scholarly journals LncRNA SNHG20 predicts a poor prognosis and promotes cell progression in epithelial ovarian cancer

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Dandan Wang ◽  
Jianrong Dai ◽  
Shunyu Hou ◽  
Yonghong Qian
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cancer Progression ◽  
Noncoding Rna ◽  
Histological Grade ◽  
Underlying Mechanism ◽  
Cell Counting ◽  
Immunofluorescent Staining ◽  
Migration And Invasion ◽  
Qrt Pcr

AbstractThe long noncoding RNA small nucleolar RNA host gene 20 (SNHG20) has been demonstrated to play a crucial role in cancer progression. However, the functions of SNHG20 in epithelial ovarian cancer (EOC) are not well established. The aim of the present study was to investigate SNHG20 clinical significance and its underlying mechanism in proliferation and metastasis in EOC. The expression level of SNHG20 was identified via in situ hybridization (ISH) and quantitative RT-PCR (qRT-PCR). The proliferative and metastatic capacities by silencing SNHG20 expression in A2780 and CAOV-3 cells were measured by cell counting kit-8 (CCK-8) and transwell assays. The molecular mRNA and protein expressions were examined using qRT-PCR, Western blot, and double immunofluorescent staining. SNHG20 expression was markedly higher in serous EOC tissues than that in adjacent tissues and closely correlated with histological grade and lymph node (LN) status. Patients with high SNHG20 showed a shorter overall survival (OS) and SNHG20 was an independent risk factor for the prognosis of serous EOC. Knockdown of SNHG20 remarkably inhibited EOC cell proliferation, migration, and invasion, which was associated with dysregulation of P21, Cyclin D1, E-cadherin, and Vimentin. These results suggest that SNHG20 may serve as an independent prognostic predictor and function as a noncoding oncogene in EOC progression, which might be a possible novel diagnostic marker and treatment target.

Silencing of Long Noncoding RNA LINC01132 Alleviates the Oncogenicity of Epithelial Ovarian Cancer by Regulating the microRNA-431-5p/SOX9 Axis

2021 ◽  
Author(s):  
Wei Zhu ◽  
Xiangming Xiao ◽  
Jinqin Chen
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Noncoding Rna ◽  
Xenograft Model ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Molecular Events

Abstract Background: To date, long intergenic nonprotein coding RNA 1132 (LINC01132) expression in epithelial ovarian cancer (EOC) and the underlying mechanisms have not been explored. In this study, we measured LINC01132 expression in EOC and assessed the effects of LINC01132 on the malignant behaviours of EOC cells in vitro and in vivo. Additionally, mechanistic studies were performed to elucidate the molecular events that occurred downstream of LINC01132 in EOC cells. Methods: Reverse-transcription quantitative PCR (RT-qPCR) was utilized to verify LINC01132 expression in EOC. The effects of LINC01132 on the malignant behaviours of EOC cells were determined using a Cell Counting Kit-8 assay, flow cytometry analysis, cell migration and invasion assays and a tumour xenograft model. The targeting interaction among LINC01132, microRNA-431-5p (miR-431-5p) and SRY-Box 9 (SOX9) was verified by RNA immunoprecipitation and luciferase reporter assays. Results: LINC01132 was overexpressed in EOC and was obviously associated with poor patient prognosis. Functionally, cell experiments revealed that LINC01132 depletion could inhibit EOC cell proliferation, migration and invasion and promote cell apoptosis in vitro. Additionally, loss of LINC01132 attenuated tumour growth in vivo. Mechanistically, LINC01132 acted as a competing endogenous RNA by sequestering miR-431-5p and thereby increasing SOX9 expression in EOC cells, forming a LINC01132/miR-431-5p/SOX9 axis. In rescue experiments, miR-431-5p inhibition or SOX9 re-expression eliminated the inhibitory effects of LINC01132 silencing on the pathological behaviours of EOC cells. Conclusions: Generally, LINC01132 exhibited oncogenic activities in EOC cells in vitro and in vivo by regulating the outcome of the miR-431-5p/SOX9 axis, providing an effective target for EOC diagnosis, therapy and prognosis evaluation.

