scholarly journals Long noncoding RNA UCA1 facilitates cell proliferation and inhibits apoptosis via activating PI3K/Akt pathway in retinoblastoma

2019 ◽  
Author(s):  
Zhongfang Yuan ◽  
Zhaona Li
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cell Counting ◽  
Akt Pathway ◽  
Promote Cell Proliferation ◽  
Cell Clones ◽  
Y79 Cells ◽  
The Relationship

Abstract Background Retinoblastoma (RB) is the most common intraocular malignancy of childhood. This study is aimed to explored the effect of lncRNA-UCA1 on RB and its potential molecular mechanisms.Methods In our study, the expression of lncRNA-UCA1 was measured by qRT-RCR in both RB tissues and RB HXO-RB44 and Y79 cells. The relationship between lncRNA-UCA1 expression and clinical parameters in RB patients were evaluated. Cell proliferation, cell clones, apoptosis and cell cycle of HXO-RB44 and Y79 cells were measured by cell counting kit-8 (CCK-8) assay, colony formation assay and flow cytometry, respectively. In addition, the expressions of PCNA, Caspase-3, survivin, p16, p21, CDK2, PI3K, p-PI3K, Akt, p-Akt and S6k in HXO-RB44 and Y79 cells were measured by western blot.Results lncRNA-UCA1 was highly expressed in both RB tissues and RB HXO-RB44 and Y79 cells. Moreover, the expression of lncRNA-UCA1 in RB patients was remarkedly correlated with tumor size, optic nerve invasion and pathologic grade. lncRNA-UCA1 markedly facilitated cell proliferation and cell cycle procession, as well as inhibited cell apoptosis in HXO-RB44 and Y79 cells. lncRNA-UCA1 dramatically increased the expression of S6k and the phosphorylation of PI3K and Akt in RB cells. LY294002 (PI3K inhibitor) reversed the effects of lncRNA-UCA1 on RB cell proliferation, apoptosis and cell cycle procession.Conclusions Our study indicated that lncRNA-UCA1 could promote cell proliferation and cell cycle procession, as well as inhibit cell apoptosis in RB via activating PI3K/Akt pathway.

scholarly journals Long noncoding RNA UCA1 facilitates cell proliferation and inhibits apoptosis via activating PI3K/Akt pathway in retinoblastoma

2019 ◽  
Author(s):  
Zhongfang Yuan ◽  
Zhaona Li
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cell Counting ◽  
Akt Pathway ◽  
Promote Cell Proliferation ◽  
Cell Clones ◽  
Y79 Cells ◽  
The Relationship

Abstract Background This study aimed to explored the effect of lncRNA-UCA1 on retinoblastoma (RB) and its potential molecular mechanisms.Methods In our study, the expression of lncRNA-UCA1 was measured by qRT-RCR in both RB tissues and RB HXO-RB44 and Y79 cells. The relationship between lncRNA-UCA1 expression and clinical parameters in RB patients were evaluated. Cell proliferation, cell clones, apoptosis and cell cycle of HXO-RB44 and Y79 cells were measured by cell counting kit-8 (CCK-8) assay, colony formation assay and flow cytometry, respectively. In addition, the expressions of PCNA, Caspase-3, survivin, p16, p21, CDK2, PI3K, p-PI3K, Akt, p-Akt and S6k in HXO-RB44 and Y79 cells were measured by western blot.Results lncRNA-UCA1 was highly expressed in both RB tissues and RB HXO-RB44 and Y79 cells. Moreover, the expression of lncRNA-UCA1 in RB patients was remarkedly correlated with tumor size, optic nerve invasion and pathologic grade. lncRNA-UCA1 markedly facilitated cell proliferation and cell cycle procession, as well as inhibited cell apoptosis in HXO-RB44 and Y79 cells. lncRNA-UCA1 dramatically increased the expression of S6k and the phosphorylation of PI3K and Akt in RB cells. LY294002 (PI3K inhibitor) reversed the effects of lncRNA-UCA1 on RB cell proliferation, apoptosis and cell cycle procession.Conclusions Our study indicated that lncRNA-UCA1 could promote cell proliferation and cell cycle procession, as well as inhibit cell apoptosis in RB via activating PI3K/Akt pathway.

