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 miR-330-5p suppresses glioblastoma cell proliferation and invasiveness through targeting ITGA5

2017 ◽  
Vol 37 (3) ◽  
Author(s):  
Linsen Feng ◽  
Jianhua Ma ◽  
Haiming Ji ◽  
Yichun Liu ◽  
Weixing Hu
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Biological Effects ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Normal Brain ◽  
Luciferase Reporter Gene ◽  
Invasion And Migration ◽  
Gene Assay ◽  
And Migration

The present study intended to investigate the biological effects of miR-330-5p on glioblastoma (GBM) cell proliferation and invasiveness by targeting integrin α5 (ITGA5). The expressions of miR-330-5p and ITGA5 mRNA in GBM cell lines (U87, U251, and U373) and normal brain glial cell line (HEB) were detected using RT-qPCR. Protein expression of ITGA5 was examined using Western blot. The present study used MTT assay, colony formation assay, Transwell assay, wound healing assay, and flow cytometry analysis in order to determine the biological functions of GBM cells (including cell proliferation, invasion, migration, apoptosis, and cell cycle). The present study applied dual-luciferase reporter gene assay to identify the target relationship between miR-330-5p and ITGA5. miR-330-5p was low-expressed in GBM cell lines while ITGA5 was high-expressed compared with HEB. miR-330-5p could directly target ITGA5 as well as suppress its expression in GBM cells. Up-regulation of miR-330-5p and down-regulation of ITGA5 both have an inhibitory effect on cell proliferation, invasion, and migration. Meanwhile, they could also promote GBM cell apoptosis. miR-330-5p could suppress proliferation and invasion of GBM cells through targeting ITGA5.

Interaction between miR-572 and PPP2R2C, and their effects on the proliferation, migration, and invasion of nasopharyngeal carcinoma (NPC) cells

2017 ◽  
Vol 95 (5) ◽  
pp. 578-584 ◽  
Author(s):  
Lei Yan ◽  
Kerui Cai ◽  
Jun Liang ◽  
Haifeng Liu ◽  
Yang Liu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Luciferase Reporter Gene Assay ◽  
Normal Tissues ◽  
Gene Assay ◽  
And Migration ◽  
Proliferation And Invasion ◽  
Lower Expression

We investigated the how miR-572 regulates PPP2R2C, and studied the effects of miR-572 and PPP2R2C on proliferation and migration as well as invasion of nasopharyngeal carcinoma (NPC) cells. NPC tissues and normal tissues were collected, and the expressions of miR-572 and PPP2R2C were detected by real-time PCR. Western blot was applied to detect the expression of PPP2R2C protein. The target relationship between miR-572 and PPP2R2C was confirmed by dual luciferase reporter gene assay. MTT assay and flow cytometry were applied to investigate the viability and apoptosis levels of NPC cells. Transwell as well as wound healing assays were used, respectively, to detect the invasiveness and migration of NPC cells. MiR-572 was highly expressed in NPC tissues as well as NPC cells, and there was lower expression of PPP2R2C in NPC tissues compared with normal samples. MiR-572 could bind to the 3′ UTR of PPP2R2C and decrease its expression. Over-expressed miR-572 and decreased PPP2R2C expression could both inhibit proliferation and invasion and induce apoptosis of NPC cells. Thus, miR-572 promotes the proliferation and invasion of NPC by directly down-regulating PPP2R2C.

scholarly journals miR-495-3p Depresses Cell Proliferation and Migration By Down-Regulating HMGB1 in Colorectal Cancer

2021 ◽  
Author(s):  
Zhang Jieling ◽  
Li Kai ◽  
Zheng Huifen ◽  
Zhu Yiping
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
And Migration ◽  
Cancer Tissues

Abstract Background: MicroRNAs play an important role in the genesis and progression of tumors, including colorectal cancer (CRC), which has a high morbidity and mortality rate. In this research, the role of miR-495-3p and HMGB1 in CRC was investigated.Methods: We performed qRT-PCR to detect the expression of miR-495-3p in colorectal cancer tissues and cell lines. Functional experiments such as CCK-8 assay, EDU assay, Transwell assay and apoptosis assay were conducted to explore the effects of miR-495-3p on the proliferation, migration and apoptosis of CRC cells in vitro. Then, the use of database prediction, dual-luciferase reporter gene assay and functional experiments verified the role of miR-495-3p target gene HMGB1 in CRC. Finally, rescue experiments was performed to investigate whether overexpression of HMGB1 could reverse the inhibitory effect of miR-495-3p on CRC cell proliferation in vivo and in vitro.Results: miR-495-3p was down-regulated in colorectal cancer tissues and cell lines, and could inhibit the proliferation and migration of colorectal cancer cells, and promote cell apoptosis. The database prediction and dual-luciferase reporter gene assay showed that HMGB1 was the downstream target gene of miR-495-3p. We finally demonstrated that miR-495-3p inhibited CRC cell proliferation by targeting HMGB1 in vitro and in vivo.Conclusion: Our research shows that miR-495-3p inhibits the progression of colorectal cancer by down-regulating the expression of HMGB1, which indicates that miR-495-3p may become a potential therapeutic target for colorectal cancer.

