scholarly journals Long Non-coding RNA FEZF1-AS1 Promotes Growth and Reduces Apoptosis Through Regulation of miR-363-3p/PAX6 Axis in Retinoblastoma

2021 ◽  
Author(s):  
Xiuming Liu ◽  
Xiaofeng Li ◽  
Jianchang Li
Keyword(s):  
Cell Viability ◽  
Antisense Rna ◽  
Tumor Formation ◽  
Retinoblastoma Cell ◽  
Non Coding Rna ◽  
High Incidence ◽  
Non Coding Rnas ◽  
Long Non Coding Rna ◽  
Common Malignancy

AbstractRetinoblastoma is the most common malignancy in children's eyes with high incidence. Long non-coding RNAs (lncRNAs) play important roles in the progression of retinoblastoma. LncRNA FEZF1 antisense RNA 1 (FEZF1-AS1) has been found to stimulate retinoblastoma. However, the mechanism of FEZF1-AS1 underlying progression of retinoblastoma is still unclear. In current study, FEZF1-AS1 was up-regulated in retinoblastoma tissues and cells. FEZF1-AS1 overexpression enhanced retinoblastoma cell viability, promoted cell cycle, and inhibited apoptosis. Conversely, FEZF1-AS1 knockdown reduced cell viability, cycle, and elevated apoptosis. The interaction between FEZF1-AS1 and microRNA-363-3p (miR-363-3p) was confirmed. FEZF1-AS1 down-regulated miR-363-3p and up-regulated PAX6. PAX6 was a target gene of miR-363-3p. EZF1-AS1 promoted retinoblastoma cell viability and suppressed apoptosis via PAX6. Further, we demonstrated that FEZF1-AS1 contribute to tumor formation in vivo. In conclusion, FEZF1-AS1 elevated growth and inhibited apoptosis by regulating miR-363-3p/PAX6 in retinoblastoma, which provide a new target for retinoblastoma treatment.

scholarly journals Silencing of Long Non-Coding RNA LINC00607 Prevents Tumor Proliferation of Osteosarcoma by Acting as a Sponge of miR-607 to Downregulate E2F6

2021 ◽  
Vol 10 ◽  
Author(s):  
Yuehuan Zheng ◽  
Zhe Chen ◽  
Zezhu Zhou ◽  
Xiangyang Xu ◽  
Huilin Yang
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Bioinformatic Analysis ◽  
Transcriptional Factor ◽  
Migration And Invasion ◽  
Tumor Proliferation ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Osteosarcoma (OS), a type of malignant bone tumor, is commonly found in children and adolescents. Although previous studies have identified that long non-coding RNAs (lncRNAs) regulate OS, it is unclear whether lncRNAs impact the progression of OS. Here, we identified LINC00607, a lncRNA that facilitates OS proliferation, migration, and invasion. Based on the RNA-sequencing results, LINC00607 expression was significantly upregulated in pulmonary metastasis within OS. Functional experiments revealed that LINC00607 promoted migration and invasion of endothelial cells to exacerbate epithelial-mesenchymal transition (EMT). Furthermore, the results of RNA pull-down assay and invasion assay suggested that the binding between LINC00607 and miR-607 promoted OS invasion. Bioinformatic analysis and rescue experiments demonstrated that E2F6, a transcriptional factor, functioned downstream of LINC00607/miR-607. Finally, we found that LINC00607 promoted OS progression in vivo. This work revealed that LINC00607 worked as an miR-607 sponge to upregulate E2F6 expression, which promoted tumor proliferation in OS. These results identified a novel therapeutic target for treating OS.

scholarly journals Angelica polysaccharide promotes proliferation and osteoblast differentiation of mesenchymal stem cells by regulation of long non-coding RNA H19