scholarly journals Knockdown of long noncoding RNA HOTAIR inhibits osteoarthritis chondrocyte injury by miR-107/CXCL12 axis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Jipeng Lu ◽  
Zhongxiong Wu ◽  
Ying Xiong
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Underlying Mechanism ◽  
Joint Disease ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Cxcl12 Expression ◽  
Ecm Degradation

Abstract Background Osteoarthritis (OA) is a joint disease characterized via destruction of cartilage. Chondrocyte damage is associated with cartilage destruction during OA. Long noncoding RNAs (lncRNAs) are implicated in the regulation of chondrocyte damage in OA progression. This study aims to investigate the role and underlying mechanism of lncRNA homeobox antisense intergenic RNA (HOTAIR) in OA chondrocyte injury. Methods Twenty-three OA patients and healthy controls without OA were recruited. Chondrocytes were isolated from OA cartilage tissues. HOTAIR, microRNA-107 (miR-107) and C-X-C motif chemokine ligand 12 (CXCL12) levels were measured by quantitative real-time polymerase chain reaction and western blot. Cell proliferation, apoptosis and extracellular matrix (ECM) degradation were measured using cell counting kit-8, flow cytometry and western blot. The target interaction was explored by bioinformatics, luciferase reporter and RNA immunoprecipitation assays. Results HOTAIR expression was enhanced, and miR-107 level was reduced in OA cartilage samples. HOTAIR overexpression inhibited cell proliferation, but induced cell apoptosis and ECM degradation in chondrocytes. HOTAIR knockdown caused an opposite effect. MiR-107 was sponged and inhibited via HOTAIR, and knockdown of miR-107 mitigated the effect of HOTAIR silence on chondrocyte injury. CXCL12 was targeted by miR-107. CXCL12 overexpression attenuated the roles of miR-107 overexpression or HOTAIR knockdown in the proliferation, apoptosis and ECM degradation. CXCL12 expression was decreased by HOTAIR silence, and restored by knockdown of miR-107. Conclusion HOTAIR knockdown promoted chondrocyte proliferation, but inhibited cell apoptosis and ECM degradation in OA chondrocytes by regulating the miR-107/CXCL12 axis.

Long noncoding RNA THOR is highly expressed in colorectal cancer and predicts a poor prognosis

2020 ◽  
Vol 16 (25) ◽  
pp. 1911-1920
Author(s):  
Feifei Chu ◽  
Yuanbo Cui ◽  
Kunkun Li ◽  
Xingguo Xiao ◽  
Li Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Prognostic Biomarker ◽  
Cell Counting ◽  
Tumor Node Metastasis ◽  
Tumor Node Metastasis Stage

Aim: Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. This study aimed to investigate the role of long noncoding RNA THOR in CRC. Materials & methods: The expression of THOR in 103 cases of CRC tissues and four CRC cell lines was examined by quantitative real-time PCR. Cell counting kit-8 and colony formation assays were applied to detect cell proliferation, and flow cytometry was used for testing cell cycle and apoptosis of CRC. Results: We found that THOR was highly expressed in CRC and correlated with tumor node metastasis stage, histological subtype, tumor size and differentiation and survival in CRC patients. Meanwhile, knockdown of THOR significantly suppressed cell proliferation and cell cycle of CRC, whereas promoted cell apoptosis. Conclusion: Our findings suggest that THOR is an oncogenic long noncoding RNA in CRC and a potential prognostic biomarker for this cancer.

MiR-129-5p promotes radio-sensitivity of NSCLC cells by targeting SOX4 and RUNX1

2021 ◽  
Vol 21 ◽  
Author(s):  
Tongqing Xue ◽  
Gang Yin ◽  
Weixuan Yang ◽  
Xiaoyu Chen ◽  
Cheng liu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Transcription Factor ◽  
Cell Lines ◽  
Cell Apoptosis ◽  
Colony Formation ◽  
Nsclc Cell ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Radio Sensitivity