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 miR-636 Inhibits EMT, Cell Proliferation and Cell Cycle of Ovarian Cancer by Directly Targeting the Transcription Factor Gli2 of Hedgehog Pathway

2020 ◽  
Author(s):  
Jiong Ma ◽  
Chunxia Zhou ◽  
Xuejun Chen
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Cell Proliferation And Migration ◽  
Gene Assay ◽  
And Migration ◽  
Proliferation And Migration

Abstract Objective: Ovarian cancer (OVC) is the fifth leading cause of cancer-related deaths in women and has a significant impact on physical and mental health of women. This study explores the molecular mechanism of miR-636 acting as a tumor suppressor in OVC in vitro and in vivo, and provides new insight into the treatment of OVC.Methods: Protein-protein interaction (PPI) analysis was performed to identify the hub gene in Hedgehog (Hh) pathway. TargetScan database was used to predict the upstream regulatory miRNAs of Gli2 to obtain the target miRNA. qRT-PCR was performed to test the expression of miR-636, while Western blot were conducted to detect the expression of Hh and EMT (epithelial-mesenchymal transition) related genes in OVC cell lines. MTT assay and wound healing assay were used to measure the effect of miR-636 on OVC cell proliferation and migration. Flow cytometry was carried out to examine the effect of miR-636 on cell cycle, and Western blot was used for identification of changes in expression of Hh and EMT related proteins. Dual-luciferase reporter gene assay was implemented to detect the targeted relationship between miR-636 and Gli2. The xenotransplantation model was used to detect the effect of miR-636 on OVC cell proliferation in vivo.Results: PPI interaction analysis found that Gli2 was the hub gene in Hh pathway. Based on TargetScan and GEO databases, Gli2 was found to be targeted regulated by the upstream miR-636. In vitro experiments discovered that miR-636 was significantly lowly expressed in OVC cell lines. Overexpressing miR-636 significantly inhibited HO-8910PM cell proliferation and migration abilities as well as induced cell cycle arrest in G0/G1 phase, while the inhibition of miR-636 promoted cell proliferation and migration abilities. Dual-luciferase reporter gene assay revealed that Gli2 was a target gene of miR-636. Besides, overexpressing miR-636 decreased protein expression of Gli2, while the inhibition of miR-636 increased protein expression of Gli2. Furthermore, the overexpression and inhibition of miR-636 both affected the expression of proteins related to Hh signaling pathway and EMT. Rescue experiments verified that overexpression of Gli2 reversed the inhibitory effect of miR-636 on HO-8910PM cell proliferation and migration abilities, and attenuated the blocking effect of miR-636 on HO-8910PM cell cycle. The xenotransplantation model suggested that miR-636 inhibited cell growth of OVC by decreasing Gli2 expression. Besides, overexpressing Gli2 potentiated the EMT process in OVC via decreasing E-cadherin protein expression and increasing Vimentin protein expression, and it reversed the inhibitory effect of miR-636 on OVC cell proliferation and migration abilities in vivo.Conclusion: miR-636 inhibits the Hh pathway activation via targeted binding to Gli2, thus inhibiting EMT, cell proliferation and migration in OVC.

scholarly journals Long Noncoding RNA HCG11 Acts as a Tumor Suppressor in Gastric Cancer by Regulating miR-942-5p/BRMS1 Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Qingmei Zhang ◽  
Keli Yang ◽  
Jie Li ◽  
Fang Chen ◽  
Yan Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Noncoding Rna ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Metastasis Suppressor ◽  
Invasion And Migration ◽  
And Migration

