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.

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.

miR-9-5p Increases Sensitivity to Cisplatin in Thyroid Cancer Cells by Down-Regulating BRAF Expression

2019 ◽  
Vol 9 (6) ◽  
pp. 751-759
Author(s):  
Wanzhi Chen ◽  
Jichun Yu ◽  
Rong Xie ◽  
Meijun Zhong
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Cell Number ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Thyroid Cancer Cells ◽  
Dual Luciferase Reporter Assay

Objective: To explore the expression of miR-9-5p and BRAF in cisplatin resistant strain thyroid cancer cells and reversal effect of drug resistance as well as the possible mechanism. Methods: The cisplatin-resistant thyroid cancer cells (FTC-133/DDP and TPC-1/DDP) were respectively divided into 3 groups as NC, DDP and DDP + miRNA groups. Measuring cell proliferation by MTT assay and cell apoptosis by flow cytometry; Evaluating invasion cell number and wound healing rates by transwell and wound healing assay. The relative proteins (BRAF, Mek and Erk1/2) were measured by WB assay. The correlation between miR-9-5p and BRAF by dual-luciferase reporter assay in FTC-133/DDP and TPC-1/DDP cells. Results: In FTC-133/DDP and TPC-1/DDP cells experiment, compared with DDP group, with miR-9-5p supplement, the cell proliferation rats were significantly depressed with cell apoptosis increasing (P < 0.001, respectively); invasion cell number and wound healing rats were significantly down-regulation (P < 0.001, respectively) in DDP + miRNA groups. Meanwhile, the BRAF, Mek and Erk1/2 proteins expressions were significantly depressed in DDP + miRNA groups were significantly suppressed compared with those in DDP groups (P < 0.001, respectively). By dual-luciferase reporter assay, BRAF was the target gene of miR-9-5p in FTC133/DDP and TPC-1/DDP cells. Conclusion: miR-9-5p increases sensitivity to cisplatin in thyroid cancer cells by down-regulating BRAF expression.

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.

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.

miR-29b-3p’s Effects on Prostate Cancer

2022 ◽  
Vol 12 (4) ◽  
pp. 681-689
Author(s):  
Zhou Hongyi ◽  
Yan Zhiqiang ◽  
Zhu Leilei ◽  
Li Maolin ◽  
Shao Jianfeng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Cell Apoptosis ◽  
Cell Number ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
Nuclear Levels

Objection: Our research wanted to discuss miR-29b-3p in PCa occurrence and development and relative mechanisms. Methods: Collecting adjacent and cancer tissues from prostate cancer patients and measuring miR-29b-3p expressions by RT-qPCR and ISH assay. Using DU145 and PC3 cell lines which the miR-29b-3p were high expression in our study. Using miR inhibitor to knockdown miR-29b-3p in DU145 and PC3. Using CCK-8 and flow cytometry to measure cell proliferation and cell apoptosis, invasion cell number by transwell and wound healing rate by wound healing assay. The relative proteins expressions were measured using WB assay. p-AKT nuclear levels were evaluated using Cell immunofluorescence test. Using dual-luciferase reporter gene assay to analysis correlation miR-29b-3p and PTEN. Results: miR-29b-3p gene significantly increased. miR-29b-3p knockdown had effects to depress cell proliferation, increase cell apoptosis, depress invasion cells number and wound healing rates. PTEN proteins were significantly up-regulation and p-AKT and MMP-9 proteins expressions were significantly down-regulation (P < 0.001, respectively). And p-AKT nuclear volume were significantly depressed. And miR-29b-3p could target PTEN. Conclusion: miR-29b-3p played an oncology gene in prostate cancer via regulation PTEN/AKT pathway in vitro study.

Effects of miR-1305 on Proliferation and Apoptosis of Non-Small Cell Lung Cancer Cells via Regulating High Mobility Group Box-1 Level

2020 ◽  
Vol 10 (12) ◽  
pp. 1837-1842
Author(s):  
Wenpu Zhao ◽  
Xiaolian Yang ◽  
Yishan Dong ◽  
Jin Quan ◽  
Li Huang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Mrna Level ◽  
Small Cell ◽  
Small Cell Lung ◽  
Hmgb1 Level ◽  
Proliferation And Apoptosis

Abnormal expression of HMGB1 is closely related to non-small cell lung cancer (NSCLC). miR-1305 regulates HMGB1 level by MiRDB analysis. Therefore, we investigated whether miR-1305 affects NSCLC cell proliferation and apoptosis by regulating HMGB1. The control group (NC group), miR-1305 Mimics group and miR-1305 Mimics+pcDNA-HMGB1 group were set followed by analysis of miR-1305 and HMGB1 mRNA level real time-PCR, relationship between miR-1305 and HMGB1 by dual fluorescein reporter assay, HMGB1 and Tubulin level by Western blot, cell proliferation by clone formation assay, cell apoptosis by Annexin V-FITC/PI staining. Compared with normal tissues, miR-1305 was significantly downregulated in NSCLC tissues (P <0.01), while HMGB1 mRNA was upregulated (P <0.01). HMGB1 was the target gene of miR-1305. Compared to NC group, HMGB1 level in miR-1305 Mimics group was significantly reduced (P <0.01). Compared with miR-1305 Mimics group, HMGB1 level was significantly increased in miR-1305 Mimics+pcDNA-HMGB1group (P <0.05). HMGB1 mRNA level was not significantly changed. In addition, the number of cell clones and proliferation ability was decreased in miR-1305 Mimics group, which were reversed in miR-1305 Mimics+pcDNA-HMGB1 group. miR-1305 can bind HMGB1 3′-UTR, reduce its protein level, thereby inhibiting NSCLC cell proliferation and promoting cell apoptosis. HMGB1 overexpression can prevent the effect of miR-1305.

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