LncRNA-IMAT1 Promotes Invasion of Meningiomas by Suppressing KLF4/hsa-miR22-3p/Snai1 Pathway.
Ontology highlight
ABSTRACT:
SUBMITTER: Ding Y
PROVIDER: S-EPMC9200663 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Objective Non-small cell lung cancer (NSCLC) explains about 80 percent of whole lung cancers, and its 5-year survival rate is impoverished, as when people are first diagnosed, 68% of whom are identified at a dangerous stage. The molecular mechanisms of NSCLC are still being explored. Methods GSE18842 and GSE19804 were exerted to scan for diversely expressed genes (DEGs) in NSCLC, and then we used GEPIA for the validation of DEGs expression. The prognostic values were determined through Kaplan–Meier analysis. Three target prediction databases indicated potential microRNAs (miRNAs), while miRNet predicted hsa-miR-1-3p′s upstream long non-coding RNAs (lncRNAs) and pseudogenes. UALCAN was utilized to identify the co-expressed genes of PAICS, while enrichment analysis on them was managed with Enrichr. Results We initially found that the gene expression level of cyclin B1 (CCNB1), cyclin-dependent kinases1 (CDK1), and phosphoribosylaminoimidazole succinocarboxamide synthetase (PAICS) had a notable increase in NSCLC. We predicted 6, 10, and 7 microRNAs to target CCNB1, CDK1, and PAICS, respectively. Among miRNA-mRNA (microRNA-messenger RNA) pairs, we deduced that the hsa-miR-1-PAICS axis was the most potential one to inhibit the occurrence of NSCLC. We also noted that the hsa-miR-1-3p-PAICS axis participated in regulating the process of mitosis with mechanical functions. Moreover, we identified 5 pseudogenes and 33 long non-coding RNAs (lncRNAs) that might inhibit the hsa-miR-1-3p-PAICS axis in NSCLC. Conclusions The pseudogene/lncRNA-hsa-miR-1-3p-PAICS is very important in NSCLC on the basis of this study, thus providing us with effective treatments and promising biomarkers for the diagnosis of NSCLC.
| S-EPMC9448537 | biostudies-literature
Project description:Purpose: It remains unclear that long noncoding RNAs' role in cancer initiation and progression, including osteosarcoma. Long noncoding RNA LINC00963 was found to be participated in carcinogenesis and progression of osteosarcoma. However, the molecular mechanisms of LINC00963 engaged in osteosarcoma (OS) still needs to be explored. Methods: LINC00963 and miR-204-3p RNA expression levels were quantified by PCR in OS tissues and cells. CCK 8 assay, wound healing assay and transwell migration and invasion assay were chosen to assess cell growth, viability, migration, and invasion. Luciferase reporter assays were performed to verify direct interaction between LINC00963 and miR-204-3p and miR-204-3p and Fibronectin-1. Western blot was conducted to evaluate Fibronectin-1 expression in OS cells. Results: LINC00963 was verified to be highly expressed in OS samples and cells. Specifically, elevated expression of LINC00963 was correlated with poor prognosis in patients. Furthermore, LINC00963 overexpression was found to promote proliferation, migration, and invasion in vitro. The luciferase reporter assay showed that LINC00963 can suppress miR-204-3p by directly binding miR-204-3p. Rescue experiment results indicated that function of LINC00963 in osteosarcoma was miR-204-3p dependant. Besides, we initially explored Fibronectin-1 (FN1) as the target of LINC00963/miR-204-3p axis in osteosarcoma. Conclusions: Our findings implied that LINC00963/miR-204-3p/FN1 can play an important role in proliferation and progression in osteosarcoma. LINC00963 has the potential to be a therapeutic target for osteosarcoma treatment.