LncRNA SNHG14 Promotes Progression of Ovarian Cancer by Regulating miR-206 Expression

2021 ◽  
Vol 7 (5) ◽  
pp. 3997-4004
Author(s):  
Zhibo Zou ◽  
Lin Peng
Keyword(s):  
Ovarian Cancer ◽  
Flow Cytometry ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Cancer Progression ◽  
Nude Mice ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Qrt Pcr ◽  
Research Objects

Objective: This study aimed to probe into the effect of LncRNA SNHG14 on ovarian cancer progression by regulating miR-206.Methods: Fifty-seven ovarian cancer (OC) patients who were treated in our hospital from December 2017 to December 2019 were collected as the research objects. During the operation, OC tissues and paracancerous tissues of patients were collected, and the effect of SNHG14 on OC tumor growth in nude mice was detected, and SNHG14 inhibitor was transfected into OC cells. The relative expression of SNHG14 in tissues and cells was detected by qRT-PCR, cell proliferation was testedvia CCK8, migration and invasion were detected through Transwell, apoptosis was assessedvia flow cytometry, and the targeted relationship between SNHG14 and miR-206 was detected by dual luciferase reporter gene.Results: SNHG14 is highly expressed in OC tissues, cells and nude mice. Down-regulating it can inhibit the biological ability of OC cells and inhibit the growth of nude mice tumors. It can directly target miR-206 to regulate CCND1 expression and promote OC progression.Conclusion: LncRNA SNHG14 can act as miR-206 sponge to regulate CCND1 expression downstream of miR-206 and promote OC progression.

scholarly journals Snail Driving Alternative Splicing of CD44 by ESRP1 Enhances Invasion and Migration in Epithelial Ovarian Cancer

2017 ◽  
Vol 43 (6) ◽  
pp. 2489-2504 ◽  
Author(s):  
Le Chen ◽  
Ying Yao ◽  
Lijuan Sun ◽  
Jiajia Zhou ◽  
Minmin Miao ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Alternative Splicing ◽  
Epithelial Ovarian Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Regulatory Protein ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Mesenchymal Transition

Background/Aims: Our study aims to investigate the role, effect and mechanisms of ESRP1 (epithelial splicing regulatory protein 1) in epithelial-mesenchymal transition (EMT) in epithelial ovarian cancer (EOC). Methods: Microarray and immunohistochemical analysis of ESRP1 expression were performed in EOC cases. The correlations between ESRP1 expression and clinical factors on EOC were assessed. Lentivirus-mediated RNA interference and EGFP vector which contains ESRP1 gene were used to down-regulate and up-regulate ESRP1 expression in human EOC cell lines. Roles of ESRP1 in cell growth, migration and invasion of EOC cells were also measured by Cell Counting Kit-8 and Transwell systems in vitro and by a nude mice intraperitoneal transplantation model in vivo. Results: By the analysis of Gene Expression Omnibus (GEO) (p<0.05) and our own microarray data (p<0.001), ESRP1 expression in EOC was significantly different from normal ovarian tissue. It was abundant in the nuclei of cancer cells and in malignant lesions. However, it was weakly expressed or negative in both normal and benign lesions. High ESRP1 expression in EOC was associated with poor clinical outcomes. Decreased ESRP1 expression significantly increased cell migration and invasion both in vivo and in vitro. Snail strongly repressed ESRP1 transcription through binding to the ESRP1 promoter in EOC cells. Furthermore, ESRP1 regulated the expression of CD44s. Down-regulated ESRP1 resulted in an isoform switching from CD44v to CD44s, which modulated epithelial-mesenchymal transition (EMT) program in EOC. Up-regulatin of ESRP1 was detected in mesenchymal to epithelial transition (MET) in vivo. Conclusions: ESRP1 regulates CD44 alternative splicing during the EMT process which plays an important role in EOC carcinogenesis. In addition, ESRP1 is associated with disease prognosis in EOC.

scholarly journals miR-125 inhibits colorectal cancer proliferation and invasion by targeting TAZ

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Meiyuan Yang ◽  
Xiaoli Tang ◽  
Zheng Wang ◽  
Xiaoqing Wu ◽  
Dong Tang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Underlying Mechanism ◽  
Cell Counting ◽  
Binding Motif ◽  
Cancer Proliferation ◽  
Qrt Pcr ◽  
Sirna Knockdown ◽  
Proliferation And Invasion ◽  
Hct116 Cells

