Long noncoding RNA lnc‐ABCA12‐3 promotes cell migration, invasion, and proliferation by regulating fibronectin 1 in esophageal squamous cell carcinoma

Ma, Junliang; Xiao, Yuhang; Tian, Bo; Chen, Shaolin; Zhang, Baihua; Wu, Jie; Wu, Zhining; Xu, Li; Tang, Jinming; Yang, Desong; Zhou, Yong; Wang, Hui; Su, Min; Wang, Wenxiang

doi:10.1002/jcb.29373

Cited by 25 publications

(16 citation statements)

References 58 publications

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“…Additionally, fibronectin may also be regulated by long noncoding RNAs (lncRNAs). It has been already reported that co-overexpression of fibronectin 1 and lncRNAs, such as lnc-ABCA12-3 (ATP Binding Cassette Subfamily A Member 12-3), in ESCC tissues is associated with tumor expansion, metastasis, and patients' poor prognosis [140]. Furthermore, increased expression of lncRNA SPRY4-IT1 (sprouty RTK signaling antagonist 4-Intronic Transcript 1) observed in ESCC cell lines increased cell motility and favored EMT, an event strongly related to an increase in the cell motility that could be corroborated by fibronectin-positive staining [141].…”

Section: Glycoproteins and Ecm Adhesion And Migrationmentioning

confidence: 99%

Esophageal Cancer Development: Crucial Clues Arising from the Extracellular Matrix

Palumbo

Costa

Pontes

et al. 2020

Cells

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In the last years, the extracellular matrix (ECM) has been reported as playing a relevant role in esophageal cancer (EC) development, with this compartment being related to several aspects of EC genesis and progression. This sounds very interesting due to the complexity of this highly incident and lethal tumor, which takes the sixth position in mortality among all tumor types worldwide. The well-established increase in ECM stiffness, which is able to trigger mechanotransduction signaling, is capable of regulating several malignant behaviors by converting alteration in ECM mechanics into cytoplasmatic biochemical signals. In this sense, it has been shown that some molecules play a key role in these events, particularly the different collagen isoforms, as well as enzymes related to its turnover, such as lysyl oxidase (LOX) and matrix metalloproteinases (MMPs). In fact, MMPs are not only involved in ECM stiffness, but also in other events related to ECM homeostasis, which includes ECM remodeling. Therefore, the crucial role of distinct MMPs isoform has already been reported, especially MMP-2, -3, -7, and -9, along EC development, thus strongly associating these proteins with the control of important cellular events during tumor progression, particularly in the process of invasion during metastasis establishment. In addition, by distinct mechanisms, a vast diversity of glycoproteins and proteoglycans, such as laminin, fibronectin, tenascin C, galectin, dermatan sulfate, and hyaluronic acid exert remarkable effects in esophageal malignant cells due to the activation of oncogenic signaling pathways mainly involved in cytoskeleton alterations during adhesion and migration processes. Finally, the wide spectrum of interactions potentially mediated by ECM may represent a singular intervention scenario in esophageal carcinogenesis natural history and, due to the scarce knowledge on the cellular and molecular mechanisms involved in EC development, the growing body of evidence on ECM’s role along esophageal carcinogenesis might provide a solid base to improve its management in the future.

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Section: Glycoproteins and Ecm Adhesion And Migrationmentioning

confidence: 99%

Esophageal Cancer Development: Crucial Clues Arising from the Extracellular Matrix

Palumbo

Costa

Pontes

et al. 2020

Cells

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“…[10][11][12] Aberrant lncRNA expression in ESCC has been widely reported and is implicated in multiple malignant characteristics of ESCC. [13][14][15] LncRNAs play an important part during ESCC initiation and progression by performing either oncogenic or tumor-suppressive functions. [16][17][18] These observations have collectively uncovered the crucial regulatory role of lncRNAs in the pathogenesis of ESCC, suggesting that lncRNAs might be promising targets for the diagnosis, prognosis, prevention, and treatment of ESCC.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Noncoding RNA <em>FGD5-AS1</em> Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression</p>

Jia

Zhang

Hong

et al. 2020

CMAR

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These authors contributed equally to this workPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms. Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment. Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown. Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383-SP1 axis, which may represent a novel target for ESCC therapy.

