LncRNA EIF3J-AS1 enhanced esophageal cancer invasion via regulating AKT1 expression through sponging miR-373-3p

Wei, Wei‐Tian; Wang, Liang; Liang, Jinxiao; Li, Qing; Zeng, Jing

doi:10.1038/s41598-020-70886-2

Cited by 19 publications

(21 citation statements)

References 29 publications

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“…In recent years, an increasing number of studies have shown that the dysregulation of lncRNAs, such as lncRNA MALAT1 and DRAIC, plays important roles in the initiation and development of PCa [17][18][19][20]. LncRNA EIF3J-AS1 was found to function as an oncogene in different kinds of cancer [8,10] and to induce chemoresistance [21]. However, the role of EIF3J-AS1 has not been described with regard to PCa.…”

Section: Discussionmentioning

confidence: 99%

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LncRNA EIF3J-AS1 functions as an oncogene by regulating MAFG to promote prostate cancer progression

Wang¹,

Qin²,

Guo³

et al. 2022

J. Cancer

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Long non-coding RNAs (lncRNAs) can modulate various biological processes and behaviors in most human cancers. LncRNA EIF3J-AS1 has been reported as an oncogene in various tumors, but whether it exerts functions in malignant progression and gene expression in prostate cancer (PCa) remains unknown. In this study, we investigated the high level of EIF3J-AS1 in PCa tissues and cells, and used functional assays to show that knocking down EIF3J-AS1 inhibited PCa cell proliferation and metastatic ability. A preliminary mechanistic investigation also showed that EIF3J-AS1 may increase the expression of MAF bZIP transcription Factor G (MAFG) in PCa. The expression correlation between EIF3J-AS1 and MAFG was found to be positive in PCa tissues. Finally, rescue assays showed that MAFG might be involved in the EIF3J-AS1-mediated malignant phenotype in PCa cells. This study demonstrated that EIF3J-AS1/MAFG may play a key role in facilitating PCa progression.

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Section: Discussionmentioning

confidence: 99%

“…Recently, lncRNA EIF3J antisense RNA 1 (EIF3J-AS1) was found to function as an oncogene in glioma, colorectal cancer, esophageal cancer, etc. [8][9][10], demonstrating its clinical potential as a biomarker and therapeutic target. However, the role of EIF3J-AS1 in PCa remains unclear.…”

Section: Introductionmentioning

confidence: 99%

LncRNA EIF3J-AS1 functions as an oncogene by regulating MAFG to promote prostate cancer progression

Wang¹,

Qin²,

Guo³

et al. 2022

J. Cancer

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“…ZFAS1 was validated to be directly targeted by miR-373-3 p . Actually, miR-373-3 p was found to inhibit cancer development through targeting different lncRNAs [ 17 , 18 ]. Here, miR-373-3 p functioned as a tumor suppressor miRNA in TPC-1 cells.…”

Section: Discussionmentioning

confidence: 99%

CREB3 Transactivates lncRNA ZFAS1 to Promote Papillary Thyroid Carcinoma Metastasis by Modulating miR-373-3p/MMP3 Regulatory Axis

Wang

Wei

et al. 2021

International Journal of Endocrinology

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The incidence rate of thyroid carcinoma ranks ninth among human malignancies, and it accounts for the most frequent malignancy in endocrine-related tumors. This study aimed to investigate the role of long noncoding RNA (lncRNA) ZFAS1 in the metastasis of papillary thyroid carcinoma (PTC) and the potential molecular mechanisms. Both ZFAS1 and MMP3 were highly expressed in thyroid carcinoma and PTC cell, as measured by the q-PCR and TCGA database. In addition, ZFAS1 induced TPC-1 metastasis through inducing the epithelial–mesenchymal transition (EMT) process. Besides, ZFAS1 knockdown by siRNA induced miR-373-3p expression and reduced MMP3 expression, as quantified by q-PCR and Western blotting. According to the luciferase assay, both ZFAS1 and MMP3 were classified as the direct targets of miR-373-3p. However, MMP3 itself did not affect ZFAS1. Using the online prediction tool, CREB3 was predicted as the transcription factor (TF) of ZFAS1 that contained two binding sites on its promoter region, and CREB3 was positively correlated with ZFAS1 in thyroid carcinoma cohorts. Results from the dual-luciferase assay and ChIP-qPCR indicated that both the two binding sites were essential for the transcription of ZFAS1. In conclusion, CREB3 activated lncRNA ZFAS1 at the transcriptional level to promote PTC metastasis by modulating miR-373-3p/MMP3.