| S-EPMC6605988 | biostudies-literature
Project description:BackgroundOvarian cancer is the most common female gynecological malignancy. SNHG20, as a long non-coding RNA, has been proven to be an important regulator in the occurrence and development of various tumors. However, the potential mechanism of SNHG20 in ovarian cancer is unclear.ObjectiveThe present study was aimed to investigate the functions and mechanisms of SNHG20 in ovarian cancer.MethodsThe expression of SNHG20 and miR-217 in ovarian cancer tissues and cell lines was detected by qRT-PCR. CCK-8 assay was used to measure cell proliferation in transfected cells. The transwell assay was used to detect the relative invasion rate of transfected cells. The putative binding sites between SNHG20 and miR-217 were predicted by software LncBase v.2, and the interaction between SNHG20 and miR-217 was confirmed by dual-luciferase reporter assays and RIP assay. The rescue experiments were used to illustrate potential mechanisms.ResultsSNHG20 was upregulated in ovarian cancer tissues and cell lines. Overexpression of SNHG20 promoted ovarian cancer cell proliferation and invasion. MiR-217 was downregulated in ovarian cancer tissues and cells, and was negatively regulated by SNHG20. Moreover, miR-217 overexpression inhibited ovarian cancer cell proliferation and invasion. Furthermore, miR-217 mimic reversed the inhibitory effect of SNHG20 overexpression on the biological behavior of ovarian cancer cells.ConclusionsSNHG20 promoted cell proliferation and invasion by sponging miR-217 in ovarian cancer. These results suggested that SNHG20 and miR-217 might provide new targets for therapeutic application in ovarian cancer.
| S-EPMC8376724 | biostudies-literature
Project description:Glioblastoma (GBM) is one of the most prevalent and aggressive central nervous tumors with high mobility and mortality. The prognosis of patients with GBM is poor. It is therefore essential to explore the therapeutic strategies for the treatment of GBM. Previous studies have demonstrated that the long non?coding RNA (lncRNA) Kinectin 1?Antisense RNA 1 (KTN1?AS1) can participate in the development of several types of cancer. However, the underlying mechanism of KTN1?AS1 in GBM remains unknown. The present study aimed to determine the potential role of KTN1?AS1 in GBM. In this study, reverse transcription quantitative PCR analysis was conducted and the results demonstrated that KTN1?AS1 was upregulated in GBM tissues and cell lines compared with normal tissues and astrocytes (NHA). Furthermore, KTN1?AS1 knockdown decreased the viability and invasive ability of glioma cells in vitro and in vivo. In addition, high level of KTN1?AS1 was correlated with poor prognosis in TCGA GBM database. Furthermore, microRNA?505?3p (miR?505?3p) was a promising target of KTN1?AS1, and the suppressing effects of miR?505?3p on cell proliferation and invasive ability was reversed by downregulating KTN1?AS1. Taken together, the results from the present provided novel insights into the roles of KTN1?AS1 in GBM, and suggested that the KTN1?AS1/miR?505?3p axis may be considered as a novel therapeutic target for the treatment of patients with GBM.
| S-EPMC7640367 | biostudies-literature
Project description:Neuroblastoma (NB) is the most common pediatric extra-cranial solid tumor with heterogeneous characteristics, and the prognosis of patients with high-risk NB is usually poor. Discovery of novel biomarkers for early detection and investigation of the underlying mechanisms governing invasion and metastasis of NB are urgently needed. Recently, exosomal microRNAs (miRNAs) have been shown to play vital regulatory or communication roles in the process of various types of cancers. However, the roles and mechanisms of exosomal miRNAs in NB remain unknown. Thus, the present study aims to investigate the detailed functions of tumor-derived exosomal miRNAs in progression and migration of NB in vivo and in vitro. By examining different exosomal miRNA expression profiles in the plasma of NB patients, we identified that the expression of hsa-miR199a-3p from exosomes was significantly upregulated, which was correlated with the severity of NB patients. Furthermore, we confirmed that exosomal hsa-miR199a-3p could facilitate proliferation and migration of NB via regulating NEDD4 expression. In summary, our data, for the first time, revealed that exosomal hsa-miR199a-3p could promote tumor proliferation and migration via decreasing NEDD4 expression in NB, suggesting that exosomal hsa-miR199a-3p may be applicated as a fast, easy, and non-invasive detection biomarker and contribute to the development of novel therapeutic strategies for NB in the future.