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“…The dysregulation of lncRNAs is increasing linked to tumorigenesis, with both oncogenic and tumor suppressor functions reported [22][23][24][25] . In this study, higher levels of EIF3J-AS1 expression were observed in ECa tumors and cells, which was associated with advantaged TNM staging (P = 0.014), invasion depth (P = 0.001), metastasis (P < 0.001), and poor survival.…”

Section: Discussionmentioning

confidence: 99%

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

Wei

Wang

Liang

et al. 2020

Sci Rep

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Esophageal cancer (ECa) remains a major cause of mortality across the globe. The expression of EIF3J-AS1 is altered in a plethora of tumors, but its role in ECa development and progression are undefined. Here, we show that EIF3J-AS1 is up-regulated in ECa and that its expression correlates with advanced TNM stage (P = 0.014), invasion depth (P = 0.001), positive lymph node metastasis (P < 0.001) and poor survival (OS: P = 0.0059; DFS: P = 0.0037) in ECa. Functional experiments showed that knockdown EIF3J-AS1 inhibited ECa growth and metastasis through in vitro and in vivo experiments. Regarding the mechanism, EIF3J-AS1/miR-373-3p/AKT1 established the ceRNA network involved in the modulation of cell progression of ECa cells. Overall, EIF3J-AS1 may exhibit an oncogenic function in ECa via acting as a sponge for miR-373-3p to up-regulate AKT1 mRNA level, and may serve as a potential therapeutic target and a prognostic biomarker for ECa patients. Esophageal cancer (ECa) is of particularly high incidence in Chinese males compared to other regions and remains a global threat to human health. Up to ~ 450,000 new cases of ECa are diagnosed annually, of which up to ~ 400,000 of those afflicted do not survive 1. Diagnostic and therapeutic advances have been made to improve ECa therapeutics, including biopsies, chromo endoscopy and narrow-band imaging 2. However, despite these improvements, the efficiency of ECa therapies and subsequent patient prognosis remains poor. ECa therefore remains a global health burden for which new diagnostics and effective therapeutic strategies are urgently required 3. A further understanding of the molecular regulators of ECa tumorigenesis is required to expedite the discovery of novel anti-ECa strategies. While lncRNAs (long noncoding RNAs; more than 200 bases long 4-8 are not capable of translating proteins, their dysregulation is observed several cancers, such as ECa 9-12. For instance, the process of EMT (epithelialmesenchymal transition) is enhanced by lncRNA PVT1 via E-cadherin suppression in ECa 13. Further, significantly enhanced level of CASC11 was observed in ECa tissues while its silencing impeded the progression of ECa by regulating KLF6 expression 14. Previous study reported that up-regulated a novelty EIF3J-AS1 was associated with poor survival and accelerated HCC progression via targeting miR-122e5p/CTNND2 axis under hypoxia 15. Meanwhile, EIF3J-AS1 induced by H3K27 promoted colorectal cancer proliferation and inhibited apoptosis via miR-3163/YAP1 axis 16. Nevertheless, the role and inherent mechanisms of EIF3J-AS1 in human ECa development remains to be assessed. In this research, we examined the increased expression of EIF3J-AS1 in ECa cell lines and tissues, the effect of EIF3J-AS1 knocked down on inhibiting the metastasis and growth of ECa cell lines in vitro and vivo. We also examined the role of EIF3J-AS1 in ECa cells' aggressive phenotypes by miR-373-3p binding and assessing the AKT1 expression. Materials and methods Tissue specimens. Collection of a total of 182 ECa cases...

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Long noncoding RNA lnc‐ABCA12‐3 promotes cell migration, invasion, and proliferation by regulating fibronectin 1 in esophageal squamous cell carcinoma

Cited by 25 publications

References 58 publications

Esophageal Cancer Development: Crucial Clues Arising from the Extracellular Matrix

Esophageal Cancer Development: Crucial Clues Arising from the Extracellular Matrix

<p>Long Noncoding RNA <em>FGD5-AS1</em> Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression</p>

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

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