2019 ◽  
Vol 8 (7) ◽  
pp. 323-332 ◽  
Author(s):  
Xiaoyan Xie ◽  
Miao Liu ◽  
Qiang Meng
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Western Blot ◽  
Cell Viability ◽  
Osteoblast Differentiation ◽  
Signalling Pathways ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Objectives Osteoporosis is a systemic bone metabolic disease, which often occurs among the elderly. Angelica polysaccharide (AP) is the main component of angelica sinensis, and is widely used for treating various diseases. However, the effects of AP on osteoporosis have not been investigated. This study aimed to uncover the functions of AP in mesenchymal stem cell (MSC) proliferation and osteoblast differentiation. Methods MSCs were treated with different concentrations of AP, and then cell viability, Cyclin D1 protein level, and the osteogenic markers of runt-related transcription factor 2 (RUNX2), osteocalcin (OCN), alkaline phosphatase (ALP), bone morphogenetic protein 2 (BMP-2) were examined by Cell Counting Kit-8 (CCK-8) and western blot assays, respectively. The effect of AP on the main signalling pathways of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and Wnt/β-catenin was determined by western blot. Following this, si-H19#1 and si-H19#2 were transfected into MSCs, and the effects of H19 on cell proliferation and osteoblast differentiation in MSCs were studied. Finally, in vivo experimentation explored bone mineral density, bone mineral content, and the ash weight and dry weight of femoral bone. Results The results revealed that AP significantly promoted cell viability, upregulated cyclin D1 and increased RUNX2, OCN, ALP, and BMP-2 protein levels in MSCs. Moreover, we found that AP notably activated PI3K/AKT and Wnt/β-catenin signalling pathways in MSCs. Additionally, the relative expression level of H19 was upregulated by AP in a dose-dependent manner. The promoting effects of AP on cell proliferation and osteoblast differentiation were reversed by H19 knockdown. Moreover, in vivo experimentation further confirmed the promoting effect of AP on bone formation. Conclusion These data indicate that AP could promote MSC proliferation and osteoblast differentiation by regulating H19. Cite this article: X. Xie, M. Liu, Q. Meng. Angelica polysaccharide promotes proliferation and osteoblast differentiation of mesenchymal stem cells by regulation of long non-coding RNA H19: An animal study. Bone Joint Res 2019;8:323–332. DOI: 10.1302/2046-3758.87.BJR-2018-0223.R2.

scholarly journals Long non-coding RNA NEAT1/miR-320b/MSI2 axis regulates cisplatin resistance in ovarian cancer

2021 ◽  
Author(s):  
Chunling Zhao ◽  
Pingfen Zi ◽  
Degang Zhou
Keyword(s):  
Ovarian Cancer ◽  
Cell Viability ◽  
Cisplatin Resistance ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Novel Therapy ◽  
Non Coding Rna ◽  
Long Non Coding Rna

IntroductionOvarian cancer (OC) frequently occurs in postmenopausal women and it has higher mortality rate. Accumulating researches proved that long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) involved in the progression of chemoresistance in human OC. Here, the study aimed to investigate the partial molecular mechanism of OC chemoresistance.Material and methodsThe levels of NEAT1 and microRNA-320b (miR-320b) were measured by qRT-PCR. Western blot was carried out to determine the protein levels that used in this research. Cell viability was identified via Cell Counting Kit-8 (CCK-8). Transwell assay was employed to determine migration and invasion. The relationship between miR-320b and NEAT1 or MSI2 was clarified by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) and RNA pull down assay. Also, a murine xenograft assay was used to explore the effect of NEAT1 on cisplatin resistance in OC in vivo.ResultsThe level of NEAT1 was significantly increased in cisplatin resistant OC cell lines. Downregulation of NEAT1 enhanced cisplatin sensibility in OVCAR-3/DDP and HEY/DDP cells. Furthermore, miR-320b was a target of NEAT1, and the effects of knockdown of NEAT1 on the cell viability, IC50 of cisplatin, migration and invasion in OVCAR-3/DDP and HEY/DDP were restored by the inhibitor of miR-320. In addition, miR-320b directly targeted MSI2 to regulate cisplatin sensibility in cisplatin resistant OC cells. In addition, downregulation of NEAT1 decreased cisplatin resistance in OC in vivo.ConclusionsNEAT1 regulated cisplatin resistance through NEAT1/miR-320b/MSI2 axis in OC, which might offer a novel therapy target for the chemotherapy of OC.

