Long non-coding RNA AGAP2-AS1 promotes cell proliferation and invasion through regulating miR-193a-3p/LOXL4 axis in laryngeal squamous cell carcinoma

Ren, Pengyu; Niu, Xiaorong; Zhao, Ren; Liu, Junsong; Ren, Wanli; Dai, Hao; Chen, Jiayu; Yan, Jinfeng; Li, Baiya; Shao, Yuan; Bai, Yang; Han, Peng

doi:10.1080/15384101.2021.2016197

Cited by 8 publications

(6 citation statements)

References 31 publications

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“…Loss of cell adhesion causes loss of contact inhibition, which results in increased cell migration, cell proliferation and cancer progression (41, 42). We also found that downregulated LOXL4 pathway in laryngeal squamous cell carcinoma (45). Yan et al confirmed that AGAP2-AS1 regulated the migration, invasion, proliferation and apoptosis of glioma cells via the miR-628-5p/PTN axis (46).…”

Section: Discussionmentioning

confidence: 53%

“…We also found that downregulated GOLGA7B led to enhanced proliferation, invasion and metastasis of CCA cells. Meanwhile, AGAP2−AS1 is a lncRNA and was recognized as an oncogene in several types of cancer, such as adenocarcinoma, laryngeal squamous cell carcinoma, breast cancer and lung cancer ( 43 – 45 ). Some studies have elucidated the molecular process by which AGAP2−AS1 promotes cancer progression.…”

Section: Discussionmentioning

confidence: 99%

“…Pengyu et al. reported that AGAP2-AS1 promoted cell invasion and proliferation by upregulating the miR-193a-3p/LOXL4 pathway in laryngeal squamous cell carcinoma ( 45 ). Yan et al.…”

Section: Discussionmentioning

confidence: 99%

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Identification of therapeutic targets and prognostic biomarkers in cholangiocarcinoma via WGCNA

Xiao

et al. 2022

Front. Oncol.

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BackgroundCholangiocarcinoma (CCA) is a highly aggressive malignant tumor for which limited treatment methods and prognostic signatures are available. This study aims to identify potential therapeutic targets and prognostic biomarkers for CCA.MethodsBased on differentially expressed genes (DEGs) identified from The Cancer Genome Atlas (TCGA) data, our study identified key gene modules correlated with CCA patient survival by weighted gene coexpression network analysis (WGCNA). Cox regression analysis identified survival-related genes in the key gene modules. The biological properties of the survival-related genes were evaluated by CCK-8 and transwell assays. Then, these genes were used to construct a prognostic signature that was internally and externally validated. Additionally, by combining clinical characteristics with the gene−based prognostic signature, a nomogram for survival prediction was built.ResultsWGCNA divided the 1531 DEGs into four gene modules, and the yellow gene module was significantly associated with overall survival (OS) and histologic neoplasm grade. Our study identified the lncRNA AGAP2−AS1 and a novel gene, GOLGA7B, that are closely related to survival. GOLGA7B downregulation promoted the invasion, migration and proliferation of CCA cells, but AGAP2−AS1 had the opposite effect. AGAP2−AS1 and GOLGA7B were integrated into a gene−based prognostic signature, and both internal and external validation studies confirmed that this two-gene prognostic signature and nomogram could accurately predict CCA patient prognosis.ConclusionAGAP2−AS1 and GOLGA7B are potential therapeutic targets and prognostic biomarkers for CCA.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 99%

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Identification of therapeutic targets and prognostic biomarkers in cholangiocarcinoma via WGCNA

Xiao

et al. 2022

Front. Oncol.

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“…However, previous studies have reported the function of LOXL4 in cancer cells to be controversial. LOXL4 was found to promote tumor development in laryngeal squamous cell carcinoma ( 40 ), liver cancer ( 41 , 42 ), and breast cancer ( 43 ), while Zhang ( 32 ) and Xie et. al ( 30 ) reported it may have tumor suppressive properties in lung cancer.…”

Section: Discussionmentioning

confidence: 99%

miR-183-5p regulates ECM and EMT to promote non-small cell lung cancer progression by targeting LOXL4

