The Regulatory Role of Non-coding RNAs on Programmed Cell Death Four in Inflammation and Cancer

Zhao, Mengxiang; Zhu, Nisha; Hao, Fengyao; Song, Yuxian; Wang, Zhiyong; Ni, Yanhong; Ding, Liang

doi:10.3389/fonc.2019.00919

Cited by 30 publications

(15 citation statements)

References 91 publications

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“…Given the critical role of epigenetic regulation in BC, lncRNAs play comprehensive roles in BC recurrence and metastasis 17 , 18 . Moreover, m 6 A acts as one of the most common RNA modifications in eukaryotes.…”

Section: Discussionmentioning

confidence: 99%

m6A-induced LINC00958 promotes breast cancer tumorigenesis via the miR-378a-3p/YY1 axis

Rong

Dong

et al. 2021

Cell Death Discov.

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Increasing evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in human breast cancer (BC) tumorigenesis. However, the mechanisms by which lncRNA and N6-methyladenosine (m6A) regulate BC tumorigenesis are still unclear. In the present research, LINC00958 was markedly overexpressed in BC tissue and cells, and LINC00958 upregulation promoted the tumor progression of BC cells. Mechanistically, m6A methyltransferase-like 3 (METTL3) gave rise to the upregulation of LINC00958 by promoting its RNA transcript stability. Moreover, LINC00958 acted as a competitive endogenous RNA for miR-378a-3p to promote YY1. Overall, these data provide novel insight into how m6A-mediated LINC00958 regulates BC tumorigenesis.

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Section: Discussionmentioning

confidence: 99%

m6A-induced LINC00958 promotes breast cancer tumorigenesis via the miR-378a-3p/YY1 axis

Rong

Dong

et al. 2021

Cell Death Discov.

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“…36,37 Approximately one fifth of lncRNAs are predicted to control the aggressive phenotype of human cancers. 38 Regarding melanoma, a variety of lncRNAs are abnormally expressed and are closely related to the patients' prognosis. [39][40][41] They play an important part in the malignant characteristics of melanoma in vitro and in vivo because these lncRNAs exert oncogenic or tumor-suppressive effects.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Noncoding RNA <em>LINC00173</em> Promotes the Malignancy of Melanoma by Promoting the Expression of IRS4 Through Competitive Binding to microRNA-493</p>

Yang¹,

Lei²,

Zeng³

et al. 2020

CMAR

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Purpose: Long intergenic non-protein-coding RNA 173 (LINC00173) plays crucial roles in lung cancer. However, the expression and biological functions of LINC00173 in melanoma have not yet been investigated. In this study, we aimed to characterize the involvement of LINC00173 in melanoma and elucidate its mechanisms of action. Materials and Methods: Reverse-transcription quantitative PCR was performed to measure LINC00173 expression in melanoma. A CCK-8 assay, flow cytometry, and migration and invasion assays were applied to examine melanoma cell proliferation, apoptosis, migration, and invasion, respectively. A xenograft tumor experiment was performed to determine the tumorous growth of melanoma cells in vivo. Results: We found that LINC00173 was upregulated in melanoma tissues and cell lines. High LINC00173 expression was closely associated with TNM stage, lymph node metastasis, and shorter overall survival of patients with melanoma. Functional assays revealed that LINC00173 downregulation inhibited melanoma cell proliferation, migration, and invasion and induced apoptosis, suggesting that LINC00173 acts as an oncogenic RNA. LINC00173 knockdown retarded the tumorous growth of melanoma cells in vivo. Mechanistically, LINC00173 increased insulin receptor substrate 4 (IRS4) expression by sponging microRNA-493 (miR-493), thereby acting as a competing endogenous RNA. The effects of LINC00173 knockdown on the malignant phenotype of melanoma cells were reversed by overexpression of IRS4 or knockdown of miR-493. Conclusion: The LINC00173-miR-493-IRS4 pathway regulates melanoma characteristics by increasing the expression of IRS4 via competitive binding of LINC00173 to miR-493, suggesting that this pathway is a potential target for the diagnosis, prognosis, and/or treatment of melanoma.

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“…Furthermore, PDCD4 downregulation in tumor cells is associated with drug resistance, whereas its expression enhances sensitivity to chemo- and radio-therapy [ 24 , 31 , 32 , 33 , 34 ]. Besides its primary function in carcinogenesis, a new role for PDCD4, as a regulator of the inflammatory process has recently emerged [ 29 , 35 ]. PDCD4 downregulation is associated with an anti-inflammatory phenotype [ 29 , 35 ].…”

Section: Introductionmentioning

confidence: 99%

Clinical Significance of PDCD4 in Melanoma by Subcellular Expression and in Tumor-Associated Immune Cells

Tran

Rane

Zito

et al. 2021

Cancers

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Little is known about the subcellular localization and function of programmed cell death 4 (PDCD4) in melanoma. Our past studies suggest PDCD4 interacts with Pleckstrin Homology Domain Containing A5 (PLEKHA5) to influence melanoma brain metastasis outcomes, as high intracranial PDCD4 expression leads to improved survival. We aimed to define the subcellular distribution of PDCD4 in melanoma and in the tumor microenvironment during neoplastic progression and its impact on clinical outcomes. We analyzed multiple tissue microarrays with well-annotated clinicopathological variables using quantitative immunofluorescence and evaluated single-cell RNA-sequencing on a brain metastasis sample to characterize PDCD4+ immune cell subsets. We demonstrate differences in PDCD4 expression during neoplastic progression, with high tumor and stromal PDCD4 levels associated with improved survival in primary melanomas and in intracranial metastases, but not in extracranial metastatic disease. While the expression of PDCD4 is well-documented on CD8+ T cells and natural killer cells, we show that it is also found on B cells and mast cells. PDCD4 expression in the tumor microenvironment is associated with increased immune cell infiltration. Further studies are needed to define the interaction of PDCD4 and PLEKHA5 and to evaluate the utility of this pathway as a therapeutic target in melanoma brain metastasis.

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The Regulatory Role of Non-coding RNAs on Programmed Cell Death Four in Inflammation and Cancer

Cited by 30 publications

References 91 publications

m6A-induced LINC00958 promotes breast cancer tumorigenesis via the miR-378a-3p/YY1 axis

m6A-induced LINC00958 promotes breast cancer tumorigenesis via the miR-378a-3p/YY1 axis

<p>Long Noncoding RNA <em>LINC00173</em> Promotes the Malignancy of Melanoma by Promoting the Expression of IRS4 Through Competitive Binding to microRNA-493</p>

Clinical Significance of PDCD4 in Melanoma by Subcellular Expression and in Tumor-Associated Immune Cells

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