The essential role of long non-coding RNA GAS5 in glioma: interaction with microRNAs, chemosensitivity and potential as a biomarker

Tan, Xiaosheng; Jiang, Hua; Fang, Yingying; Han, Dafei; Guo, Yawei; Wang, Xinming; Gong, Xun; Hong, Wenming; Tu, Jiajie; Wei, Wei

doi:10.7150/jca.49203

Cited by 12 publications

(10 citation statements)

References 67 publications

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“…Numerous lncRNAs have also been reported to be involved in the malignant progression of glioma. For example, GAS5 and HOTAIR were dysregulated in gliomas and related to the proliferation, migration, invasion and chemosensitivity of glioma cells [28,[35][36][37]. FGF14-AS2 was reported to function as a suppressor gene in breast cancer and colorectal cancer [13,15]; however, its role in glioma has not been reported to date.…”

Section: Discussionmentioning

confidence: 99%

FGF14-AS2 accelerates tumorigenesis in glioma by forming a feedback loop with miR-320a/E2F1 axis

Zhang¹,

Gu²,

Zhang³

et al. 2021

J. Cancer

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Glioma is the most common primary tumour in the central nervous system in adults, and at present, there is no effective treatment to cure this malignancy. Long noncoding RNAs (lncRNAs) are closely related to tumour progression and have attracted increasing attention in tumour research. However, the role of lncRNA FGF14-AS2 in glioma tumorigenesis has not been determined. In the present study, we found that FGF14-AS2 expression was significantly elevated in glioma tissues and was associated with poor survival in glioma patients. Silencing FGF14-AS2 inhibited the proliferation, migration and invasion ability of glioma cells. In vivo assay showed that silencing FGF14-AS2 led to inhibition of tumour growth. In addition, FGF14-AS2 was observed to promote glioma progression via the miR-320a/E2F1 axis. Moreover, E2F1 could bind to the promoter region of FGF14-AS2, thereby enhancing FGF14-AS2 expression. In conclusion, FGF14-AS2 could accelerate tumorigenesis of glioma by forming a feedback loop with the miR-320a/E2F1 axis which suggested that FGF14-AS2 could serve as a therapeutic target for glioma.

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Section: Discussionmentioning

confidence: 99%

FGF14-AS2 accelerates tumorigenesis in glioma by forming a feedback loop with miR-320a/E2F1 axis

Zhang¹,

Gu²,

Zhang³

et al. 2021

J. Cancer

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“…Another example is TUG1 , which sequesters miR-29b-3p , miR-29c , miR-133b , and miR-590 [ 45 , 46 , 51 , 52 ]. As there are more miRNAs being identified to bind these two exemplified lncRNAs in other cell types (e.g., cardiomyocytes, endothelial cells), cellular statuses, and diseases [ 51 , 52 , 53 , 54 , 55 , 56 , 57 ], it is important to perform a comparative study of lncRNAs and several miRNAs being reported to be sequestered by the target lncRNAs by measuring the copy numbers of each RNA species. Without such a head-to-head comparative study, more and more miRNAs will be reported to be sequestered by one lncRNA, despite its expression level being far lower than those of the sequestered miRNAs.…”