LncRNA DLGAP1-AS2 modulates glioma development by up-regulating YAP1 expression

2020 ◽  
Vol 167 (4) ◽  
pp. 411-418 ◽  
Author(s):  
Wei Miao ◽  
Ning Li ◽  
Bin Gu ◽  
Guoqing Yi ◽  
Zheng Su ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Antisense Rna ◽  
Glioma Cells ◽  
Therapeutic Interventions ◽  
Downstream Target ◽  
Non Coding Rna ◽  
Glioma Cell Proliferation ◽  
Long Non Coding Rna ◽  
Inhibit Cell Proliferation

Abstract LncRNA DLGAP1 antisense RNA 2 (DLGAP1-AS2) is one kind cytoplasmic long non-coding RNA; however, there is rarely little information about its function in physiological process. Here, we demonstrated that LncRNA DLGAP1-AS2 was up-regulated in glioma and was quite correlated with poor prognosis of glioma patients. Depletion of DLGAP1-AS2 in glioma cells could inhibit cell proliferation and cell migration, and induce cell apoptosis, resulting in the suppression of the progression of glioma consequently. Furthermore, knockdown of DLGAP1-AS2 inhibited the growth of xenograft glioma tumour in vivo as well. Finally, we verified Yes Associated Protein 1 (YAP1) was the downstream target of DLGAP1-AS2 and DLGAP1-AS2 modulated glioma cell proliferation, migration and apoptosis via regulating YAP1. Our study revealed novel mechanism about how did lncRNA DLGAP1-AS2 execute function in glioma and thus provided potential therapeutic interventions for the treatment of glioma.

scholarly journals LncRNA ZEB1-AS1 regulates colorectal cancer cells by miR-205/YAP1 axis

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 175-184 ◽  
Author(s):  
Zhong Jin ◽  
Bing Chen
Keyword(s):  
Colorectal Cancer ◽  
Cell Viability ◽  
Luciferase Reporter ◽  
Non Coding Rna ◽  
Colorectal Cancer Cells ◽  
Non Coding Rnas ◽  
Induced Apoptosis ◽  
The Relationship ◽  
Long Non Coding Rna ◽  
Inhibit Cell Proliferation

AbstractBackgroundRecent studies demonstrated that long non-coding RNAs (lncRNAs) were involved in many biological processes. Dysregulated lncRNAs are related to many cancers, including colorectal cancer (CRC). However, the molecular mechanism of lncRNA ZEB1-AS1 in CRC is not clear.MethodsLncRNA ZEB1-AS1, miR-205, and YAP1 expression were measured by quantitative reverse transcriptase PCR (QRT-PCR). YAP1 protein expression was measured by western blotting. Cell viability was measured by MTT assay. Cell apoptosis was detected by flow cytometry. Luciferase reporter assay was used to confirm the relationship between ZEB1-AS1, miR-205, and YAP1.ResultsLncRNA ZEB1-AS1 and YAP1 was upregulated in CRC tissues. The expression of YAP1 was positively correlated with ZEB1-AS1. Knockdown of ZEB1-AS1 inhibited cell viability and induced apoptosis in CRC cell line SW480 and HCT116 which could be reversed by overexpression of YAP1. ZEB1-AS1 targeted and regulated miR-205 which could directly bind to YAP1. Meanwhile, ZEB1-AS1 regulated the expression of YAP1 via modulating miR-205.ConclusionLong non-coding RNA ZEB1-AS1 silencing could inhibit cell proliferation and induce apoptosis of colorectal cancer via regulating miR-205 and YAP1.

