LOXL1-AS1 contributes to the proliferation and migration of laryngocarcinoma cells through miR-589-5p/TRAF6 axis
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ABSTRACT:
SUBMITTER: He G
PROVIDER: S-EPMC7552551 | biostudies-literature | 2020 Jan
REPOSITORIES: biostudies-literature
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Project description:Introduction:Colorectal cancer (CRC), the third most common cancer worldwide, involves a physiological and pathological long non-coding RNA (lncRNA) paradigm shift. It has been reported that the lncRNA LOXL1-AS1 affects tumor development for many kinds of cancers, but its functions and mechanisms in CRC remain unknown. Methods:Expression levels of LOXL1-AS1 and miR-708-5p within CRC tissues and cell lines were measured using qRT-PCR. The performance of gain-of-function and loss-of-function assays was aimed at examining the effects of LOXL1-AS1 and miR-708-5p; colony formation and cell viability assays were carried out to measure cell multiplication; and Transwell migration and wound-healing assays were carried out for the measurement of cell migration and invasion. Luciferase reporter assay was used to verify the interactions between LOXL1-AS1 and miR-708-5p and between miR-708-5p and the CD44-EGFR signaling pathway. Finally, expression of CD44 and EGFR proteins was measured by Western blot and immunofluorescence assays. Results:In this study, we reveal that the regulation of lncRNA LOXL1-AS1 occurs within CRC based on the correlation with poor clinical outcomes. LOXL1-AS1 knockdown along with miR-708-5p overpresentation in CRC cell lines inhibited cell multiplication, migration, and invasion. The inhibiting effect of LOXL1-AS1 knockdown on CRC was reversed by upregulating the CD44-EGFR signal pathway. From the perspective of mechanism, LOXL1-AS1 imposes sponging upon miR-708-5p and thereby promotes the CD44-EGFR signal pathway in CRC cells. Discussion:This study demonstrated that lncRNA LOXL1-AS1 enhances multiplication, migration, invasion, and progression of CRC by sponging miR-708-5p to regulate the CD44-EGFR signal pathway.
| S-EPMC7423350 | biostudies-literature
Project description:Liver cancer is becoming one of the most lethal malignancies due to its high incidence and mortality. Accumulating studies have indicated that long non-coding RNAs (lncRNAs) are critical regulators of the tumorigenesis and development of various types of cancer, including liver cancer. LncRNA LOXL1-antisense RNA 1 (LOXL1-AS1) has been identified as an oncogene in some types of human cancer; however, its role in liver cancer remains obscure. Reverse transcription-quantitative PCR was used to measure LOXL1-AS1 expression in liver cancer tissues and cells. Western blot, MTT, colony formation, glucose uptake and wound healing assays were used to explore the biological function of LOXL1-AS1 in liver cancer cells. Bioinformatics analysis and RNA pull-down and luciferase reporter assays were used to explore the molecular mechanism of LOXL1-AS1 in liver cancer cells. Statistical analysis was used to compare the experimental results of different groups. In the present study, LOXL1-AS1 expression was significantly upregulated in liver cancer tissues and cells compared with in normal liver tissues and cells, respectively. High LOXL1-AS1 expression was associated with poor clinical outcomes in patients with liver cancer. Furthermore, LOXL1-AS1-knockdown suppressed glucose metabolism, proliferation, migration and epithelial-mesenchymal transition (EMT) of liver cancer cells. Subsequently, LOXL1-AS1 acted as a microRNA (miR)-377-3p sponge, and nuclear factor I B (NFIB) was confirmed as the downstream target of miR-377-3p in liver cancer cells. Additionally, rescue assays suggested that NFIB overexpression countervailed the inhibitory influence of LOXL1-AS1 silencing on liver cancer cellular processes. The present study demonstrated that LOXL1-AS1 promoted glucose metabolism, proliferation, migration and EMT of liver cancer cells by sponging miR-377-3p and modulating NFIB, which may provide a novel insight for the treatment of liver cancer.