Section: Lncrnas In Cardiac Fibrosismentioning

confidence: 99%

Long Non-Coding RNAs in Cardiac and Pulmonary Fibroblasts and Fibrosis

Ilieva

Uchida

2022

ncRNA

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The cardiopulmonary system delivers oxygen throughout the body via blood circulation. It is an essential part of the body to sustain the lives of organisms. The integral parts of the cardiopulmonary system—the heart and lungs—are constantly exposed to damaging agents (e.g., dust, viruses), and can be greatly affected by injuries caused by dysfunction in tissues (e.g., myocardial infarction). When damaged, mesenchymal cells, such as fibroblasts, are activated to become myofibroblasts to initiate fibrosis as part of a regenerative mechanism. In diseased states, the excess accumulation of extracellular matrices secreted by myofibroblasts results in further dysfunction in the damaged organs. These fibrotic tissues cannot easily be removed. Thus, there is a growing interest in understanding the fibrotic process, as well as finding biomolecules that can be targets for slowing down or potentially stopping fibrosis. Among these biomolecules, the interest in studying long non-coding RNAs (lncRNAs; any non-protein-coding RNAs longer than 200 nucleotides) has intensified in recent years. In this commentary, we summarize the current status of lncRNA research in the cardiopulmonary system by focusing on cardiac and pulmonary fibrosis.

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“… 3 , 4 Long noncoding RNAs can act as oncogenes (such as HOX transcript antisense RNA) 5 or tumor suppressors (such as growth arrest‐specific transcript 5 [GAS5]). 6 Evidence shows that GAS5 is abnormally expressed in a variety of cancers, such as non‐small‐cell lung cancer, hepatocellular carcinoma, breast cancer, and gastric cancer. 7 , 8 , 9 , 10 However, the function and mechanism of GAS5 in EC are largely unknown.…”

Section: Introductionmentioning

confidence: 99%

“…Increasing evidence has shown that abnormal expression of certain lncRNAs could play an important function in cancer biology 3,4 . Long noncoding RNAs can act as oncogenes (such as HOX transcript antisense RNA) 5 or tumor suppressors (such as growth arrest‐specific transcript 5 [GAS5]) 6 . Evidence shows that GAS5 is abnormally expressed in a variety of cancers, such as non‐small‐cell lung cancer, hepatocellular carcinoma, breast cancer, and gastric cancer 7‐10 .…”

Section: Introductionmentioning

confidence: 99%

Growth arrest‐specific transcript 5 represses endometrial cancer development by promoting antitumor function of tumor‐associated macrophages

Tan

Chen

et al. 2022

Cancer Science

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The tumor‐suppressor role of long noncoding RNA (lncRNA) growth arrest‐specific transcript 5 (GAS5) has been proven in various types of cancer. However, the specific function of GAS5 in tumor‐associated macrophages (TAMs) of endometrial cancer (EC) is elusive. Quantitative PCR results showed that GAS5 expression decreased in EC tissues and primary TAMs from EC tumors. Tumor‐associated macrophage infiltration was significantly positively associated with the developmental stage of EC. Direct coculture of GAS5‐overexpressing TAMs and EC cells showed that GAS5 enhanced phagocytosis, antigen presentation, and activation of cytotoxic T cells, and repressed “Don’t eat me” signals between TAMs and EC cells. Tumor formation in immunodeficient mice showed that GAS5‐overexpressing macrophages could repress EC formation in vivo. GAS5 promoted M1 polarization by activating the microRNA‐21– phosphatase and tensin homolog (PTEN)–AKT signaling pathway and directly repressing the nuclear accumulation and phosphorylation of oncogenic yes‐associated protein 1 (YAP1) in TAMs. GAS5 inhibited the development of EC from both innate and adaptive immunity by transforming TAMs from a protumor to an antitumor phenotype. These antitumor effects of GAS5 on TAMs were mediated by the activation of the miR‐21‐PTEN‐AKT pathway and inhibition of YAP1.

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The essential role of long non-coding RNA GAS5 in glioma: interaction with microRNAs, chemosensitivity and potential as a biomarker

Cited by 12 publications

References 67 publications

FGF14-AS2 accelerates tumorigenesis in glioma by forming a feedback loop with miR-320a/E2F1 axis

FGF14-AS2 accelerates tumorigenesis in glioma by forming a feedback loop with miR-320a/E2F1 axis

Long Non-Coding RNAs in Cardiac and Pulmonary Fibroblasts and Fibrosis

Growth arrest‐specific transcript 5 represses endometrial cancer development by promoting antitumor function of tumor‐associated macrophages

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