COX10-AS1 Facilitates Cell Proliferation and Inhibits Cell Apoptosis in Glioblastoma Cells at Post-Transcription Level

Zhou, Chaoyang; Jiang, Xingxing; Liang, Aijun; Zhu, Ronglan; Yang, Yu; Zhong, Liangchen; Wan, Dengfeng

doi:10.1007/s11064-020-03081-4

Cited by 17 publications

(14 citation statements)

References 23 publications

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“…At one time, LINC01354 is studied as a competing endogenous RNA in regulating cancer-related pathways in CRC [ 37 ]. Incremental LINC01354 level has been once examined in osteosarcoma, and artificially eliminating LINC01354 is conducive for retarding cell invasion in vitro and metastasis in vivo [ 10 ]. In the field of NSCLC, the overexpressed LINC01354 is also measured, manifesting a correlation with advanced TNM, while knocking down LINC01354 restricts cancer cells to proliferate and invade [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, lncRNAs-mediated networks are merged as the regulator of EC progression, such as lncRNA RP11-395G23.3-mediated microRNA (miR)-205-5p/phosphatase and tensin homolog axis [ 9 ]. LINC01354 is considered as a tumor activator in osteosarcoma, lung cancer and colorectal cancer (CRC) through promoting cell progression [ 10 – 12 ]. Nevertheless, the defined role of LINC01354, along with its regulatory network has been scarcely ever discussed in EC.…”

Section: Introductionmentioning

confidence: 99%

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RETRACTED ARTICLE: LINC01354/microRNA-216b/KRAS Axis Promotes the Occurrence and Metastasis of Endometrial Cancer

Zhang

Zhao

et al. 2022

Nanoscale Res Lett

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Objective LINC01354 has been defined as a tumor driver in several cancers. Nevertheless, whether LINC01354 involves in endometrial cancer (EC) has been little navigated. Thus, the mechanism of LINC01354 was explored in the disease. Methods Measurements of LINC01354, microRNA (miR)-216b and kirsten rat sarcoma viral oncogene (KRAS) levels in EC tissues and cells were performed. LINC01354 low expression and miR-216b overexpression vectors were introduced into EC cells (lshikawa), thereby their effects on cell viability, apoptosis, migration and invasion were manifested. Rescue experiments were also carried out by down-regulating LINC01354 and miR-216b spontaneously. Tumorigenesis in vivo was also assessed. The relationships of LINC01354/miR-216b/KRAS were analyzed. Results Increased LINC01354 and KRAS and reduced miR-216b levels were measured in EC. Silencing LINC01354 or overexpressing miR-216b retarded EC cellular development. LINC01354 counteracted with miR-216b to target KRAS. Suppression of miR-216b antagonized silenced LINC01354-induced impacts on EC cell development. LINC01354/miR-216b/KRAS axis enhanced tumorigenesis in mice with EC. Conclusion It is testified that silencing LINC01354 inhibits KRAS by up-regulating miR-216b, thereby discouraging cell malignant phenotype in EC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: LINC01354/microRNA-216b/KRAS Axis Promotes the Occurrence and Metastasis of Endometrial Cancer

Zhang

Zhao

et al. 2022

Nanoscale Res Lett

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“…Chaoyang Zhou et al found that COX10-AS1 acts as a competing endogenous RNA to positively regulate ACTG1 expression by sponging miR-361-5p and promotes glioblastoma cell proliferation and inhibits apoptosis [66]. The transcript is also upregulated in SaOS-2, and G-292 cell lines compared to hFOB by more than 2-fold in our RT-qPCR result (Figure 5D).…”