Abstract Colorectal cancer (CRC) is the third most common malignant tumor worldwide and is a serious threat to human health. MicroRNAs (miRNAs) play a key role in oncogenesis and cancer progression. MiRNA-125 (miR-125) is an important miRNA that is dysregulated in several kinds of cancers. Thus, we investigated the expression and effects of miR-125 and Transcriptional co-activator with PDZ-binding motif (TAZ) for a better understanding of the underlying mechanism of tumor progression in CRC, which may provide an emerging biomarker for diagnosis and treatment of CRC. We measured the expression levels of miR-125 in CRC tissues, adjacent tissues, and cell lines (e.g. HCT116, SW480, FHC) by quantitative real-time polymerase chain reaction (qRT-PCR). The effect of miR-125 on proliferation and invasion in CRC cells was detected by Cell Counting Kit-8 (CCK-8), clone formation assay, and transwell assay. Western blotting and qRT-PCR were used to investigate the expression of TAZ after knocking down miR-125 in HCT116 cells or overexpressing miR-125 in SW480 cells. MiR-125 was significantly down-regulated in CRC compared with pericarcinomatous tissue from 18 patients. An miR-125 inhibitor promoted CRC cell proliferation and invasion, while miR-125 mimic had the opposite effect. Moreover, we found that TAZ was an miR-125 target and the siRNA knockdown of TAZ could reverse the effect of the miR-125 inhibitor on proliferation and invasion in HCT116 cells. The present study shows that miR-125 suppresses CRC proliferation and invasion by targeting TAZ.

scholarly journals EPDR1, Which Is Negatively Regulated by miR-429, Suppresses Epithelial Ovarian Cancer Progression via PI3K/AKT Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Zhendan Zhao ◽  
Zhiling Wang ◽  
Pengling Wang ◽  
Shujie Liu ◽  
Yingwei Li ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Figo Stage ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Gynecology And Obstetrics

Epithelial ovarian cancer (EOC) is the main pathological type of ovarian cancer. In this study, we found that ependymin-related 1 (EPDR1) was remarkably downregulated in EOC tissues, and low EPDR1 expression was associated with International Federation of Gynecology and Obstetrics (FIGO) stage, metastasis, and poor prognosis. We confirmed that EPDR1 overexpression dramatically suppressed EOC cell proliferation, migration, and invasion in vitro and in vivo. Mechanistically, EPDR1 inhibited EOC tumorigenesis and progression, at least in part, through the repression of the PI3K (Phosphoinositide 3-kinase)/AKT (AKT Serine/Threonine Kinase 1) signaling pathway. Furthermore, the expression and function of EPDR1 were regulated by miR-429, as demonstrated by luciferase reporter assays and rescue experiments. In conclusion, our study validated that EPDR1, negatively regulated by miR-429, played an important role as a tumor-suppressor gene in EOC development via inhibition of the PI3K/AKT pathway. The miR-429/EPDR1 axis might provide novel therapeutic targets for individualized treatment of EOC patients in the future.

scholarly journals LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer

2018 ◽  
Vol 49 (4) ◽  
pp. 1289-1303 ◽  
Author(s):  
Lei  Chang ◽  
Ruixia Guo ◽  
Zhongfu Yuan ◽  
Huirong Shi ◽  
Dongya Zhang
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Noncoding Rna ◽  
Ovarian Cancer Cell Line ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Qrt Pcr ◽  
Gene Assay ◽  
Lncrna Hotair

Background/Aims: The long noncoding RNA homeobox (HOX) transcript antisense intergenic RNA (HOTAIR) has been demonstrated to be a vital modulator in the proliferation and metastasis of ovarian cancer cells, but its potential molecular mechanism remains to be elucidated. In the current study, we aimed to uncover the biological role of lncRNA HOTAIR and its underlying regulatory mechanism in the progression and metastasis of ovarian cancer. Methods: HOTAIR expression was detected by quantitative RT-PCR (qRT-PCR) and northern blotting. The SKOV3 ovarian cancer cell line was chosen for the subsequent assays. In addition, the molecular mRNA and protein expression levels were examined by qRT-PCR and western blotting. The competitive endogenous RNA (ceRNA) mechanism was validated by bioinformatics analysis and a dual luciferase reporter gene assay. Results: HOTAIR expression was significantly higher in ovarian carcinoma tissues and cell lines than in the control counterparts. Both CCND1 and CCND2 were downstream targets of miR-206. The inhibition of HOTAIR elevated the expression of miR-206 and inhibited the expression of CCND1 and CCND2. Moreover, CCND1 and CCND2 were highly expressed in ovarian cancer tissues, and their expression was positively correlated with HOTAIR expression. Finally, the functional assays indicated that the anticancer effects of miR-206 could be rescued by the simultaneous overexpression of either CCND1 or CCND2 in ovarian cancer. Conclusion: HOTAIR enhanced CCND1 and CCND2 expression by negatively modulating miR-206 expression and stimulating the proliferation, cell cycle progression, migration and invasion of ovarian cancer cells.

scholarly journals Long non-coding RNA AFAP1-AS1 facilitates ovarian cancer progression by regulating the miR-107/PDK4 axis