| S-EPMC8258629 | biostudies-literature
Project description:Background:Gastric cancer (GC) is a deadly disease, and its incidence is especially high in East Asia including China. Recently, some long non-coding RNA (lncRNAs) have been identified as oncogenes or tumor suppressors. This study aimed to determine the function and mechanism of lncRNA LOXL1-AS1 on the progression of GC. Methods:RT-PCR was done to measure the expression levels of LOXL1-AS1 and miR-142-5p in GC tissues. The association between pathological indexes and LOXL1-AS1 expression was also analyzed. Human GC cell lines AGS and BGC823 were used as cell models. CCK-8 and colony formation assays were conducted to assess the effect of LOXL1-AS1 on the proliferation of GC cell lines. Transwell assay was conducted to determine the influence of LOXL1-AS1 on cell migration and invasion. Furthermore, luciferase reporter assay was carried out to confirm the relationship of miR-142-5p with LOXL1-AS1. Additionally, Western blot was done to detect the regulatory function of LOXL1-AS1 on PIK3CA, a target of miR-142-5p. In vivo experiment was also performed to validate the roles and mechanism of LOXL1-AS1 on the growth and metastasis of GC cells. Results:LOXL1-AS1 expression in GC samples was significantly increased, which was correlated with unfavorable pathological indexes. Highly expressed LOXL1-AS1 was closely linked to shorter overall survival time and post-progression survival time of the patients. LOXL1-AS1 markedly modulated the malignant phenotypes of GC cells. Additionally, overexpressed LOXL1-AS1 notably reduced the expression of miR-142-5p, but enhanced the expression level of PIK3CA. In vivo experiments further validated that knockdown of LOXL1-AS1 inhibited the growth and metastasis of GC cells via regulating miR-142-5p and PIK3CA. Conclusion:LOXL1-AS1 was a sponge of tumor suppressor miR-142-5p in GC, enhanced the expression of PIK3CA indirectly and functioned as an oncogenic lncRNA.
| S-EPMC6929932 | biostudies-literature
Project description:BackgroundAbundant evidence has manifested that long noncoding RNAs (lncRNAs) are closely implicated in human cancers, including hepatocellular carcinoma (HCC). Remarkably, lncRNA FAM83H antisense RNA 1 (FAM83H-AS1) has been reported to be a tumor-propeller in multiple cancers. However, its effect on HCC progression remains unknown.MethodsFAM83H-AS1 expression was analyzed by RT-qPCR. Colony formation, EdU, and flow cytometry as well as transwell assays were implemented to analyze the biological functions of FAM83H-AS1 on HCC progression. Luciferase reporter, RIP and RNA pull-down assays were implemented to detect the interaction among FAM83H-AS1, microRNA-485-5p (miR-485-5p), and myocyte enhancer factor 2D (MEF2D) in HCC cells.ResultsFAM83H-AS1 expression in HCC cells was markedly elevated. FAM83H-AS1 accelerated cell proliferation, migration and invasion whereas inhibiting cell apoptosis in HCC. Besides, we confirmed that FAM83H-AS1 acts as a miR-485-5p sponge in HCC cells. Additionally, MEF2D was verified to be a direct target of miR-485-5p. FAM83H-AS1 could upregulate MEF2D expression via sponging miR-485-5p. Further, rescue experiments testified that MEF2D upregulation or miR-485-5p downregulation offset the repressive effect of FAM83H-AS1 depletion on HCC cell progression.ConclusionsFAM83H-AS1 facilitates HCC malignant progression via targeting miR-485-5p/MEF2D axis, suggesting that FAM83H-AS1 may be a promising biomarker for HCC treatment in the future.
| S-EPMC8650424 | biostudies-literature
Project description:ObjectiveLong non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play essential roles in the tumour progression. LncRNAs mostly act as competing endogenous RNAs (ceRNAs) by sponging miRNAs. This study aimed to study the association of a novel lncRNA MFI2-AS1 with miR-574-5p/MYCBP axis in the development of colorectal cancer (CRC).MethodsNinety-four CRC tissues and paired adjacent non-tumour tissues were included in our study. The relative expression level of MFI2-AS1 was detected, and its relationship with clinico-pathological factors was analysed. Then, the CRC cells lines (LoVo and RKO) were transfected with MFI2-AS1 siRNA, miR-574-5p mimics and inhibitors. Cell proliferation, migration, invasion, cell cycle distribution and DNA damage in response to different transfection conditions were examined. Dual-luciferase reporter assay was performed to identify the target interactions between MFI2-AS1 and miR-574-5p, miR-574-5p and MYCBP.ResultsLncRNA MFI2-AS1 and MYCBP were up-regulated in CRC tissues when compared with adjacent non-tumour tissues. The expression levels of MFI2-AS1 were significantly associated with tumour histological grade, lymph and distant metastasis, TNM stage and vascular invasion. Both MFI2-AS1 siRNA and miR-574-5p mimics inhibited proliferation, migration and invasion in LoVo and RKO cells. The transfection of miR-574-5p inhibitor showed MFI2-AS1 siRNA-induced changes in CRC cells. Dual-luciferase reporter assay revealed target interactions between MFI2-AS1 and miR-574-5p, miR-574-5p and MYCBP.ConclusionsThese findings suggested that lncRNA MFI2-AS1 and MYCBP have promoting effects in CRC tissues. LncRNA MFI2-AS1 promoted CRC cell proliferation, migration and invasion through activating MYCBP and by sponging miR-574-5p.