| S-EPMC6582313 | biostudies-literature
Project description:The present study aimed to explore whether and how microRNA‑5580‑3p (miR‑5580‑3p) affected oral cancer (OC) cell phenotypes via regulation of laminin subunit γ2 (LAMC2). Bioinformatics analysis was used to identify miR‑5580‑3p/LAMC2, a novel interactome that, to the best of our knowledge, has not been studied previously in OC. In the present study, the expression levels of miR‑5580‑3p and LAMC2 were detected by reverse transcription‑quantitative PCR, while the protein expression levels of LAMC2 were identified using western blotting. To determine the effects of miR‑5580‑3p and LAMC2 in OC, a number of experiments, including Cell Counting Kit‑8, 5‑bromo‑2'‑deoxyuridine cell proliferation and wound healing migration assays, were performed using OC SCC‑4 and Cal‑27 cell lines. Additionally, luciferase reporter assays were employed to examine the interaction between miR‑5580‑3p and LAMC2 mRNA. The results demonstrated that miR‑5580‑3p expression was downregulated, while LAMC2 expression was upregulated in OC tissues and cell lines. In addition to the observation that miR‑5580‑3p promoted the malignant phenotypes of OC, it was also revealed that miR‑5580‑3p inhibited OC cell viability, proliferation and migration by suppressing LAMC2. Therefore, the present study suggested that miR‑5580‑3p and LAMC2 may be potential biomarkers and therapeutic targets for OC diagnosis and therapies in the future.
| S-EPMC8072311 | biostudies-literature
Project description:BackgroundLncRNA was known to be closely associated with the progression of human tumors. The role of lncRNA LIFR-AS1 in the pathogenesis and progression of gastric tumor is still unclear. The aim of this study was to investigate the function of LIFR-AS1 and the underlying mechanism in the pathogenesis and progression of gastric cancer.MethodsQRT-PCR was used to evaluate the expression of LIFR-AS1, miR-29a-3p and COL1A2 in gastric tumor tissues and cells. Western blotting was used to evaluate the protein expression of COL1A2 in gastric tumor cells. CCK-8 assay, transwell assay and flow cytometry were used to evaluate the roles of LIFR-AS1, miR-29a-3p and COL1A2 in cell proliferation, invasion, migration and apoptosis. The relationship among LIFR-AS1, miR-29a-3p and COL1A2 was assessed by bioinformatics analyses and luciferase reporter assay.ResultsThe expression levels of LIFR-AS1 were significantly increased in gastric tumor tissues and cells, while the expression levels of miR-29a-3p were decreased. The expression of miR-29a-3p was negatively correlated with the expression of LIFR-AS1 in gastric cancer tumor tissues. Knocking down of LIFR-AS1 inhibited proliferation, invasion and migration of gastric tumor cells, and induced apoptosis of gastric tumor cells. Bioinformatics analyses and integrated experiments revealed that LIFR-AS1 elevated the expression of COL1A2 through sponging miR-29a-3p, which further resulted in the progression of gastric tumor.ConclusionLIFR-AS1 plays an important role as a competing endogenous RNA in gastric tumor pathogenesis and may be a potential target for the diagnosis and treatment of gastric tumor.
| S-EPMC7789183 | biostudies-literature
Project description:Hepatocellular carcinoma (HCC), with life-threatening malignant behaviours, often develops distant metastases and is the fourth most common primary cancer in the world, having taken millions of lives in Asian countries such as China. The novel miR-3677-3p is involved in a high-expression-related poor prognosis in HCC tissues and cell lines, indicating oncogenesis functions in vitro and in vivo. Initially, we confirmed the inhibition of proliferation, migration and invasion in miR-3677-3p knock-down MHCC-97H and SMMC-7721 cell lines, which are well known for their high degree of invasiveness. Then, we reversed the functional experiments in the low-miR-3677-3p-expression Hep3B cell line via overexpressing miR-3677-3p. In nude mice xenograft and lung metastasis assays, we found suppressor behaviours, smaller nodules and low density of organ spread, after injection of cells transfected with shRNA-miR-3677-3p. A combination of databases (Starbase, TargetScan and MiRgator) illustrated miR-3677-3p targets, and it was shown to suppress the expression of SIRT5 in a dual-luciferase reporter system. To clarify the conclusions of previous ambiguous research, we up-regulated SIRT5 in Hep3B cells, and rescue tests were established for confirmation that miR-3677-3p suppresses SIRT5 to enhance the migration and invasion of HCC. Interestingly, we discovered hypoxia-induced miR-3677-3p up-regulation benefited HCC malignancy and invasiveness. In conclusion, the overexpression of miR-3677-3p mediated SIRT5 inhibition, which could increase proliferation, migration and invasion of HCC in hypoxic microenvironments.
