miR-449b-5p Inhibits Cell Proliferation and Migration of Breast Cancer via Targeting Flotillin-2

2020 ◽  
Vol 10 (8) ◽  
pp. 1094-1101
Author(s):  
Delin Wu ◽  
Xiaopeng Ma
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Breast Carcinoma ◽  
Critical Role ◽  
Ectopic Expression ◽  
Luciferase Reporter ◽  
Cell Growth And Migration ◽  
Cancer Pathogenesis ◽  
And Migration

Background: MicroRNAs (miRNAs) act as a critical role in cancer pathogenesis, while the potential of miR-449b-5p in breast carcinoma remains to be fully inquired. Therefore, we purposed to probe the mechanism governing miR-449b-5p in breast cancer. Methods: Reverse transcription-PCR (RTPCR) was adopted to examine miR-449b-5p expression level in breast carcinoma. The functional experiments were implemented to estimate the role of miR-449b-5p in cell growth and migration. The interplay of miR-449b-5p with FLOT2 was validated with luciferase reporter assay. Results: miR-449b-5p level was markedly lessened in the tissue samples and cell lines of breast carcinoma. Overexpression of miR-449b-5p contributed to suppression of cell growth and migration whereas induced apoptosis in SKBr-3 and MCF-7 cells. Moreover, luciferase reporter experiment suggested that FLOT2 had a negative correlation with miR-449b-5p expression. Functionally, ectopic expression of FLOT2 reversed repressive effects of miR-449b-5p mimic on malignant behaviors of breast carcinoma cells. Conclusion: miR-449b-5p hindered cell proliferation, migration and facilitated cell apoptosis of breast carcinoma through targeting FLOT2. Our findings may offer a potent target for the therapy of breast carcinoma.

scholarly journals LINC00514 upregulates CCDC71L to promote cell proliferation, migration and invasion in triple‐negative breast cancer by sponging miR-6504-5p and miR-3139

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiao Luo ◽  
Hui Wang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Essential Gene ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cell Growth And Migration ◽  
Promote Cell Proliferation ◽  
And Migration

Abstract Background Long noncoding RNAs (lncRNAs) have recently identified as essential gene modulators in numerous cancers. Previous studies have confirmed the oncogenic role of long intergenic nonprotein-coding RNA 00514 (LINC00514) in some cancers. Nevertheless, its biological function and mechanism remain unclear in triple-negative breast cancer (TNBC). Methods Herein, we detected LINC00514 expression level in TNBC tissues and cells using RT-qPCR. The function of LINC00514 in TNBC cellular activities was assessed by colony formation, EdU, wound healing, transwell assays and flow cytometry analysis. Results The binding between miR-6504-5p/miR-3139 and LINC00514/CCDC71L was validated by luciferase reporter assay. The results indicated that LINC00514 expression was upregulated in TNBC tissues and cells. Furthermore, it was manifested that silenced LINC00514 restrained cell proliferative, migratory and invasive abilities and promoted cell apoptosis. In mechanism, LINC00514 was revealed to sequester miR-6504-5p and miR-3139 in TNBC cells. Furthermore, the low level of miR-6504-5p and miR-3139 was identified in TNBC tissues and cells. Overexpression of miR-6504-5p or miR-3139 inhibited cell growth and migration in TNBC. CCDC71L was recognized as a common downstream gene of miR-6504-5p and miR-3139. Rescue assay verified that overexpressed CCDC71L countervailed the anti-tumor influence of LINC00514 knockdown on TNBC cell proliferation, migration, invasion and apoptosis. Conclusions LINC00514 promote cell proliferation, migration and invasion in triple-negative breast cancer by targeting the miR-6504-5p/miR-3139/CCDC71L axis in TNBC.

scholarly journals MiR-188-3p and miR-133b Suppress Cell Proliferation in Human Hepatocellular Carcinoma via Post-Transcriptional Suppression of NDRG1

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Zhenzhao Luo ◽  
Yue Fan ◽  
Xianchang Liu ◽  
Shuiyi Liu ◽  
Xiaoyu Kong ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Growth ◽  
Suppressive Effect ◽  
Luciferase Reporter ◽  
Invasion And Migration ◽  
And Migration ◽  
Cancer Tissues ◽  
Suppress Cell Proliferation

Background: Previous studies reported that N-myc downstream-regulated gene 1 (NDRG1) was upregulated in various cancer tissues and decreased expression of miR-188-3p and miR-133b could suppress cell proliferation, metastasis, and invasion and induce apoptosis of cancer cells. However, the molecular mechanism of NRDG1 involved in hepatocellular carcinoma (HCC) tumorigenesis is still unknown. Methods: The expressions of miR-188-3p, miR-133b, and NRDG1 in HCC tissues and cells were quantified by qRT-PCR and Western blot. MTT assay and transwell invasion assay were performed to evaluate cell growth and cell migration, respectively. Luciferase reporter assay were performed to determine whether miR-188-3p and miR-133b could directly bind to NRDG1 in HCC cells. Results: The results showed that NRDG1 was upregulated and these 2 microRNAs were downregulated in HCC tissues. NRDG1 was negatively correlated with miR-188-3p and miR-133b in HCC tissues. MiR-188-3p and miR-133b were demonstrated to directly bind to 3′UTR of NRDG1 and inhibit its expression. Upregulation of miR-188-3p and miR-133b reduced NRDG1 expression in hepatocellular carcinoma cell lines, which consequently inhibited cell growth and cell migration. Conclusions: Our finding suggested that miR-188-3p and miR-133b exert a suppressive effect on hepatocellular carcinoma proliferation, invasion, and migration through downregulation of NDRG1.

scholarly journals miR-3188 Regulates Cell Proliferation, Apoptosis, and Migration in Breast Cancer by Targeting TUSC5 and Regulating the p38 MAPK Signaling Pathway