Background: Dysregulation of microRNAs (miRNAs) figures prominently in radio-sensitivity of non-small cell lung cancer (NSCLC). MiR-129-5p can block the development of a variety of tumors. However, whether miR-129-5p modulates radio-sensitivity of NSCLC cells remains unknown. Objective: This study was aimed to explore the role and the underlying mechanism of miR-129-5p in the radiosensitivity of NSCLC. Methods: Radio-resistant NSCLC cell lines (A549-R and H1299-R) were constructed using A549 and H1299 cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to quantify miR-129-5p, SRY-box transcription factor 4 (SOX4) mRNA, and RUNX family transcription factor 1 (RUNX1) mRNA expression levels. Cell apoptosis and cell cycle were detected by flow cytometry. Cell counting kit-8 (CCK-8) assay and colony formation experiments were used to measure cell proliferation. γ-H2AX was examined by Western blot to confirm DNA injury. Dual-luciferase reporter experiments were applied to analyze the interactions among miR-129-5p, RUNX1, and SOX4. Results: In A549-R and H1299-R cells, compared with the wild type cell lines, miR-129-5p expression was remarkably reduced while SOX4 and RUNX1 expressions were increased. The transfection of miR-129-5p into NSCLC cell lines, markedly induced cell apoptosis, DNA injury, and cell cycle arrest, and inhibited cell proliferation and colony formation. RUNX1 and SOX4 were validated as target genes of miR-129-5p, and the restoration of RUNX1 or SOX4 could counteract the influence of miR-129-5p on A549-R cells. Conclusion: MiR-129-5p sensitizes A549-R and H1299-R cells to radiation by targeting RUNX1 and SOX4.

scholarly journals UCA1, a long noncoding RNA, promotes the proliferation of CRC cells via p53/p21 signaling

2016 ◽  
Vol 11 (1) ◽  
pp. 206-210
Author(s):  
Shen Yi ◽  
Ying Xiao-jiang ◽  
Li Zhen-jun ◽  
Li Gang ◽  
Xue Wu-jin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Proliferation Rate ◽  
Cell Counting ◽  
Quantitative Real Time Pcr ◽  
Human Colorectal Cancer ◽  
Underlying Mechanisms ◽  
Hct116 Cells

AbstractObjectiveRecently, the role of long noncoding RNAs (lncRNAs) in human colorectal cancer (CRC) has been a subject of intense focus. We set out to determine the function of one lncRNA, termed urothelial carcinoma-associated 1 (UCA1) in CRC cell proliferation and its underlying mechanisms.MethodsQuantitative real-time PCR (qRT-PCR) was applied to detect the expression level of UCA1 in 50 pairs of CRC samples compared with non-tumor colon tissues. Cell growth was determined using the Cell Counting Kit-8 (CCK-8). Western blotting was carried out to analyze the related protein expression. Flow cytometry was done to evaluate cell apoptosis by UCA1 inhibition.ResultsWe found an increased expression of UCA1 in CRC samples. Knockdown of UCA1 in HCT116 cells induced a decrease in cell proliferation rate compared to control samples. This oncogenic activity may be enhanced through p53/ p21 signaling.ConclusionOur results supported the hypothesis that upregulation of UCA1 contributes to the unlimited proliferation rate of CRC cells, at least partially through the negative regulation of p53/p21 signaling pathway. Finally, we found that UCA1 merely influenced CRC cell apoptosis.

scholarly journals Circ_0082182 promotes oncogenesis and metastasis of colorectal cancer in vitro and in vivo by sponging miR-411 and miR-1205 to activate the Wnt/β-catenin pathway

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Ruijie Liu ◽  
Ping Deng ◽  
Yonglian Zhang ◽  
Yonglan Wang ◽  
Cuiping Peng
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Xenograft Model ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Mesenchymal Transition

Abstract Background Circular RNAs (circRNAs) are a class of endogenous single-strand RNA transcripts with crucial regulation in human cancers. The objective of this study is to investigate the role of circ_0082182 in CRC and its specific functional mechanism. Methods The quantitative real-time polymerase chain reaction (qRT-PCR) was performed to measure the levels of circ_0082182, microRNA-411 (miR-411) and microRNA-1205 (miR-1205). Cell proliferation was detected by Cell counting Kit-8 (CCK-8) and colony formation assays. Flow cytometry was used for determining cell cycle and cell apoptosis. Cell apoptosis was also assessed by caspase3 and caspase9 activities. Cell migration and invasion were examined using scratch assay and transwell assay. The interaction between circ_0082182 and miRNA was validated by the dual-luciferase reporter and biotinylated RNA pull-down assays. Wnt/β-catenin pathway and epithelial-mesenchymal transition (EMT)-associated proteins were quantified by Western blot. Xenograft model was established for the research of circ_0082182 in vivo. Results Circ_0082182 was upregulated in CRC and could predict the poor prognosis of CRC patients. Functionally, circ_0082182 promoted CRC cell proliferation, cell cycle progression, and metastasis while inhibited apoptosis. Subsequently, circ_0082182 was shown to act as the sponges of miR-411 and miR-1205. MiR-411 and miR-1205 were identified as tumor inhibitors in CRC. Furthermore, circ_0082182 promoted the CRC progression via sponging miR-411 and miR-1205. Moreover, circ_0082182 facilitated the Wnt/β-catenin pathway and EMT process by targeting miR-411 and miR-1205. In vivo, circ_0082182 accelerated the CRC tumorigenesis and EMT process by activating the Wnt/β-catenin pathway by downregulating the expression of miR-411 or miR-1205. Conclusion This study showed that circ_0082182 functioned as an oncogene in the developing process of CRC by sponging miR-411 or miR-1205 to activate the Wnt/β-catenin pathway. Circ_0082182 might be a molecular target in the diagnosis and treatment of CRC.

