lncRNA FOXD2-AS1 was a Key Part in Thyroid Cancer Biological Activity

2019 ◽  
Vol 9 (8) ◽  
pp. 1086-1093
Author(s):  
Shi Guohua ◽  
Bu Zibin ◽  
Lou Cen
Keyword(s):  
Cell Proliferation ◽  
Biological Activity ◽  
Thyroid Cancer ◽  
Mrna Expression ◽  
Cell Apoptosis ◽  
Proliferation Rate ◽  
Down Regulation ◽  
Invasion And Migration ◽  
Cell Proliferation Rate ◽  
And Migration

Objective: The research was wanted to discuss the effect lncRNA FOXD2-AS1 on Thyroid Cancer Biological Activity. Methods: The cells were respectively divided as NC and si-FOXD2-AS1 groups. Measuring the FOXD2-AS1 mRNA expression in difference cell lines by RT-qPCR. The cell proliferation rate were evaluated by CCK-8; Using flow cytometry to measure cell apoptosis; Using transwell and wound healing methods to evaluate invasion and migration abilities. The relative proteins levels were measured by WB assay. Results: With si-FOXD2-AS1 transfection, the FOXD2-AS1 mRNA expression of si-FOXD2-AS1 groups were significantly down-regulation (P < 0.001); Cell proliferation rate of si-FOXD2-AS1 groups were significantly depressed with cell apoptosis significantly increased (P < 0.001); The invasion and migration abilities of si-FOXD2-AS1 groups were significantly suppressed (P < 0.001). By WB assay, GRP94, cyclin D1, β-catenin and c-Myc proteins expressions of si-FOXD2-AS1 groups were significantly down-regulation (P < 0.001). Conclusion: lncRNA FOXD2-AS1 was as oncology role in Thyroid Cancer occur, FOXD2-AS1 knockdown had effects to suppress Thyroid Cancer.

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.

lncRNA UBE2R2-AS1 Had Anti-Tumor Effects in Non-Small Cell Lung Cancer

2019 ◽  
Vol 9 (12) ◽  
pp. 1685-1692
Author(s):  
Haiyun Zhang ◽  
Weidong Han ◽  
Haimei Liu ◽  
Haijun Chen
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Cell Number ◽  
Caspase 8 ◽  
Down Regulation ◽  
Invasion And Migration ◽  
Protein Levels ◽  
And Migration

Background: The purpose of our work was to discuss anti-tumor effects and mechanisms of lncRNA UBE2R2-AS1 in NSCLC. Methods : lncRNA UBE2R2-AS1 gene level was measured by RT-qPCR in BEAS-2B, A549, H1975, H1650 and HCC827. Dividing A549 and H1650 cells into NC, Vector and UBE2R2-AS1. Measuring the cell proliferation by CCK-8 assay; Using flow cytometer to evaluate cell apoptosis, using transwell and wound healing methods to evaluate invasion and migration abilities. The relative protein expressions were measured by WB assay. Results: UBE2R2-AS1 mRNA expression of A549 and H1650 were the lowest in all cells lines. With UBE2R2-AS1 transfection, the cell proliferation rates were significantly down-regulation with cell apoptosis significantly increasing (P < 0 001). Meanwhile, the invasion cell number and wound healing rates of UBE2R2-AS1 groups were significantly depressed (P < 0 001). Bcl-2, TLR4 and MyD88 proteins expressions were significantly down-regulation and Caspase-3 and Caspase-8 proteins levels were significantly upregulation in UBE2R2-AS1 groups (P < 0 001). Conclusion: UBE2R2-AS1 overexpression had antitumor in NSCLC, the mechanisms might be correlation with regulation Bcl-2, caspase-3, caspase-8, TLR4 and MyD88 protein levels.

scholarly journals LncRNA CRNDE promotes cell proliferation, invasion and migration by competitively binding miR-384 in papillary thyroid cancer

Oncotarget ◽  
2017 ◽  
Vol 8 (66) ◽  
pp. 110552-110565 ◽  
Author(s):  
Honggang Sun ◽  
Liqin He ◽  
Lan Ma ◽  
Tao Lu ◽  
Jianguo Wei ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Papillary Thyroid ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Carnosol Induces Cell Apoptosis and Inhibits Invasion and Proliferation in Skin Epidermoid Cancer in Vitro Through MMP11-EGFR Pathway

2021 ◽  
Author(s):  
Shiqiu Jiang ◽  
Hairong Liu ◽  
Jie Zhang ◽  
Fang Zhang ◽  
Jiawei Fan
Keyword(s):  
Cell Proliferation ◽  
Overall Survival ◽  
Skin Cancer ◽  
Mrna Expression ◽  
Cell Apoptosis ◽  
Survival Rates ◽  
Invasion And Migration ◽  
Egfr Expression ◽  
E Cadherin