| S-EPMC6668983 | biostudies-literature
Project description:At present, growing evidence indicates that long non-coding RNAs (lncRNAs) participate in the progression of glioma. The function of LOXL1-AS1 in vasculogenic mimicry (VM) in glioma remains unclear. First, the expressions of TIAR, the lncRNA LOXL1-AS1, miR-374b-5p and MMP14 were examined by qRT-PCR and Western blot in both, glioma tissues and glioma cell lines. Proliferation, migration, invasion and tube formation assays were conducted to evaluate the roles of TIAR, LOXL1-AS1, miR-374b-5p and MMP14 in malignant cellular behaviours in glioma cells. A nude mouse xenograft model and dual staining for CD34 and PAS were used to assess whether VM was affected by TIAR, LOXL1-AS1 or miR-374b-5p in vivo. In this study, low levels of TIAR and high levels of LOXL1-AS1 were found in glioma cells and tissues. TIAR downregulated the expression of LOXL1-AS1 by destabilizing it. LOXL1-AS1 acted like a miRNA sponge towards miR-374b-5p so that downregulation of the former greatly inhibited cell proliferation, migration, invasion and VM. Additionally, miR-374b-5p overexpression repressed malignant biological behaviours and VM in glioma by modifying MMP14. In summary, we demonstrated that TIAR combined with LOXL1-AS1 modulates VM in glioma via the miR-374b-5p/MMP14 axis, revealing novel targets for glioma therapy.
| S-EPMC8743654 | biostudies-literature
Project description:BackgroundExtensive studies revealed that long non-coding RNAs (lncRNAs) could act as a regulator in tumors, including lung adenocarcinoma (LUAD). LncRNA FTX transcript, XIST regulator (FTX) has been reported to regulate the biological behaviors of some cancers. Nevertheless, its functional role and molecular mechanism remain obscure in LUAD. Our current study concentrates on exploring the biological function of FTX in LUAD.MethodsRT-qPCR was used to test the expression of FTX, miR-335-5p or NUCB2 in LUAD cells. The effect of FTX on LUAD progression was investigated by colony formation, EdU, flow cytometry, TUNEL, transwell and western blot assays. The interaction between microRNA-335-5p (miR-335-5p) and FTX or nucleobindin 2 (NUCB2) was confirmed by luciferase reporter assay.ResultsRT-qPCR showed that FTX expression was up-regulated in LUAD cell lines. Loss-of-function assay indicated that FTX accelerated cell proliferation, migration and invasion, while inhibited cell apoptosis in LUAD. Besides, miR-335-5p, lowly expressed in LUAD cells, was discovered to be sponged by FTX. Subsequently, NUCB2 was identified as a target gene of miR-335-5p. Additionally, it was confirmed that NUCB2 functioned as an oncogene in LUAD. Rescue assays indicated that LUAD progression inhibited by FTX knockdown could be restored by NUCB2 up-regulation.ConclusionFTX played an oncogenic role in LUAD and contributed to cancer development via targeting miR-335-5p/NUCB2 axis.
| S-EPMC7092578 | biostudies-literature
Project description:Purpose:Long non-coding RNAs (lncRNAs) have been reported to be involved in a variety of cancers, including glioma. However, the exact role and underlying mechanism of lncRNA AGAP2 antisense RNA 1 (AGAP2-AS1) in glioma have not yet been fully elucidated. Methods:The expression levels of AGAP2-AS1, microRNA-628-5p (miR-628-5p) and pleiotrophin (PTN) were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, migration and invasion were detected by Cell Counting Kit-8 (CCK-8) assay, flow cytometry, transwell assay, respectively. Western blot assay was used to detect the protein level of PTN. The interaction between miR-628-5p and AGAP2-AS1 or PTN was predicted by bioinformatics software and confirmed by the dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. Murine xenograft model was established to confirm the role of AGAP2-AS1 in glioma progression in vivo. Results:AGAP2-AS1 expression was upregulated in glioma tissues and cells. Knockdown of AGAP2-AS1 inhibited the proliferation, migration and invasion, but facilitated apoptosis in glioma cells. Moreover, AGAP2-AS1 could directly bind to miR-628-5p and its overexpression reversed the anti-tumor effect of miR-628-5p restoration on the progression of glioma cells. In addition, miR-628-5p directly targeted PTN and its inhibition abolished the inhibitory effect of PTN knockdown on the progression of glioma cells. Furthermore, AGAP2-AS1 functioned as a competing endogenous RNA (ceRNA) by sponging miR-628-5p to modulate PTN expression. Besides, AGAP2-AS1 depletion reduced tumor growth by upregulating miR-628-5p and downregulating PTN. Conclusion:AGAP2-AS1 knockdown suppressed cell proliferation, migration and invasion but promoted cell apoptosis in glioma cells by regulating miR-628-5p/PTN axis, providing novel avenues for treatment of glioma.