scholarly journals Long non-coding RNA PSMA3-AS1 promotes glioma progression through modulating the miR-411-3p/HOXA10 pathway

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tianzao Huang ◽  
Yingxian Chen ◽  
Yile Zeng ◽  
Chaoyang Xu ◽  
Jinzhong Huang ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Antisense Rna ◽  
Regulatory Mechanism ◽  
Functional Assays ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna ◽  
Competitive Endogenous Rna ◽  
Glioma Progression

Abstract Background Glioma is a common type of brain tumor and is classified as low and high grades according to morphology and molecules. Growing evidence has proved that long non-coding RNAs (lncRNAs) play pivotal roles in numerous tumors or diseases including glioma. Proteasome 20S subunit alpha 3 antisense RNA 1 (PSMA3-AS1), as a member of lncRNAs, has been disclosed to play a tumor-promoting role in cancer progression. However, the role of PSMA3-AS1 in glioma remains unknown. Therefore, we concentrated on researching the regulatory mechanism of PSMA3-AS1 in glioma. Methods PSMA3-AS1 expression was detected using RT-qPCR. Functional assays were performed to measure the effects of PSMA3-AS1 on glioma progression. After that, ENCORI (http://starbase.sysu.edu.cn/) database was used to predict potential genes that could bind to PSMA3-AS1, and miR-411-3p was chosen for further studies. The interaction among PSMA3-AS1, miR-411-3p and homeobox A10 (HOXA10) were confirmed through mechanism assays. Results PSMA3-AS1 was verified to be up-regulated in glioma cells and promote glioma progression. Furthermore, PSMA3-AS1 could act as a competitive endogenous RNA (ceRNA) for miR-411-3p to regulate HOXA10 and thus affecting glioma progression. Conclusion PSMA3-AS1 stimulated glioma progression via the miR-411-3p/HOXA10 pathway, which might offer a novel insight for the therapy and treatment of glioma.

scholarly journals Long non-coding RNA SNHG5 promotes glioma progression via miR-205/E2F3 axis

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Xiaojian Li ◽  
Liang Liu ◽  
Yidan Luo ◽  
Sitong Cui ◽  
Wei Chen ◽  
...  
Keyword(s):  
Molecular Mechanism ◽  
Tumour Growth ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
E2f Transcription Factor ◽  
Non Coding Rnas ◽  
Long Non Coding Rna ◽  
Nucleolar Rna ◽  
Glioma Progression

Abstract In recent years, many studies have reported on the abnormal expression and correlation of long non-coding RNAs (lncRNAs) in tumours. However, the accurate molecular mechanism of lncRNAs in glioma is still in its infancy. In the present study, we aimed to explore the molecular mechanism of small nucleolar RNA host gene 5 (SNHG5) in glioma progression. First, we found that SNHG5 expression was higher in glioma and was related to glioma glucose uptake, migration and invasion. Second, through a series of assays, we concluded that SNHG5 acts as a sponge for miR-205, which inhibits tumour growth in glioma by targeting E2F transcription factor 3 (E2F3). Third, using a xenograft mouse model, we demonstrated that SNHG5 regulates tumourigenesis in vivo. Taken together, our results show that the SNHG5/miR-205/E2F3 axis is involved in glioma progression and may provide a new therapeutic target for the diagnosis and therapy of glioma.

Long Non-Coding RNA GATA3-AS1 Promotes 5-Fluorouracil Resistance of Ovarian Cancer via Mediating miR-6771-3p/SOX4 Target Axis