Chen¹,

Zhou²,

Liao³

et al. 2023

J Thorac Dis

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Background Non-small cell lung cancer (NSCLC) progression is mediated by changes in gene expression induced by microRNAs. However, the underlying mechanisms remain to be elucidated. In this study, we investigated the roles of miR-183-5p and its target gene in lung cancer development. Methods Relative levels of miR-183-5p and lysyl oxidase-like 4 (LOXL4) expression in lung cancer cells or tissues were measured by quantitative reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence or Western blotting as appropriate. The binding of miR-183-5p to LOXL4 sequences was verified by a dual luciferase reporter assay, and cell proliferation was assessed by Cell Counting Kit-8 (CCK-8) and Edu staining. The cell cycle stage and apoptosis were detected by flow cytometry, and Transwell assays were performed to evaluate cell migration and invasion capabilities. The tumorigenic capability of cancer cells was analyzed using a cancer cell line-based xenograft nude mouse model. Results miR-183-5p expression was decreased in the lung cancer tissues and cell lines and was negatively correlated with elevated LOXL4 expression. Treatment with miR-183-5p mimics suppressed LOXL4 expression, while treatment with an miR-183-5p inhibitor promoted LOXL4 expression in A549 cells. miR-183-5p was found to directly bind to the 3’ UTR of the LOXL4 gene in A549 cells. Overexpression of LOXL4 enhanced cell proliferation, cell cycle progression, migration, and invasion, but repressed their apoptosis, and activated extracellular matrix (ECM) and the epithelial mesenchymal transition (EMT) process in A549 cells, while LOXL4 knockdown produced the opposite effects. Treatment with an miR-183-5P inhibitor promoted the proliferation, cell cycle progression, migration, and invasion of A549 cells but suppressed their apoptosis, and activated the ECM and EMT process, while all these effects were abrogated by LOXL4 knockdown. The tumorigenic capability of A540 cells in nude mice was greatly impaired by treatment with miR-183-5p mimics. Conclusions miR-183-5p repressed the proliferation, migration, invasion, ECM formation, and EMT processes, and promoted the apoptosis of lung cancer cells by targeting LOXL4 expression.

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“…AGAP2-AS1 is an antisense lncRNA transcribed from the 12q14.1 gene, with a length of 1567 nt [ 1 ]. Studies have shown that AGAP2-AS1 is associated with the development of various cancers, including gastric cancer [ 2 ], non-small cell lung cancer (NSCLC) [ 3 ], breast cancer [ 4 ], pleomorphic glioblastoma [ 5 ], ovarian cancer [ 6 ], pancreatic cancer [ 7 ], and hepatocellular carcinoma (HCC) [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA AGAP2 antisense RNA 1 stabilized by insulin-like growth factor 2 mRNA binding protein 3 promotes macrophage M2 polarization in clear cell renal cell carcinoma through regulation of the microRNA-9-5p/THBS2/PI3K-Akt pathway

Xu,

Feng,

Wang

et al. 2023

Cancer Cell Int

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Background Increasing evidence highlights the potential role of long non-coding RNAs (lncRNAs) in the biological behaviors of renal cell carcinoma (RCC). Here, we explored the mechanism of AGAP2-AS1 in the occurrence and development of clear cell RCC (ccRCC) involving IGF2BP3/miR-9-5p/THBS2. Methods The expressions of AGAP2-AS1, IGF2BP3, miR-9-5p, and THBS2 and their relationship were analyzed by bioinformatics. The targeting relationship between AGAP2-AS1 and miR-9-5p and between miR-9-5p and THBS2 was evaluated with their effect on cell biological behaviors and macrophage polarization assayed. Finally, we tested the effect of AGAP2-AS1 on ccRCC tumor formation in xenograft tumors. Results IGF2BP3 could stabilize AGAP2-AS1 through m6A modification. AGAP2-AS1 was highly expressed in ccRCC tissues and cells. The lentivirus-mediated intervention of AGAP2-AS1 induced malignant behaviors of ccRCC cells and led to M2 polarization of macrophages. In addition, THBS2 promoted M2 polarization of macrophages by activating the PI3K/AKT signaling pathway. AGAP2-AS1 could directly bind with miR-9-5p and promote the expression of THBS2 downstream of miR-9-5p. These results were further verified by in vivo experiments. Conclusion AGAP2-AS1 stabilized by IGF2BP3 competitively binds to miR-9-5p to up-regulate THBS2, activating the PI3K/AKT signaling pathway and inducing macrophage M2 polarization, thus facilitating the development of RCC.

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Long non-coding RNA AGAP2-AS1 promotes cell proliferation and invasion through regulating miR-193a-3p/LOXL4 axis in laryngeal squamous cell carcinoma

Cited by 8 publications

References 31 publications

Identification of therapeutic targets and prognostic biomarkers in cholangiocarcinoma via WGCNA

Identification of therapeutic targets and prognostic biomarkers in cholangiocarcinoma via WGCNA

miR-183-5p regulates ECM and EMT to promote non-small cell lung cancer progression by targeting LOXL4

LncRNA AGAP2 antisense RNA 1 stabilized by insulin-like growth factor 2 mRNA binding protein 3 promotes macrophage M2 polarization in clear cell renal cell carcinoma through regulation of the microRNA-9-5p/THBS2/PI3K-Akt pathway

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