GABPB1-AS1 Promotes the Development of Osteosarcoma by Targeting SP1 and Activating the Wnt/β-Catenin Pathway

Chen, Jingyang; Bian, Mei‐Ru; Pan, Langxing; Liu, Chengdong; Yang, Hanshi

doi:10.1155/2022/8468896

Cited by 6 publications

(3 citation statements)

References 28 publications

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“…For its role in cancer, GABPB1-AS1 was found to be upregulated in glioma tissues and associated with advanced WHO grades [22]. It was also found that silencing of GABPB1-AS1 could significantly inhibit the proliferation, clonal formation, migration, and epithelial-mesenchymal transformation of osteosarcoma by acting the SP1/Wnt/β-catenin signaling pathway [23]. However, there is still no study investigated the specific role of GABPB1-AS1 in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

GABPB1-AS1 acts as a tumor suppressor and inhibits non-small cell lung cancer progression by targeting miRNA-566/F-box protein 47

LV¹,

LAI²,

ZHAO³

et al. 2021

Oncology Research

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It has been certified that GABPB1-AS1 is aberrantly expressed and plays as a vital role in some kinds of cancers.However, its expression pattern and functions in non-small cell lung cancer (NSCLC) are still largely unknown. This study aims to assess GABPB1-AS1 expression and biological roles in NSCLC. The expression of GABPB1-AS1 was detected in NSCLC specimens and adjacent normal specimens. CCK8 and Transwell assays were performed to evaluate the effects of GABPB1-AS1 on NSCLC cell proliferation, migration and invasion. Bioinformatics tools and luciferase reporter assays were applied to predict and verify GABPB1-AS1's direct targets. The results revealed that GABPB1-AS1 is sharply reduced in NSCLC specimens and cell lines. CCK8 assays indicated that overexpression of GABPB1-AS1 dramatically reduced NSCLC cell growth, and Transwell assays proved that NSCLC cell migration and invasion were distinctly inhibited by GABPB1-AS1. Exploration of the mechanism uncovered that miRNA-566 (miR-566)/F-box protein 47 (FBXO47) is directly targeted by GABPB1-AS1 in NSCLC. The study demonstrated that GABPB1-AS1 inhibited NSCLC cell proliferation, migration and invasion by targeting miR-566/FBXO47.

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Section: Discussionmentioning

confidence: 99%

GABPB1-AS1 acts as a tumor suppressor and inhibits non-small cell lung cancer progression by targeting miRNA-566/F-box protein 47

LV¹,

LAI²,

ZHAO³

et al. 2021

Oncology Research

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show abstract

“…GABPB1 associates with the alpha subunit to form a tetrameric configuration that actively enhances the transcription of a myriad of genes, including those involved in antioxidant defense mechanisms, such as Peroxiredoxin 5 (PRDX5), which is highly expressed in HCC tissues and associates with poor prognosis of patients [ 137 , 138 ]. The lncRNA GABPB1-AS1 is the antisense transcript of GABPB1 mRNA [ 139 ]. The expression of GABPB1-AS1 might fluctuate in response to stress stimuli [ 132 , 140 ].…”

Section: Ferroptosis-related Lncrnas In Hcc Progression and Prognosismentioning

confidence: 99%

The multifaceted perspectives on the regulation of lncRNAs in hepatocellular carcinoma ferroptosis: from bench-to-bedside

Jin,

Huang,

Tian

2024

Clin Exp Med

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Despite being characterized by high malignancy, high morbidity, and low survival rates, the underlying mechanism of hepatocellular carcinoma (HCC) has not been fully elucidated. Ferroptosis, a non-apoptotic form of regulated cell death, possesses distinct morphological, biochemical, and genetic characteristics compared to other types of cell death. Dysregulated actions within the molecular network that regulates ferroptosis have been identified as significant contributors to the progression of HCC. Long non-coding RNAs (lncRNAs) have emerged as influential contributors to diverse cellular processes, regulating gene function and expression through multiple mechanistic pathways. An increasing body of evidence indicates that deregulated lncRNAs are implicated in regulating malignant events such as cell proliferation, growth, invasion, and metabolism by influencing ferroptosis in HCC. Therefore, elucidating the inherent role of ferroptosis and the modulatory functions of lncRNAs on ferroptosis in HCC might promote the development of novel therapeutic interventions for this disease. This review provides a succinct overview of the roles of ferroptosis and ferroptosis-related lncRNAs in HCC progression and treatment, aiming to drive the development of promising therapeutic targets and biomarkers for HCC patients.

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“…Several reports showed the involvement of the Wnt/beta-catenin signaling pathway in OS tumor development and metastasis [81]. The SP1/Wnt/β-catenin signaling pathway plays a vital role in GABPB1-AS1-mediated OS tumorigenesis [82]. Melittin inhibits lung metastasis of human OS mediated by the Wnt/β-catenin signaling pathway [83].…”

Section: Wnt/β-catenin Signaling Pathwaymentioning

confidence: 99%

Deciphering the Signaling Mechanisms of Osteosarcoma Tumorigenesis

Nirala

Yamamichi

Yustein

2023

IJMS

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Osteosarcoma (OS) is the predominant primary bone tumor in the pediatric and adolescent populations. It has high metastatic potential, with the lungs being the most common site of metastasis. In contrast to many other sarcomas, OS lacks conserved translocations or genetic mutations; instead, it has heterogeneous abnormalities, including somatic DNA copy number alteration, ploidy, chromosomal amplification, and chromosomal loss and gain. Unfortunately, clinical outcomes have not significantly improved in over 30 years. Currently, no effective molecularly targeted therapies are available for this disease. Several genomic studies showed inactivation in the tumor suppressor genes, including p53, RB, and ATRX, and hyperactivation of the tumor promoter genes, including MYC and MDM2, in OS. Alterations in the major signaling pathways, including the PI3K/AKT/mTOR, JAK/STAT, Wnt/β-catenin, NOTCH, Hedgehog/Gli, TGF-β, RTKs, RANK/RANKL, and NF-κB signaling pathways, have been identified in OS development and metastasis. Although OS treatment is currently based on surgical excision and systematic multiagent therapies, several potential targeted therapies are in development. This review focuses on the major signaling pathways of OS, and we propose a biological rationale to consider novel and targeted therapies in the future.

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GABPB1-AS1 Promotes the Development of Osteosarcoma by Targeting SP1 and Activating the Wnt/β-Catenin Pathway

Cited by 6 publications

References 28 publications

GABPB1-AS1 acts as a tumor suppressor and inhibits non-small cell lung cancer progression by targeting miRNA-566/F-box protein 47

GABPB1-AS1 acts as a tumor suppressor and inhibits non-small cell lung cancer progression by targeting miRNA-566/F-box protein 47

The multifaceted perspectives on the regulation of lncRNAs in hepatocellular carcinoma ferroptosis: from bench-to-bedside

Deciphering the Signaling Mechanisms of Osteosarcoma Tumorigenesis

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