2018 ◽  
Vol 26 (3) ◽  
pp. 363-372 ◽  
Author(s):  
Xiaowen Chen ◽  
Jianli Chen
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Luciferase Reporter ◽  
And Migration ◽  
Mcf 7

This study intended to investigate the effects of miR-3188 on breast cancer and to reveal the possible molecular mechanisms. miR-3188 was upregulated and TUSC5 was downregulated in breast cancer tissues and MCF-7 cells compared to normal tissue and MCF-10 cells. After MCF-7 cells were transfected with miR-3188 inhibitor, cell proliferation and migration were inhibited, whereas apoptosis was promoted. Luciferase reporter assay suggested that TUSC5 was a target gene of miR-3188. In addition, miR-3188 overexpression increased the p-p38 expression, while miR-3188 suppression decreased the p-p38 expression significantly. miR-3188 regulated breast cancer progression via the p38 MAPK signaling pathway. In conclusion, miR-3188 affects breast cancer cell proliferation, apoptosis, and migration by targeting TUSC5 and activating the p38 MAPK signaling pathway. miR-3188 may serve as a potential therapeutic agent for the treatment of breast cancer.

Arsenic trioxide suppresses cell growth and migration via inhibition of miR-27a in breast cancer cells

2016 ◽  
Vol 469 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Shunhua Zhang ◽  
Cong Ma ◽  
Haijie Pang ◽  
Fanpeng Zeng ◽  
Long Cheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Breast Cancer Cells ◽  
Cell Growth And Migration ◽  
And Migration

MiR-4458 inhibits breast cancer cell growth, migration, and invasiveness by targeting CPSF4

2019 ◽  
Vol 97 (6) ◽  
pp. 722-730 ◽  
Author(s):  
Jianrong Wu ◽  
Juan Miao ◽  
Ye Ding ◽  
Yayun Zhang ◽  
Xiaohao Huang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Target Genes ◽  
Human Lung ◽  
Lung Tumor ◽  
Luciferase Reporter ◽  
Bioinformatics Analyses ◽  
Cox 2

Numerous studies have reported that CPSF4 is over-expressed in a large percentage of human lung cancers, and CPSF4 has been identified as a potential oncogene of human lung tumor. Downregulation of CPSF4 inhibits the proliferation and promotes the apoptosis of lung adenocarcinoma cells. A previous study by our group also found overexpression of CPSF4 in breast cancer (BC), and was closely associated with a poor prognosis for the patient. This study investigates microRNAs (miRNAs) that target CPSF4 to modulate BC cell proliferation. We found that miR-4458 was noticeably reduced in BC tissues and cells. Using a miR-4458 mimic, we found that cell proliferation, migration, and invasiveness were suppressed by miR-4458 overexpression, and were enhanced by reducing the expression of miR-4458. Moreover, the results from bioinformatics analyses suggest a putative target site in the CPSF4 3′-UTR. Furthermore, using luciferase reporter assays and Western blotting, we verified that miR-4458 directly targets the 3′-UTR of CPSF4 and downregulates COX-2 and h-TERT, which are downstream target genes of CPSF4. Additionally, PI3K/AKT and ERK were shown to be inhibited by miR-4458 overexpression in BC cells. Moreover, miR-4458 suppresses BC cell growth in vivo. Consequently, these results suggest that the miR-4458–CPSF4–COX-2–hTERT axis might serve as a potential target for the treatment of BC patients.

scholarly journals Down-regulation of uPA and uPAR by 3,3′-diindolylmethane contributes to the inhibition of cell growth and migration of breast cancer cells

2009 ◽  
Vol 108 (4) ◽  
pp. 916-925 ◽  
Author(s):  
Aamir Ahmad ◽  
Dejuan Kong ◽  
Zhiwei Wang ◽  
Sanila H. Sarkar ◽  
Sanjeev Banerjee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Down Regulation ◽  
Cell Growth And Migration ◽  
And Migration

scholarly journals Down-regulated Long Noncoding RNAHOXA11-ASaffects trophoblast cell proliferation and migration by regulatingRND3andHOXA7expression in preeclampsia

2018 ◽  
Author(s):  
Yetao Xu ◽  
Dan Wu ◽  
Jie Liu ◽  
Zhonghua Ma ◽  
Bingqing Hui ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Noncoding Rna ◽  
Trophoblast Cell ◽  
Rna Seq ◽  
Biological Mechanisms ◽  
Aberrant Expression ◽  
Cell Growth And Migration ◽  
And Migration ◽  
Proliferation And Migration

AbstractThe long noncoding RNAHOXA11-ASreveals abnormal expression in numerous human diseases. However, its function and biological mechanisms remain unclear in Preeclampsia (PE). In this study, we report thatHOXA11-ASwas significantly downregulated in preeclampsic placental tissues and could contribute to the occurrence and development of Preeclampsia. Silencing ofHOXA11-ASexpression could significantly suppress trophoblast cell growth and migration, whereasHOXA11-ASoverexpression facilitated cell growth in HTR-8/SVneo, JEG3 and JAR cell lines. RNA-seq analysis also indicated thatHOXA11-ASsilencing preferentially regulated numerous genes associated with cell proliferation and cell migration. Mechanistic analyses showed thatHOXA11-AScould recruit Ezh2 and Lsd1 protein, and regulateRND3mRNA expression in nucleus. In cytoplasm,HOXA11-ASmodulateHOXA7expression by sponged miR-15b-5p, thus affecting trophoblast cell proliferation. Together, these resulting data confirm that aberrant expression ofHOXA11-ASis involved in the occurrence and development of Preeclampsia, and may act as a prospective diagnosis and therapeutic target in PE.

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