scholarly journals TAZ promotes cell growth and inhibits Celastrol-induced cell apoptosis

2016 ◽  
Vol 36 (5) ◽  
Author(s):  
Shuren Wang ◽  
Kai Ma ◽  
Lechuang Chen ◽  
Hongxia Zhu ◽  
Shufang Liang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase ◽  
Cell Growth ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
Protein Kinase B ◽  
B Cell Lymphoma ◽  
Akt Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Promote Cell Proliferation

TAZ could promote cell proliferation and inhibit Celastrol-induced cell apoptosis. Up-regulation of B-cell lymphoma-2 (Bcl-2), down-regulation of Bcl-2 associated X protein (Bax) and activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway may be the mechanism underlying anti-apoptosis of TAZ.

scholarly journals PTENInhibits Cell Proliferation, Promotes Cell Apoptosis, and Induces Cell Cycle Arrest via Downregulating the PI3K/AKT/hTERTPathway in Lung Adenocarcinoma A549 Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Xiao-Xiao Lu ◽  
Lan-Yu Cao ◽  
Xi Chen ◽  
Jian Xiao ◽  
Yong Zou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Cell Cycle Arrest ◽  
Cell Apoptosis ◽  
A549 Cells ◽  
Akt Pathway ◽  
Wild Type ◽  
Cycle Arrest ◽  
Lung Adenocarcinoma A549

PTENplays an essential role in tumorigenesis and both its mutation and inactivation can influence proliferation, apoptosis, and cell cycle progression in tumor cells. However, the precise role ofPTENin lung cancer cells has not been well studied. To address this, we have generated lung adenocarcinoma A549 cells overexpressing wild-type or mutantPTENas well as A549 cells expressing a siRNA directed toward endogenousPTEN. Overexpression of wild-typePTENprofoundly inhibited cell proliferation, promoted cell apoptosis, caused cell cycle arrest at G1, downregulated p-AKT, and decreased expression of the telomerase proteinhTERT. In contrast, in cells expressing aPTENdirected siRNA, the opposite effects on cell proliferation, apoptosis, cell cycle arrest, p-AKT levels, andhTERTprotein expression were observed. A549 cells transfected with aPTENmutant lacking phosphatase activity (PTEN-C124A) or an empty vector (null) did not show any effect. Furthermore, using the PI3K/AKT pathway blocker LY294002, we confirmed that the PI3K/AKT pathway was involved in mediating these effects ofPTEN. Taken together, we have demonstrated thatPTENdownregulates the PI3K/AKT/hTERTpathway, thereby suppressing the growth of lung adenocarcinoma cells. Our study may provide evidence for a promising therapeutic target for the treatment of lung adenocarcinoma.

scholarly journals LncRNA-SRA1 Suppresses Osteosarcoma Cell Proliferation While Promoting Cell Apoptosis

2019 ◽  
Vol 18 ◽  
pp. 153303381984143 ◽  
Author(s):  
Wen Guo ◽  
Haitao Jiang ◽  
Haijun Li ◽  
Fang Li ◽  
Qing Yu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Steroid Receptor ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Normal Tissues