2021 ◽  
Vol 11 (6) ◽  
pp. 1099-1107
Author(s):  
Yafei Hao ◽  
Changzhou Li ◽  
Teng Zhao ◽  
Hansheng Liu
Keyword(s):  
Ovarian Cancer ◽  
Cell Apoptosis ◽  
Opposite Effect ◽  
Inhibitory Concentration ◽  
Chemotherapy Resistance ◽  
Non Coding Rna ◽  
Associated Proteins ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Ovarian cancer (OC) ranks as the 5th highest cause of cancer-related deaths worldwide. Long non-coding RNAs (lncRNAs) exert significant effects on chemotherapy resistance. The effects of lncRNA GATA3-AS1 on the 5-Fluorouracil (5-FU) resistance in ovarian carcinoma were explored in the current study. The results showed that GATA3-AS1 was highly expressed in OC tissues and 5-FU resistant OC cells. Moreover, GATA3-AS1 knockdown reduced 50% inhibitory concentration (IC50) of 5-Fluorouracil and promoted cell apoptosis, while GATA3-AS1-overexpression showed the opposite effect. In vivo experiment and murine xenograft assay indicated GATA3-AS1 knockdown inhibited neoplasm growth, promoted cell apoptosis, and altered the expression level of apoptosis-associated proteins. GATA3-AS1 promoted SOX4 expression, a well-known transcription factor regulating apoptosis, via targeting miR-6771-3p. In summary, our findings suggested GATA3-AS1 was associated with OC 5-Fluorouracil viaregulating miR-6771-3p/SOX4, providing novel insights into OC chemoresistance.

scholarly journals LINC00636 promotes lymph node metastasis and cervical cancer through targeting NM23

2020 ◽  
Vol 40 (10) ◽  
Author(s):  
Yue Zhong ◽  
Qiang Lu ◽  
Wei Qiu ◽  
Yan Luo
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Non Coding Rna ◽  
Genes Expression ◽  
Cervical Cancer Cells ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Abstract Background: Metastasis is a major obstacle in treatment of cervical cancer, and long non-coding RNA (lncRNA) mediated regulatory effect on associated genes expression is found to be involved in metastasis. However, its mechanisms have not been fully elucidated. Materials and methods: Specimens from patients with cervical cancer metastasis and non-metastasis were used to screen out candidate non-coding RNAs (ncRNAs) and possible downstream targets. And then, effects were determined in vitro and in vivo through knockdown and overexpression techniques. Results: LINC00636 was significantly higher in serum and solid tumor cells of metastatic cervical cancer patients than non-metastatic patients. And knockdown of LINC00636 significantly suppressed invasion, proliferation of cervical cancer cells. NM23 expression was negatively regulated by LINC00636 and it mediated anti-tumor effects was partially blocked by overexpression of LINC00636. Conclusion: LINC00636 might promote metastasis of cervical cancer cells through inhibiting NM23 expression.

Long non-coding RNA ABHD11-AS1 boosts gastric cancer development by regulating miR-361-3p/PDPK1 signalling

2020 ◽  
Vol 168 (5) ◽  
pp. 465-476
Author(s):  
Hairong Xin ◽  
Zhifeng Yan ◽  
Jie Cao
Keyword(s):  
Gastric Cancer ◽  
Antisense Rna ◽  
Suppressive Effect ◽  
Malignant Tumours ◽  
Protein Levels ◽  
Non Coding Rna ◽  
Wide Range ◽  
Non Coding Rnas ◽  
Long Non Coding Rna ◽  
Expression Status

Abstract Gastric cancer (GC) is one of the most common cancers in gastrointestinal malignant tumours. Long non-coding RNAs were widely reported to play a significant role in the regulation of occurrence or development of tumours. Bioinformatics analysis and a wide range of experiments were conducted to explore the expression status, specific function and molecular mechanism of long non-coding RNA ABHD11 antisense RNA 1 (ABHD11-AS1). ABHD11-AS1 knockdown repressed cell proliferation but enhanced cell apoptosis in function. We proved that miR-361-3p directly combines with the 3′wUTR of PDPK2 and ABHD11-AS1 cooperated with miR-361-3p to modulate PDPK2 mRNA and protein levels. Rescue assays confirmed that the miR-361-3p silence reversed the suppressive effect of ABHD11-AS1 deficiency. In summary, ABHD11-AS1 boosts GC development by regulating miR-361-3p/PDPK1 signalling.

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