The functions of long noncoding RNAs (lncRNAs) have been widely investigated in human cancers, including gastric cancer (GC). The purpose of this study was to elucidate the role of lncRNA HCG11 in GC. In this study, mRNA and protein expressions were detected by quantitative real-time polymerase chain reaction assays (RT-qPCR) and Western blot analysis. The proliferation ability of GC cells was examined by (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyl Tetrazolium Bromide) MTT assays. The invasion and migration abilities of GC cells were evaluated by Transwell assays. The binding sites between miR-942-5p and HCG11/BRMS1 were confirmed by dual-luciferase reporter assays. Results showed that LncRNA HCG11 was downregulated in GC cells. Functionally, overexpression of HCG11 inhibited GC cell proliferation, migration, and invasion. In addition, lncRNA HCG11 was found to act as a molecular sponge of miR-942-5p. Furthermore, miR-942-5p promoted GC progression by suppressing lncRNA HCG11 expression. Besides that, BRMS1 was confirmed as a direct target of miR-942-5p. More importantly, breast cancer metastasis suppressor 1 (BRMS1) inhibited GC progression by upregulating lncRNA HCG11 and downregulating miR-942-5p. In conclusion, LncRNA HCG11 inhibited cell proliferation, migration, and invasion in GC by sponging miR-942-5p and upregulating BRMS1.

scholarly journals LncRNA SNHG3 Promotes Gastric Cancer Cells Proliferation, Migration, and Invasion by Targeting miR-326

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jun Rao ◽  
Jinjin Fu ◽  
Chuchen Meng ◽  
Jin Huang ◽  
Xiangrong Qin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Gastric Cancer Cells ◽  
Invasion And Migration ◽  
Protein Levels ◽  
Rna Immunoprecipitation ◽  
And Migration

The function and possible mechanism of lncRNA Small Nucleolar RNA Host Gene 3 (SNHG3) in GC have not been fully studied. The aim of our study was to investigate the role of SNHG3 in the proliferation, migration, and invasion of GC cell lines. The expressions of SNHG3, miR-326, and TWIST in GC9811-P GC cell lines were detected by RT-qPCR. Western blotting was performed to detect the protein levels of TWIST and EMT-related genes. Luciferase reporter gene analysis and RNA immunoprecipitation (RIP) analysis confirmed the interaction between lncRNA SNHG3, miR-326, and TWIST. CCK-8 and Transwell assays were performed to detect cell proliferation, invasion, and migration abilities. The results showed that lncRNA SNHG3 and TWIST were highly expressed in GC cell lines, while miR-326 was expressed to a low degree. Moreover, lncRNA SNHG3 knockdown or miR-326 overexpression significantly inhibited cell proliferation, migration, and invasion of GC cell lines. In addition, TWIST overexpression can reverse the inhibition of lncRNA SNHG3 knockdown or miR-326 overexpression on cell proliferation, migration, and invasion. In conclusion, lncRNA SNHG3 may promote GC progression through the miR-326/TWIST axis, which may provide a new diagnostic and prognostic biomarker for GC.

scholarly journals PCGEM1 Promotes Proliferation, Migration And Invasion In Prostate Cancer By Sponging miR-506 To Upregulate TRIAP1

2021 ◽  
Author(s):  
He Liu ◽  
Xin He ◽  
Tianjiao Li ◽  
Yi Qu ◽  
Lina Xu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Noncoding Rna ◽  
Suppressive Effect ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Gene Level ◽  
And Migration

Abstract Background: The important role of long noncoding RNAs (lncRNAs) in cancer has been demonstrated in many studies. Prostate cancer gene expression marker 1 (PCGEM1) is a lncRNA specifically expressed within the prostate and overexpressed in many cancer cells. Numerous studies have shown that PCGEM1 promotes cell proliferation, invasion and migration. However, the specific mechanism of PCGEM1 within prostate cancer (PCa) has not been elucidated. MicroRNA-506-3p (miR-506-3p) is a noncoding RNA, and studies have indicated that miR-506-3p is downregulated in prostate cancer cell lines and functions as a tumor suppressor.Methods: The TCGA (GEPIA) database (http://gepia.cancer-pku.cn/) was employed to measure PCGEM1 levels in PCa. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the PCGEM1 gene level. CCK-8 (Cell Counting Kit-8) and colony formation assays were used to detect cell proliferation, and Transwell assays were applied to assess cell invasion and migration. The interacting ability of miR-506-3p with PCGEM1 or TRIAP1 was validated through a dual-luciferase reporter assay. TRIAP1 protein expression was detected by Western blotting.Results: PCGEM1 expression was increased in PCa tissues and cells. In PCa tissues, High PCGEM1 expression was associated with high Gleason score, distant metastasis and extracapsular extension. In addition, PCGEM1 knockdown inhibited PCa cell (C4-2B and PC-3) proliferation, invasion and migration. miR-506-3p may interact with PCGEM1 or TRIAP1, and the suppressive effect of PCGEM1 knockdown was reversed when TRIAP1 or a miR-506-3p inhibitor was cotransfected.Conclusion: PCGEM1 expression increased in PCa cells and tissues, enhancing PCa cell proliferation, migration and invasion by sponging miR-506 to upregulate TRIAP1.

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