Objective: Osteosarcoma is a common malignant bone tumor that is frequently found in the long bones of children and adolescents. The aim of this study is to examine long noncoding RNA-steroid receptor RNA activator 1 expression in osteosarcoma to explore the biological function of long noncoding RNA steroid receptor RNA activator 1 on proliferation, migration, and invasion along with apoptosis and its regulatory mechanism, which would facilitate the early diagnosis and targeted therapy of osteosarcoma. Methods: First, microarray analysis was applied to determine the expression of long noncoding RNAs in osteosarcoma tissues and paired normal tissues. Then, quantitative real-time polymerase chain reaction was utilized to validate microarray findings. Next, osteosarcoma cancerous cell lines SJSA-1 and U2OS were transfected with pcDNA3.1-SRA1 or pCMV-sh-SRA1 to increase or decrease steroid receptor RNA activator 1 expression levels, and microRNA-208a inhibitors, mimic to investigate the effects of microRNA-208a on osteosarcoma as well as the regulatory relation between long noncoding RNA steroid receptor RNA activator 1 and microRNA-208a. Cell proliferation was evaluated through Cell Counting Kit-8 and colony formation assays. Flow cytometry analysis was conducted to evaluate the apoptosis ratio. The migration and invasion abilities were measured using wound-healing and transwell assays. Results: Long noncoding RNA-steroid receptor RNA activator 1 expression was downregulated in osteosarcoma tissues and cells compared with that in corresponding normal tissues, whereas microRNA-208a expression was upregulated in osteosarcoma tissues. Moreover, the restoration of long noncoding RNA steroid receptor RNA activator 1 inhibited cell proliferation, and upregulation of long noncoding RNA steroid receptor RNA activator 1 restrained cell migration and invasion but boosted the apoptosis rate in osteosarcoma cells. In addition, long noncoding RNA steroid receptor RNA activator 1 targeting microRNA-208a was involved in the progression of osteosarcoma. Furthermore, upregulating microRNA-208a exerted similar roles of silencing long noncoding RNA steroid receptor RNA activator 1 in cell apoptosis, proliferation, migration, and invasion, which were reversed by enhancing the expression of long noncoding RNA steroid receptor RNA activator 1. Conclusions: In our study, long noncoding RNA steroid receptor RNA activator 1 played an antitumor role in osteosarcoma as it reduced cell migration, invasion, and proliferation, but facilitated cell apoptosis via sponging microRNA-208a, which could be regarded as a potential therapeutic target of osteosarcoma treatment.

scholarly journals MiR-221 Promotes Capan-2 Pancreatic Ductal Adenocarcinoma Cells Proliferation by Targeting PTEN-Akt

2016 ◽  
Vol 38 (6) ◽  
pp. 2366-2374 ◽  
Author(s):  
Wenzhuo Yang ◽  
Yanning Yang ◽  
Lu Xia ◽  
Yuefeng Yang ◽  
Fei Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cancer Cell ◽  
Cell Counting ◽  
Ductal Adenocarcinoma ◽  
Akt Pathway ◽  
Cancer Cell Growth ◽  
Cell Vitality

Background/Aims: MicroRNAs (miRNAs, miRs) have emerged as critical regulators of cancer cell proliferation. The effect of miR-221 on cancer cell growth could be significantly changeable in different cell lines. Although miR-221 was reported to promote the cell growth of pancreatic ductal adenocarcinoma (PDAC) cells, its role in Capan-2 cell line is largely unknown. Methods: Capan-2 cells were transfected with miR-221 mimics, inhibitors, or negative controls. Cell Counting Kit-8 was used to determine cell viability. EdU staining and cell cycle analysis were used to measure cell proliferation. Western blotting was used to detect the expression levels of PTEN and phospho-Akt. The PI3K-Akt pathway activator SC-79 and inhibitor LY294002 were used to perform the rescue experiment in determining cell proliferation. Results: Overexpressing miR-221 significantly increased cell vitality and promoted cell proliferation and G1-to-S phase transition of the cell cycle in Capan-2 cells, while inhibition of miR-221 decreased that. The protein level of PTEN in Capan-2 cells was downregulated by overexpressing miR-221, while upregulated by inhibiting miR-221. Consistently, enhanced phosphorylation of AktSer473 was observed in miR-221 overexpressed Capan-2 cells, and the opposite result was found in miR-221 inhibited cells. LY294002 restored the pro-proliferation effect of miR-221 on Capan-2 cells, while SC-79 had no additional effect on cell proliferation in Capan-2 cells transfected with miR-221 mimics. Conclusion: Our study indicates that miR-221 is an oncogenic miRNA which promotes Capan-2 cells proliferation by targeting PTEN-Akt pathway.

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