Abstract Background and purpose: The anti-tumor effect of carnosol has been revealed in cancers. This research intends to explore the role and underlying mechanisms of carnosol in the skin cancer in vitro. Methods: Online database GEPIA was used to preliminarily analyze MMP11 expression in skin cancer and further performed overall survival evaluation based on TCGA data. 0, 5µM, 10 µM, 20 µM carnosol was added into the skin cancer A431 cell culture. Later, RT-PCR method detected the mRNA expression of MMP-11 and Elisa kits measured the concentrations of MMP11, phosphor-EGFR and total EGFR proteins as well as the biomarkers related to proliferation (Ki67) and EMT (E-cadherin and Vimentin) as well as Casepase-3. The 20µM carnosol group was selected to further study the regulatory effect of MMP11 in A431 cells.Colony formation examined the cell proliferation. Flow cytometry method checked cell apoptosis while Transwell method explored the cell invasion and migration. Results: MMP11 is upregulated in skin cancer and lower level of MMP11 or EGFR expression is correlated with higher overall survival rates. Carnosol addition inhibited the mRNA expression of MMP11 and lowered the protein concentrations of MMP11 and phosphor-EGFR. In addition, Ki67 and Vimentin concentration was inhibited by carnosol while E-cadherin was instead promoted. Caspase-3 activity was enhanced by carnosol. Upregulation of MMP11 recovered EGFR activation, cell proliferation and invasion while inhibited apoptosis, partly counteracted the function of carnosol in cells. Conclusion: Carnosol might induce cell apoptosis and inhibits invasion and proliferation in skin epidermoid cancer in vitro through MMP11-EGFR pathway.

scholarly journals Overexpression of long intergenic noncoding RNA LINC00312 inhibits the invasion and migration of thyroid cancer cells by down-regulating microRNA-197-3p

2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Kai Liu ◽  
Wen Huang ◽  
Dan-Qing Yan ◽  
Qing Luo ◽  
Xiang Min
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Noncoding Rna ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Invasion And Migration ◽  
Normal Tissues ◽  
Gene Assay ◽  
Long Intergenic Noncoding Rna ◽  
And Migration

The study evaluated the ability of long intergenic noncoding RNA LINC00312 (LINC00312) to influence the proliferation, invasion, and migration of thyroid cancer (TC) cells by regulating miRNA-197-3p. TC tissues and adjacent normal tissues were collected from 211 TC patients. K1 (papillary TC), SW579 (squamous TC), and 8505C (anaplastic TC) cell lines were assigned into a blank, negative control (NC), LINC00312 overexpression, miR-197-3p inhibitors, and LINC00312 overexpression + miR-197-3p mimics group. The expression of LINC00312, miR-197-3p, and p120 were measured using quantitative real-time PCR (qRT-PCR) and Western blotting. Cell proliferation was assessed via CCK8 assay, cell invasion through the scratch test, and cell migration via Transwell assay. In comparison with adjacent normal tissues, the expression of LINC00312 is down-regulated and the expression of miR-197-3p is up-regulated in TC tissues. The dual luciferase reporter gene assay confirmed that P120 is a target of miR-197-3p. The expression of LINC00312 and p120 was higher in the LINC00312 overexpression group than in the blank and NV groups. However, the expression of miR-197-3p was lower in the LINC00312 overexpression group than in the blank and NC groups. The miR-197-3p inhibitors group had a higher expression of miR-197-3p, but a lower expression of p120 than the blank and NC groups. The LINC00312 overexpression and miR-197-3p inhibitor groups had reduced cell proliferation, invasion and migration than the blank and NC groups. These results indicate that a LINC00312 overexpression inhibits the proliferation, invasion, and migration of TC cells and that this can be achieved by down-regulating miR-197-3p.

scholarly journals Long noncoding RNA CASC7 inhibits the proliferation and migration of papillary thyroid cancer cells by inhibiting miR-34a-5p

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Wencong Sun ◽  
Detao Yin
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cancer Susceptibility ◽  
Luciferase Reporter ◽  
Papillary Thyroid ◽  
And Migration ◽  
Proliferation And Migration

AbstractLong noncoding RNAs (lncRNAs) play an essential role in the progression of papillary thyroid cancer (PTC). However, the expression and function of lncRNA cancer susceptibility candidate 7 (CASC7) in PTC remain unknown. The purpose of this study was to investigate the role and molecular mechanism of CASC7 in regulating PTC cell behavior. The expression of CASC7, miR-34a-5p, and tumor protein P73 (TP73) was determined by qRT-PCR and western blot. Cell proliferation was examined by MTT assay. Cell apoptosis was assessed by flow cytometry following Annexin V and PI staining. Cell migration was determined by Transwell migration assay. The interaction between miR-34a-5p and CASC7 or TP73 was examined by luciferase reporter assay. CASC7 and TP73 expression were significantly lower, whereas miR-34a-5p expression was higher in PTC tissues than the adjacent normal tissues. Furthermore, CASC7 overexpression inhibited cell proliferation and migration, whereas facilitated cell apoptosis in human PTC cell lines (K1 and TPC-1). Mechanistically, CASC7 acted as a sponge of miR-34a-5p to upregulate TP73 expression. Moreover, miR-34a-5p mimic transfection could abate the CASC7-regulated PTC cell proliferation, migration, and apoptosis. Collectively, CASC7 inhibited the proliferation and migration of PTC cells by sponging miR-34a-5p to upregulate TP73 expression.