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Bao Liu ◽  
Li Yan ◽  
Yugang Chi ◽  
Yuhan Sun ◽  
Xiaoyu Yang
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Tumor Development ◽  
Figo Stage ◽  
Pyruvate Dehydrogenase Kinase ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Expression Levels ◽  
Gene Reporter Assay

Abstract Background Abnormally expressed in various tumors, long non-coding RNAs (lncRNAs) feature prominently in tumor development, yet little is still known regarding the functional roles of lncRNA AFAP1 antisense RNA 1 (AFAP1-AS1) in ovarian cancer (OC). Methods The relative expression levels of lncRNA AFAP1-AS1, microRNA (miR)-107 and pyruvate dehydrogenase kinase isozyme 4 (PDK4) mRNA were assessed by quantitative real-time PCR. PDK4, PCNA and cyclin D1 expression levels were determined using Western blot analysis. Bioinformatics analysis and dual-luciferase gene reporter assay were conducted for identifying and validating the binding sequences between AFAP1-AS1 and miR-107, as well as between miR-107 and PDK4. Cell counting kit-8 assay was employed for detecting cell proliferation. Cell migration and invasion abilities were examined using Transwell assays. Results The present study revealed that AFAP1-AS1 expression was elevated in OC cells and tissues. AFAP1-AS1 expression and FIGO stage were positively correlated. AFAP1-AS1 knockdown repressed OC cell proliferation, migration and invasion. AFAP1-AS1 functioned as a sponge of miR-107, and miR-107 reversed the effects of AFAP1-AS1 on OC cells. It was validated that miR-107 was able to bind to PDK4, and AFAP1-AS1 regulated PDK4 expression by competitively binding with miR-107. Additionally, miR-107 modulated OC cell proliferation, migration and invasion via targeting PDK4. Conclusions LncRNA AFAP1-AS1 serves as a tumor driver in the pathogenesis of OC via the miR-107/PDK4 axis.

scholarly journals Long noncoding RNA MAPKAPK5-AS1 promotes colorectal cancer progression by cis-regulating the nearby gene MK5 and acting as a let-7f-1-3p sponge

2020 ◽  
Author(s):  
Ting Yang ◽  
Wei-Cong Chen ◽  
Pei-Cong Shi ◽  
Man-Ru Liu ◽  
Tao Jiang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Noncoding Rna ◽  
Vital Role ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Colorectal Cancer Progression ◽  
Molecular Therapeutic

Abstract Background: Long noncoding RNAs (lncRNAs) are considered critical regulators in cancers; however, the clinical significance and mechanisms of MAPKAPK5-AS1 (hereinafter referred to as MK5-AS1) in colorectal cancer (CRC) remain mostly unknown.Methods: In this study, quantitative real-time PCR (qPCR) and western blotting were utilized to detect the levels of MK5-AS1, let-7f-1-3p and MK5 (MAPK activated protein kinase 5) in CRC tissues and cell lines. The biological functions of MK5-AS1, let-7f-1-3p and MK5 in CRC cells were explored using Cell Counting Kit-8 (CCK8), colony formation and transwell assays. The potential mechanisms of MK5-AS1 were evaluated by RNA pull-down, RNA immunoprecipitation (RIP), dual luciferase reporter assay, chromatin immunoprecipitation (CHIP) and bioinformatics analysis. The effects of MK5-AS1 and MK5 on CRC were investigated by a xenotransplantation model. Results: We confirmed that MK5-AS1 was significantly increased in CRC tissues. Knockdown of MK5-AS1 suppressed cell migration and invasion in vitro and inhibited lung metastasis in mice. Mechanistically, MK5-AS1 regulated SNAI1 expression by sponging let-7f-1-3p and cis-regulated the adjacent gene MK5. Moreover, MK5-AS1 recruited RBM4 and eIF4A1 to promote the translation of MK5. Our study verified that MK5 promoted the phosphorylation of c-Jun, which activated the transcription of SNAI1 by directly binding to its promoter. Conclusions: MK5-AS1 cis-regulated the nearby gene MK5 and acted as a let-7f-1-3p sponge, playing a vital role in CRC tumorigenesis. This study could provide novel insights into molecular therapeutic targets of CRC.

scholarly journals T-cadherin in epithelial ovarian cancer: relationship with cancer progression and drug resistanceT-cadherin in epithelial ovarian cancer: relationship with cancer progression and drug resistance