| S-EPMC7412699 | biostudies-literature
Project description:The long non‑coding (lnc)RNA named tissue differentiation inducing non‑protein coding RNA (TINCR) is a tumor marker that has not been studied in breast cancer. The present study aimed to investigate the TINCR‑targeting micro (mi)RNAs and the regulatory mechanisms of TINCR in breast cancer. Following prediction by TargetScan and confirmation by dual‑luciferase reporter assay, TINCR was demonstrated to be a target gene for miR‑589‑3p. The expression of TINCR and miR‑589‑3p in breast cancer and adjacent tissues was detected by reverse transcription‑quantitative (RT‑q)PCR, and the correlation between TINCR and miR‑589‑3p expression was determined by using Spearman correlation analysis. The 5‑years survival was analyzed in patients with breast cancer according to TINCR expression (high or low). The effects of TINCR and miR‑589‑3p on the proliferation, apoptosis, migratory and invasive abilities of some breast cancer cell lines were detected by MTT assay, flow cytometry, wound healing assay and Transwell assay. The target gene of miR‑589‑3p was predicted and verified by TargetScan and dual‑luciferase reporter assay, and the mechanism of miR‑589‑3p involvement in breast cancer cells was explored by overexpression or downregulation of miR‑589‑3p in breast cancer cells. RT‑qPCR and western blotting were used to determine the expression of the insulin‑like growth factor 1 receptor (IGF1R)/AKT pathway‑related genes. The results demonstrated that TINCR expression level was negatively correlated with miR‑589‑3p expression level in breast cancer tissues and that patients with high expression of TINCR presented with lower survival rates. In addition, TINCR overexpression in cancer cells inhibited miR‑589‑3p expression, and cell transfection with miR‑589‑3p mimic partially reversed the effect of TINCR overexpression on the promotion of cancer cell proliferation, migration and invasion, and on the inhibition of cancer cell apoptosis. Furthermore, IGF1R, which is a target gene of miR‑589‑3p, increased cancer cell proliferation, migration and invasion and inhibited cancer cell apoptosis; however, these effects were partially reversed by miR‑589‑3p mimic. Furthermore, the results demonstrated that miR‑589‑3p mimic could downregulate the protein expression of IGF1R and p‑AKT. In addition, TINCR overexpression downregulated miR‑589‑3p expression level. miR‑589‑3p partially reversed the effects of TINCR overexpression on cancer cell proliferation, migration and invasion, and inhibited cancer cell apoptosis by inhibiting the IGF1R‑Akt pathway. The results from the present study demonstrated that TINCR may sponge miR‑589‑3p in order to inhibit IGF1R‑Akt pathway activation in breast cancer cells, promoting therefore cancer cell proliferation, migration and invasion.
| S-EPMC7388824 | biostudies-literature
Project description:SNAI1 is widely regarded as a master driver of epithelial-mesenchymal transition (EMT) and associated with breast cancer progression and metastasis. This pro-malignant role is strongly linked to posttranslational modification, especially phosphorylation, which controls its protein levels and subcellular localization. While multiple kinases are implicated in regulation of SNAI1 stability, the precise mechanism by which SNAI1 is stabilized in tumors remains to be fully elucidated. Methods: A series of in vitro and in vivo experiments were conducted to reveal the regulation of SNAI1 by Serine/Threonine Kinase 39 (STK39) and the role of STK39 in breast cancer metastasis. Results: We identified STK39, a member of Stem 20-like serine/threonine kinase family, as a novel posttranslational regulator that enhances the stability of SNAI1. Inhibition of STK39 via knockdown or use of a specific inhibitor resulted in SNAI1 destabilization. Mechanistically, STK39 interacted with and phosphorylated SNAI1 at T203, which is critical for its nuclear retention. Functionally, STK39 inhibition markedly impaired the EMT phenotype and decreased tumor cell migration, invasion, and metastasis both in vitro and in vivo. These effects were rescued by ectopic SNAI1 expression. In addition, depletion of STK39 dramatically enhanced sensitivity to chemotherapeutic agents. Conclusions: Our study demonstrated that STK39 is a key mediator of SNAI1 stability and is associated with the pro-metastatic cellular process, highlighting the STK39-SNAI1 signaling axis as promising therapeutic targets for treatments of metastatic breast cancer.
| S-EPMC8315073 | biostudies-literature