Upregulation of LINC00319 indicates a poor prognosis and promotes cell proliferation and invasion in cutaneous squamous cell carcinoma

Liao, Jinfeng; Duan, Xiaohong; He, Yide; Liao, Yongmei

doi:10.1002/jcb.27388

Cited by 31 publications

(24 citation statements)

References 36 publications

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“…Here, we have identified a novel lncRNA LINC00319 as a key regulator of miR-3127, and showed that LINC00319 can downregulate the expression of miR-3127 in BCA cells by functioning as a miRNA sponge. LINC00319 was highly expressed in many human tumors and associated with poorer survival of patients (Zhou et al, 2017;Li et al, 2018;Zhang et al, 2018Zhang et al, , 2019Song and Yin, 2019). LINC00319 was shown to promote the proliferative, migratory and invasive capabilities of tumor cells by stabilizing SIRT6 (Zhang et al, 2019) or by interacting with miR-1207 (Song and Yin, 2019), miR-450 (Zhang et al, 2018) and miR-32 (Zhou et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

Wang

Meng

2020

Front. Genet.

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Recent studies suggested that microRNA-3127 (miR-3127) was dysregulated in multiple tumor types and has important roles in tumorigenesis and cancer progression. However, its biological roles and the mechanisms that regulate its expression in bladder cancer (BCA) remain to be determined. The expression level of miR-3127 was measured in BCA tissues and its cellular functions were examined using both in vitro and in vivo experiments. The interaction between miR-3127 and long non-coding RNA (lncRNA) LINC00319 was explored using RNA immunoprecipitation assay and luciferase reporter assays. We showed that miR-3127 expression was significantly downregulated in human BCA tissues and BCA cell lines. Lower miR-3127 levels were associated with worse survival in BCA patients. The overexpression of miR-3127 impaired BCA cell proliferation and invasion, and the knockdown of miR-3127 enhanced BCA cell proliferation and invasion in vitro. Importantly, miR-3127 was able to suppress cell growth in vivo. We demonstrated that miR-3127 repressed the proliferation and invasion of BCA cells though directly targeted the 3-UTR of RAP2A, which served as a novel oncogene in BCA cells. The suppression of cell proliferation and invasion caused by miR-3127 overexpression could be partially abrogated by ectopic expression of RAP2A. Furthermore, high expression of LINC00319 was correlated with adverse survival in BCA patients. LINC00319 could bind directly with miR-3127 and inhibited its expression, and the tumor-promoting effects of LINC00319 could be reversed by re-expression of miR-3127 in BCA cells. Our findings indicated that lncRNA LINC00319-mediated miR-3127 repression promotes BCA progression through the upregulation of RAP2A. The re-introduction of miR-3127 or inhibition of LINC00319 might represent a promising therapeutic strategy for BCA treatment.

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Section: Discussionmentioning

confidence: 99%

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

Wang

Meng

2020

Front. Genet.

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“…The present study using lncRNA sequencing identified LINC00319 to be significantly upregulated in rCCL18treated OSCC cells. LINC00319 is located in the intergenic region of chromosome 21 and acts as an oncogene in various tumors including ovarian cancer, cutaneous squamous cell carcinoma, glioma, and lung cancer [27][28][29][30] . Previously, the upregulation of LINC00319 was found to be associated with a poor prognosis of cutaneous squamous cell carcinoma patients 28 .…”

Section: Discussionmentioning

confidence: 99%

“…LINC00319 is located in the intergenic region of chromosome 21 and acts as an oncogene in various tumors including ovarian cancer, cutaneous squamous cell carcinoma, glioma, and lung cancer [27][28][29][30] . Previously, the upregulation of LINC00319 was found to be associated with a poor prognosis of cutaneous squamous cell carcinoma patients 28 . In addition, LINC00319 was also found to accelerate tumor growth and metastasis in glioma and lung cancer 29,30 .…”

Section: Discussionmentioning

confidence: 99%

CCL18-induced LINC00319 promotes proliferation and metastasis in oral squamous cell carcinoma via the miR-199a-5p/FZD4 axis

Jiang

Liu

et al. 2020

Cell Death Dis

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Long non-coding RNAs (lncRNAs), which may be modulated by chemokines, are key regulators in many cancers including oral squamous cell carcinoma (OSCC). An understanding of lncRNAs involved in chemokine (CC motif) ligand 18 (CCL18)-induced OSCC promotion remains elusive. The present study using lncRNA sequencing found LINC00319 to be significantly upregulated in OSCC cells subjected to rCCL18 stimulation. Furthermore, LINC00319 knockdown was found to attenuate the carcinogenic function of CCL18 in OSCC, reducing OSCC proliferation, metastasis, epithelial-mesenchymal transition (EMT), and angiogenesis. LINC00319 was demonstrated to act as a ceRNA in OSCC, which directly responded to miR-199a-5p and rescued the repression of FZD4 by miR-199a-5p. Functionally, in vitro and in vivo experiments showed that LINC00319 promoted OSCC growth and metastasis via downregulating miR-199a-5p and upregulating FZD4. In vitro rescue assays demonstrated that miR-199a-5p inhibitor or FZD4 overexpression reversed the effects of LINC00319 silencing in OSCC. Importantly, the expression of miR-199a-5p and FZD4 were found to be mediated by CCL18, and miR-199a-5p mimics inhibited the CCL18-promoting effects in oral cancer cells. Taken together, these results evidenced a mechanism of CCL18 action in OSCC mediated through the LINC00319/miR-199a-5p/FZD4 signaling pathway, which may comprise a potential target for OSCC therapeutic development.

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“…LINC00319 is a recently identified lncRNA with elevated expression in cSCC shown to correlate with larger tumor size and lymphovascular invasion of cSCC [130]. LINC00319 promotes cSCC cell migration and invasion, and upregulates expression of MMP-2, MMP-9, and markers for epithelial-mesenchymal transition, E-cadherin, and vimentin [130].…”

Section: Precsit and Linc00319 Regulate Invasion Of Csccmentioning

confidence: 99%

Long non-coding RNAs in cutaneous biology and keratinocyte carcinomas

Piipponen

Nissinen

Kähäri

2020

Cell. Mol. Life Sci.

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Long non-coding RNAs (lncRNAs) are a largely uncharacterized group of non-coding RNAs with diverse regulatory roles in various biological processes. Recent observations have elucidated the functional roles of lncRNAs in cutaneous biology, e.g. in proliferation and differentiation of epidermal keratinocytes and in cutaneous wound repair. Furthermore, the role of lncRNAs in keratinocyte-derived skin cancers is emerging, especially in cutaneous squamous cell carcinoma (cSCC), which presents a significant burden to health care services worldwide and causes high mortality as metastatic disease. Elucidation of the functions of keratinocyte-specific lncRNAs will improve understanding of the molecular pathogenesis of epidermal disorders and skin cancers and can be exploited in development of new diagnostic and therapeutic applications for keratinocyte carcinomas. In this review, we summarize the current evidence of functionally important lncRNAs in cutaneous biology and in keratinocyte carcinomas.

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Upregulation of LINC00319 indicates a poor prognosis and promotes cell proliferation and invasion in cutaneous squamous cell carcinoma

Cited by 31 publications

References 36 publications

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

CCL18-induced LINC00319 promotes proliferation and metastasis in oral squamous cell carcinoma via the miR-199a-5p/FZD4 axis

Long non-coding RNAs in cutaneous biology and keratinocyte carcinomas

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