| S-EPMC7398883 | biostudies-literature
Project description:Long noncoding RNA (lncRNA) MAF BZIP transcription factor G antisense RNA 1 (MAFG?AS1) has been demonstrated to serve an important role in the progression of various types of cancer, whereas its role in breast cancer has not been fully elucidated. The present study aimed to explore the potential role and underlying mechanism of MAFG?AS1 in breast cancer. To achieve this, the expression of MAFG?AS1, microRNA (miR)?150?5p and MYB was detected by reverse transcription?quantitative PCR. The binding between miR?150?5p and MAFG?AS1 or MYB was verified using a luciferase reporter assay. Cell proliferation was analyzed by MTS, apoptosis and cell cycle were detected by Annexin V/propidium iodide, and cell migration was analyzed by wound healing assay. The results demonstrated that the expression levels of MAFG?AS1 were significantly upregulated in breast cancer tissues and cells compared with those in normal breast tissues and cells. High MAFG?AS1 expression promoted the proliferation, migration and epithelial?mesenchymal transition of breast cancer cells. By contrast, miR?150?5p expression was reduced in breast cancer tissues compared with that in healthy breast tissues, and low expression of miR?150?5p was associated with poor overall survival in patients with breast cancer. Bioinformatics and luciferase assay revealed that MAFG?AS1 served as a sponge of miR?150?5p, and that miR?150?5p bound to MYB. The functional rescue assay results demonstrated that MAFG?AS1 knockdown suppressed the proliferation and migration of breast cancer cells by regulating miR?150?5p, which in turn targeted MYB. In conclusion, the results of the present study demonstrated that MAFG?AS1 functioned as a novel oncogenic lncRNA in the development of human breast cancer via regulating the miR?150?5p/MYB axis, which suggested that MAFG?AS1 may be a novel biomarker for the diagnosis and prognosis of human breast cancer.
| S-EPMC7721084 | biostudies-literature
Project description:MAFG-AS1 is an oncogenic lncRNA in multiple types of cancer. However, its role in bladder cancer (BC) remains unclear. The present study aimed to investigate the function of MAFG-AS1 in BC. BC and paired non-tumor tissues were collected. Two BC cell lines HT01197 and HT-1376 were used. Dual luciferase activity assay, RT-qPCR, western blot, CCK-8, transwell invasion assay, and wound healing assay were performed. We found that MAFG-AS1 was significantly up-regulated in BC tissues and predicted a poor survival rate. MAFG-AS1 interacted with miR-125b-5p. However, the expression levels of MAFG?AS1 and miR-125b-5p were not obviously correlated in BC tissues, and MAFG?AS1 and miR-125b-5p did not regulate the expression of each other. Interestingly, we found that SphK1, a downstream target of miR-125b-5p, was negatively correlated with miR-125b-5p, while it was positively correlated with MAFG-AS1 across BC tissues. In addition, overexpression of MAFG?AS1 upregulated the expression of SphK1 in BC cells, and attenuated the inhibitory effects of miR-125b-5p on the expression of SphK1. Functional assays showed that overexpression of MAFG?AS1 promoted BC cell proliferation, migration, and invasion, while its effects were attenuated by overexpression of miR-125b-5p. Moreover, overexpression of miR-125b-5p inhibited BC cell proliferation, migration, and invasion, while its effects were alleviated by overexpression of SphK1. Taken together, our findings demonstrated that MAFG-AS1 has an oncogenic role in BC by regulating the miR-125b-5p/SphK1 axis. MAFG-AS1 might serve as a good diagnostic marker and a potential therapeutic target of BC.
| S-EPMC7900043 | biostudies-literature