Section: Discussionmentioning

confidence: 51%

Upregulation of 15 Antisense Long Non-Coding RNAs in Osteosarcoma

Rothzerg

et al. 2021

Genes

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The human genome encodes thousands of natural antisense long noncoding RNAs (lncRNAs); they play the essential role in regulation of gene expression at multiple levels, including replication, transcription and translation. Dysregulation of antisense lncRNAs plays indispensable roles in numerous biological progress, such as tumour progression, metastasis and resistance to therapeutic agents. To date, there have been several studies analysing antisense lncRNAs expression profiles in cancer, but not enough to highlight the complexity of the disease. In this study, we investigated the expression patterns of antisense lncRNAs from osteosarcoma and healthy bone samples (24 tumour-16 bone samples) using RNA sequencing. We identified 15 antisense lncRNAs (RUSC1-AS1, TBX2-AS1, PTOV1-AS1, UBE2D3-AS1, ERCC8-AS1, ZMIZ1-AS1, RNF144A-AS1, RDH10-AS1, TRG-AS1, GSN-AS1, HMGA2-AS1, ZNF528-AS1, OTUD6B-AS1, COX10-AS1 and SLC16A1-AS1) that were upregulated in tumour samples compared to bone sample controls. Further, we performed real-time polymerase chain reaction (RT-qPCR) to validate the expressions of the antisense lncRNAs in 8 different osteosarcoma cell lines (SaOS-2, G-292, HOS, U2-OS, 143B, SJSA-1, MG-63, and MNNG/HOS) compared to hFOB (human osteoblast cell line). These differentially expressed IncRNAs can be considered biomarkers and potential therapeutic targets for osteosarcoma.

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“…Experimentally measured, miR-361-5p level trends to fall in gliomas and if elevated, miR-361-5p could prevent gliomas cells to migrate and invade [ 8 ]. From a novel perspective, miR-361-5p is surveyed to be sponged by COX10 antisense RNA 1, thus driving actin gamma 1-mediated proliferation and straining apoptosis of GBM cells [ 9 ]. Commonly proved, miR-361-5p is indeed the tumor suppressor in human cancers, including but not limited to gliomas.…”

Section: Discussionmentioning

confidence: 99%

“…Of significance, the process of epithelial-to-mesenchymal transition (EMT) in gliomas can be delayed by miR-361-5p targeting Twist1 [ 8 ]. Interestingly, a novel regulatory pattern of miR-361-5p in glioblastoma (GBM) implies its involvement in cancer progression and therapeutic potential [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-361-5p slows down gliomas development through regulating UBR5 to elevate ATMIN protein expression

et al. 2021

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MicroRNA (miR)-361-5p has been studied to suppress gliomas development. Based on that, an insight into the regulatory mechanism of miR-361-5p in gliomas was supplemented from ubiquitin protein ligase E3 component N-recognin 5 (UBR5)-mediated ubiquitination of ataxia-telangiectasia mutated interactor (ATMIN). miR-361-5p, ATMIN, and UBR5 levels were clinically analyzed in gliomas tissues, which were further validated in gliomas cell lines. Loss/gain-of-function method was applied to determine the roles of miR-361-5p and UBR5 in gliomas, as to cell viability, migration, invasion, colony formation ability, and apoptosis in vitro and tumorigenesis in vivo. The relationship between miR-361-5p and UBR5 was verified and the interaction between UBR5 and ATMIN was explored. It was detected that reduced miR-361-5p and ATMIN and enhanced UBR5 levels showed in gliomas. Elevating miR-361-5p was repressive in gliomas progression. UBR5 was directly targeted by miR-361-5p. UBR5 can ubiquitinate ATMIN. miR-361-5p suppressed gliomas by regulating UBR5-mediated ubiquitination of ATMIN. Downregulating UBR5 impeded gliomas tumor growth in vivo. Upregulating miR-361-5p targets UBR5 to promote ATMIN protein expression, thus to recline the malignant phenotype of gliomas cells.

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COX10-AS1 Facilitates Cell Proliferation and Inhibits Cell Apoptosis in Glioblastoma Cells at Post-Transcription Level

Cited by 17 publications

References 23 publications

RETRACTED ARTICLE: LINC01354/microRNA-216b/KRAS Axis Promotes the Occurrence and Metastasis of Endometrial Cancer

RETRACTED ARTICLE: LINC01354/microRNA-216b/KRAS Axis Promotes the Occurrence and Metastasis of Endometrial Cancer

Upregulation of 15 Antisense Long Non-Coding RNAs in Osteosarcoma

MicroRNA-361-5p slows down gliomas development through regulating UBR5 to elevate ATMIN protein expression

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