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“…Abnormal and uncontrolled cell proliferation is a hallmark of cancer, and is caused by the misregulation of the expression of various crucial molecules. Although numerous oncogenes, tumor suppressor genes, and tumor-related signaling pathways have been identified and confirmed in recent years, the pathogenesis of EC remains unclear (24)(25)(26). In total, 18% of ncRNAs are associated with human tumors, while lncRNAs account for 9%, suggesting that lncRNAs may be a major factor in carcinogenesis and cancer progression (27).…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA HAGLROS regulates the proliferation, migration, and apoptosis of esophageal cancer cells via the HAGLROS-miR-206-NOTCH3 axis

Gai¹,

Huang²,

Zhao³

et al. 2021

J Gastrointest Oncol

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Background: Esophageal cancer (EC) is a common malignant tumor of the digestive tract, the treatment of which involves surgery combined with radiotherapy and chemotherapy, as well as other comprehensive types of treatment. The pathogenesis of EC remains unclear, which hinders the development of clinical therapy and the identification of molecular targets for this disease. Long non-coding RNAs (lncRNAs) have been shown to be associated with the malignant biological behavior of EC, but the specific molecular mechanisms underlying the carcinogenesis of EC are not fully understood. Methods: Reverse transcription-quantitative PCR (RT-qPCR) was applied to measure the lncRNA HAGLR opposite strand lncRNA (HAGLROS) levels in EC cell lines and tissues. Cell Counting Kit-8 (CCK-8) detection, scratch test, and Transwell assay were performed to determine the proliferation, migration and invasion of EC cell. The interaction between HAGLROS, microRNA (miR)-206, and notch receptor 3 (NOTCH3) was confirmed by RNA immunoprecipitation and dual luciferase reporter gene assays. Results: HAGLROS is upregulated in esophageal squamous cell carcinoma (ESCC) tissues and predicts poor prognosis. Silent HAGLROS is negatively associated with malignant behavior in EC cells. Low expression of HAGLROS can induce decreased invasive and migratory abilities in EC cells. Downregulated HAGLROS significantly inhibits the proliferation of EC cells and accelerates apoptosis. HAGLROS promotes EC cell tumorigenesis in vivo. HAGLROS participates in the HAGLROS/miR-206/NOTCH3 regulatory axis in EC cells. Conclusions: HAGLROS may play a role in the progression of EC by modulating the miR-206/NOTCH3 signaling axis, and may be a novel target for the diagnosis and treatment of EC.

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LncRNA EIF3J-AS1 enhanced esophageal cancer invasion via regulating AKT1 expression through sponging miR-373-3p

Cited by 19 publications

References 29 publications

LncRNA EIF3J-AS1 functions as an oncogene by regulating MAFG to promote prostate cancer progression

LncRNA EIF3J-AS1 functions as an oncogene by regulating MAFG to promote prostate cancer progression

CREB3 Transactivates lncRNA ZFAS1 to Promote Papillary Thyroid Carcinoma Metastasis by Modulating miR-373-3p/MMP3 Regulatory Axis

Long non-coding RNA HAGLROS regulates the proliferation, migration, and apoptosis of esophageal cancer cells via the HAGLROS-miR-206-NOTCH3 axis

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