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.

MicroRNA-150 Inhibits Cell Invasion and Migration and Is Downregulated in Human Osteosarcoma

2015 ◽  
Vol 146 (2) ◽  
pp. 124-135 ◽  
Author(s):  
Xiao Li ◽  
Li Chen ◽  
Wei Wang ◽  
Fan-Bin Meng ◽  
Ren-Tao Zhao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Expression Level ◽  
Luciferase Reporter ◽  
Inhibitory Effects ◽  
Invasion And Metastasis ◽  
Invasion And Migration ◽  
Protein Levels ◽  
Mg63 Cells ◽  
And Migration

miR-150 expression in osteosarcoma (OS) cell lines and human osteoblast cells was detected, and OS cell models were transfected with exogenous miR-150 to investigate its role in cell proliferation, invasion, and apoptosis. Our results showed that miR-150 expression in OS cells (MG63, Saos-2, SOSP-9607, and U2OS) was significantly lower compared to the osteoblast hFOB1.19 cell line (all p < 0.01). The expression level of miR-150 in MG63 cells that were transfected with exogenous miR-150 mimics was markedly upregulated, while the miR-150 expression level in the inhibitor group was significantly downregulated (both p < 0.01). Similar results were also found in SOSP-9607 cells. Importantly, exogenous miR-150 expression stimulated cell apoptosis and inhibited proliferation, invasion, and migration. A luciferase reporter assay displayed that miR-150 also regulated Sp1 expression by targeting its 3′-UTR, and qRT-PCR and Western blotting showed that elevated levels of miR-150 may reduce Sp1 protein expression. The mRNA and protein levels of Sp1 were upregulated after transfection with a Sp1-expression plasmid and partially reversed the inhibitory effects of miR-150 on cell proliferation, invasion, and metastasis in MG63 and SOSP-9607 cells, as well as promoted cell apoptosis. In conclusion, miR-150 inhibits cell proliferation, invasion, and metastasis and stimulates cell apoptosis by regulating the expression of Sp1. Therefore, miR-150 may be a potential clinical target for the treatment of OS patients.

scholarly journals miR-21 down-regulation promotes apoptosis and inhibits invasion and migration abilities of OVCAR3 cells

2011 ◽  
Vol 34 (5) ◽  
pp. 281 ◽  
Author(s):  
Yanhui Lou ◽  
Zhumei Cui ◽  
Fuling Wang ◽  
Xingsheng Yang ◽  
Jinhua Qian
Keyword(s):  
Cell Proliferation ◽  
Migration And Invasion ◽  
Control Group ◽  
Control Groups ◽  
Down Regulation ◽  
Transfected Cells ◽  
Invasion And Migration ◽  
Scratch Wound ◽  
Scratch Wound Assay ◽  
And Migration

Purpose: To investigate the influence of miR-21 down-regulation on cell proliferation, apoptosis, invasion and migration of ovarian papillary adenocarcinoma cell lines (OVCAR3). Methods: Short-hairpin RNA (shRNA), specifically targeting miR-21, was constructed and transfected into OVCAR3 cells using the pSIREN-RetroQ linear vector (pSIREN-miR-21). The expression of miR-21 was detected with stem-loop real-time RT-PCR in OVCAR3 cells. Cell proliferation and apoptosis were monitored using the MTT assay and flow cytometry, respectively. Cell migration and invasion were assessed using the transwell migration and scratch-wound assay, respectively. Western-bloting was used for PDCD4 protein expression. Results: pSIREN-miR-21 suppressed miR-21 expression in OVCAR3 cells. miR-21 expression levels in pSIREN-miR-21 cells was 0.3 ± 0.1, which was significantly lower when compared with pSIREN-miR-21-Neg and control groups (P < 0.01). Cell inhibition rate in the pSIREN-miR-21 group was higher than the control group (29.4% vs 9.0%, P < 0.01), as was the percentage of apoptotic and necrotic cells. By transwell migration assay, the number of cells migrating in the pSIREN-miR-21 group was significantly lower than in the control group. In addition, fewer cells were observed in the wounded area of the pSIREN-miR-21 group following the scratch-wound assay. PDCD4 expression was increased in OVCAR-3 cells transfected by pSIREN-miR-21 compared with vector-control transfected cells. Moreover, the optical density of the transfected cells was significantly lower than the two control groups.

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