2020 ◽  
Author(s):  
Yutao Guan ◽  
Yi Lin ◽  
Fubin Zhang ◽  
Ling-ling Zhou ◽  
Yang-ping Chen ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Drug Resistance ◽  
Ovarian Carcinoma ◽  
Epithelial Ovarian Cancer ◽  
Cancer Progression ◽  
Carcinoma Cell ◽  
Ovarian Tumour ◽  
Epithelial Ovarian Carcinoma ◽  
Migration And Invasion ◽  
Benign Ovarian Tumour

Abstract Background: T-cadherin plays a crucial role in maintaining normal tissue structure by regulating specific cell adhesion, cellular recognition and signal transduction. The purpose of this study was to evaluate whether T-cadherin influences epithelial ovarian cancer (EOC) progression, differentiation and drug resistance and its possible mechanisms.Methods: Epithelial ovarian carcinoma (EOC, n=63) and relevant contralateral normal ovarian (CNO, n=41) fresh tissues were collected from epithelial ovarian carcinoma patients, and benign ovarian tumour fresh tissues were collected from 55 patients with benign ovarian tumours. The human epithelial ovarian carcinoma cell line A2780 was cultured. T-cadherin expression was assessed by real-time RT-PCR and Western blotting, and the expression of matrix metalloproteinase-2 (MMP-2) was detected by Western blotting. pcDNA‑T‑cad plasmid technology was used to upregulate T-cadherin expression. In addition, A2780 cell migration and invasion ability, viability, colony formation, proliferation, apoptosis and sensitivity to paclitaxel were measured.Results: T‑cadherin mRNA and protein expression in EOC tissues from EOC patients was significantly downregulated, and there was no significant difference between the matched contralateral normal ovarian fresh tissue from the same patient and the benign ovarian tumour tissues from other patients. The migration and invasion abilities, viability, colony formation, and proliferation were attenuated by restoration of T‑cadherin expression in A2780 cells via pcDNA‑T‑cad transfection; apoptosis, MMP-2 expression and sensitivity to Taxol were also enhanced by restored T‑cadherin expression. The T‑cadherin expression level was well correlated with the clinical characteristics and symptoms of EOC patients, including tumour stage, histology, lymph node metastasis, tumour size, distant metastasis and cisplatin resistance.Conclusions: T‑cadherin participates in the processes of epithelial ovarian carcinoma cell migration, invasion, proliferation, apoptosis and sensitivity to paclitaxel and can regulate the expression of MMP-2. Downregulation of T‑cadherin expression may contribute to epithelial ovarian cancer progression, differentiation and drug resistance.

scholarly journals Sevoflurane but not propofol enhances ovarian cancer cell malignancy through regulating cellular metabolic and signalling mechanisms

2021 ◽  
Author(s):  
Cong Hu ◽  
Bincheng Wang ◽  
Zhigang Liu ◽  
Qiling Chen ◽  
Masashi Ishikawa ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Cell Counting ◽  
Immunofluorescent Staining ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Cellular Signalling

Background and Purpose: Surgery remains the first-line treatment of ovarian cancer. However, perioperative risk factors including the choice of anaesthetics may influence its recurrence after surgery. In the current study, it was hypothesised that inhalational anaesthetic sevoflurane and intravenous anaesthetic propofol might affect cancer cellular metabolism and signalling, which might interfere the malignancy of ovarian cancer cells. Experimental Approach: Cultured ovarian cancer cells were exposed to 2.5% sevoflurane or administered with 4 μg/mL propofol for 2 hours followed by 24 hours recovery. Their cell viability, proliferation, migration and invasion were assessed using cell counting kit-8, Ki-67 staining, wound healing and Transwell assay. Cellular signalling biomarkers were measured using immunofluorescent staining and/or Western blot. Cultured media were collected for 1H-NMR spectroscopy-based metabolomics analysis. Key Results: The cell viability, proliferation, migration, and invasion of ovarian cancer cells were enhanced by sevoflurane but suppressed by propofol. Sevoflurane increased the GLUT1, MPC1, GLUD1, p-Erk1/2, and HIF-1α expressions but decreased the PEDF expression. In contrast to the sevoflurane treatment, the “mirror changes” of these cellular markers were observed with propofol. Sevoflurane increased levels of isopropanol but decreased glucose and glutamine levels in the media, but the opposite changes of those metabolites were found after propofol treatment. Conclusion and Implications: These data indicated that unlike propofol, sevoflurane enhanced ovarian cancer cell metabolism and activated PEDF/Erk/HIF-1α cellular signalling pathway, suggesting that sevoflurane might have pro-tumour property but propofol might afford an anti-tumour property. The translational value of this work warrants further study.

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