal carcinoma is one of the most common malignant tumors of the head, neck, and respiratory tract. The aim of the present study is to explore the biological function of SRY-related HMG-box 18 (SOX18) in laryngeal carcinoma cells and study the molecular mechanism involved. Initial findings indicate that the expression of SOX18 was increased in laryngeal carcinoma cell lines and tissues. The effect of SOX18 on laryngeal carcinoma cell proliferation, cell cycle, apoptosis, invasion, and migration was also identified. The results indicated that down-regulation of SOX18 significantly inhibited cell proliferation, migration, and invasion, and induced cell-cycle arrest in G0/G1 phase and apoptosis of laryngeal carcinoma cells. However, overexpression of SOX18 promoted cell proliferation, invasion, and migration, and inhibited cell apoptosis. The expression of cyclin D1, active-caspase-3, N-cadherin, MTA1, MMP-2, and MMP-7 was also regulated by the overexpression of siSOX18 or SOX18. In addition, it was found that SOX18 could also accelerate the phosphorylation of JAK2/STAT3 signaling in laryngeal carcinoma cells. Furthermore, our study indicated that SOX18 could stimulate cell proliferation, migration, and invasion of laryngeal carcinoma cells via regulation of JAK2/STAT3 signaling, which could provide a new strategy for laryngeal carcinoma diagnosis and molecular therapies.

Study on the Mechanism of Long Non-Coding RNA-An Antisense Transcript of SATB Homeobox 2 in Promoting the Growth, Invasion and Migration of Nasopharyngeal Carcinoma

2021 ◽  
Vol 11 (1) ◽  
pp. 99-105
Author(s):  
Hualong Qiang ◽  
Shiyin Ma ◽  
Xiaodong Zhan ◽  
Chengyi Jiang ◽  
Yuefeng Han ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Invasion And Migration ◽  
Potential Marker ◽  
Non Coding Rna ◽  
Gene Test ◽  
And Migration

This study intends to clarify lncRNA SATB2-AS1’s role in growth, invasion and migration of nasopharyngeal carcinoma cells and its effect on radiotherapy. The lncRNA array was used to analyze the differential expression of lncRNA in nasopharyngeal carcinoma biopsy tissues. QRT-PCR measured the levels of SATB2-AS1 and TIMP2 along with analysis of cell growth, migration, and invasion ability by MTT method and colony formation experiment. Luciferase reporter gene test assessed the relationship between SATB2-AS1 and TIMP2. LncRNA array analysis found significantly increased SATB2-AS1 expression in nasopharyngeal carcinoma tissues. Ectopic SATB2-AS1 overexpression in CNE1 cells promoted cell proliferation, migration, invasion and enhanced radiotherapy sensitivity. Bioinformatics and experiments confirmed that TIMP2 was a target of SATB2-AS1 and it participated in the upregulation of MMP-10 induced by SATB2-AS1. lncRNA SATB2-AS1 can promote the migration and invasion of nasopharyngeal carcinoma cells, indicating that it could be a potential marker for the treatment and prognosis.

scholarly journals Long noncoding RNA UCA1 promotes the proliferation, invasion, and migration of nasopharyngeal carcinoma cells via modulation of miR-145

2018 ◽  
Vol Volume 11 ◽  
pp. 7483-7492 ◽  
Author(s):  
Jing Wu ◽  
Mingyu Du ◽  
Qian Zhang ◽  
Wenjun Zhang ◽  
Yanxin Fan ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Carcinoma Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals miR-17-5p promotes the invasion and migration of colorectal cancer by regulating HSPB2

2020 ◽  
Author(s):  
Wei fang Yu ◽  
Jia Wang ◽  
Chao Li ◽  
Mingda Xuan ◽  
Shuangshuang Han ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Lymph Node ◽  
Target Genes ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Normal Tissues ◽  
Node Metastasis ◽  
Rescue Experiment ◽  
And Migration

Abstract Background: MicroRNA (miRNA) can affect tumor progression by regulating cell proliferation, apoptosis and metastasis. After miRNA microarray chip analysis of colorectal cancer (CRC) tissues and adjacent normal tissues, a significant upregulation of miR-17-5p expression was found in CRC tissues. However, the underlying mechanism of miR-17-5p in CRC is still unclear.Methods: The levels of miR-17-5p in 47 paired CRC and adjacent normal tissue samples were determined by quantitative real-time PCR (qRT-PCR). CCK-8, colony formation, flow cytometry and transwell assays were used to explore the biological effects of miR-17-5p on CRC cells. In addition, the transcriptome sequencing and miRNA target prediction software were employed to identify targets of miR-17-5p. Luciferase reporter detection was used to demonstrate the direct binding of target genes by miR-17-5p. The rescue experiment was conducted to investigate the biological function of target genes and regulatory mechanism of miR-17-5p on target genes.Results: The expression of miR-17-5p was significantly higher in CRC tissues than in adjacent normal tissues. In CRC group, the expression of miR-17-5p in cancer tissues with lymph node metastasis was higher compared with those without lymph node metastasis. Overexpression of miR-17-5p inhibited CRC cell apoptosis, as well as promoting proliferation, migration and invasion. We hypothesized that HSPB2 might be a target gene of miR-17-5p and validated for the first time that miR-17-5p binds directly to the 3’-UTR of HSPB2. In the rescue experiment, the tumor suppressive effect of HSPB2 was detected and miR-17-5p could promote cell proliferation, migration and invasion by targeting HSPB2.Conclusion: MiR-17-5p promotes invasion and migration by inhibiting HSPB2 in CRC, thereby implicating its potential as a novel diagnostic biomarker and therapeutic target for CRC.

LncRNA PCAT18/miR-301a/TP53INP1 axis is involved in gastric cancer cell viability, migration and invasion

2020 ◽  
Vol 168 (5) ◽  
pp. 547-555
Author(s):  
Jin Dou ◽  
Daoyuan Tu ◽  
Haijian Zhao ◽  
Xiaoyu Zhang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Cell Lines ◽  
Underlying Mechanism ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Proliferation And Metastasis ◽  
And Migration ◽  
Cell Proliferation And Metastasis

Abstract MiR-301a is as an oncogene involved in the regulation of gastric cancer (GC) progression, but the underlying mechanism is unclear. This study was to explore the lncRNA PCAT18/miR-301a/TP53INP1 axis in regulating the GC cell proliferation and metastasis. In the present study, GC tissues and cell lines were collected for the detection of PCAT18 expression. Herein, we found that PCAT18 is significantly decreases in human GC tissues and five GC cell lines. Overexpression of PCAT18 inhibits cell viability, invasion and migration of GC cells and tumour growth of GC xenograft tumours. PCAT18 negatively regulates the expression level of miR-301a. The interaction between PCAT18 and miR-301a is confirmed by RIP and RNA pull down. MiR-301a mimic increases cell viability and promotes cell migration and invasion and reverses the inhibitory action of PCAT18. TP53INP1 expression is negatively regulated by miR-301a and TP53INP1/miR-301a is involved in GC viability, migration and invasion. The promoting of PCAT18 on TP53INP1 expression is abolished by miR-301a overexpression. In conclusion, lncRNA PCAT18 acts as a tumour suppressor for GC and lncRNA PCAT18, miR-301a and TP53INP1 comprise a signal axis in regulating GC cell proliferation, migration and invasion.

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