Long non-coding RNA FENDRR inhibits migration and invasion of cutaneous malignant melanoma cells

Xue, Chen; Chen, Pu; Chen, Shanshan; Jin, Lu; Ma, Ting; Shi, Guang; Sheng, Liang

doi:10.1042/bsr20191194

Cited by 14 publications

(10 citation statements)

References 29 publications

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“…A similar story emerged when we compared lncRNA enriched with SFPQ in PM and melanoma cell backgrounds. The SFPQenriched lncRNA transcripts most specific to PM were EMX2OS and FENDRR, the latter reported to function as a tumour suppressor in most cancers, including melanoma [27,[46][47][48][49]. The function of EMX2OS in cancer differs depending on cell background [28,50].…”

Section: Discussionmentioning

confidence: 99%

“…Discerning the functional importance of enriched lncRNA gene lists from RNA-seq studies such as the one reported here is problematic, as the vast majority of lncRNAs remain functionally uncharacterised. However, it is interesting to note that the most PM-specific SFPQ-lncRNA interactors included genes associated with tumour suppressor function, such as EMX2OS and FENDRR [27,28], whereas the most A2058-specific SFPQ-lncRNA interactors comprise genes widely reported as oncogenic, such as LINC00511 [29][30][31]. We next sought to validate the top hits from our A2058 RIP-seq data in additional melanoma cell lines.…”

Section: Sfpq Knockdown Decelerates Cancer Cell Phenotype In Melanomamentioning

confidence: 99%

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SFPQ promotes an oncogenic transcriptomic state in melanoma

Anene

Nsengimana

et al. 2021

Oncogene

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The multifunctional protein, splicing factor, proline- and glutamine-rich (SFPQ) has been implicated in numerous cancers often due to interaction with coding and non-coding RNAs, however, its role in melanoma remains unclear. We report that knockdown of SFPQ expression in melanoma cells decelerates several cancer-associated cell phenotypes, including cell growth, migration, epithelial to mesenchymal transition, apoptosis, and glycolysis. RIP-seq analysis revealed that the SFPQ-RNA interactome is reprogrammed in melanoma cells and specifically enriched with key melanoma-associated coding and long non-coding transcripts, including SOX10, AMIGO2 and LINC00511 and in most cases SFPQ is required for the efficient expression of these genes. Functional analysis of two SFPQ-enriched lncRNA, LINC00511 and LINC01234, demonstrated that these genes independently contribute to the melanoma phenotype and a more detailed analysis of LINC00511 indicated that this occurs in part via modulation of the miR-625-5p/PKM2 axis. Importantly, analysis of a large clinical cohort revealed that elevated expression of SFPQ in primary melanoma tumours may have utility as a prognostic biomarker. Together, these data suggest that SFPQ is an important driver of melanoma, likely due to SFPQ–RNA interactions promoting the expression of numerous oncogenic transcripts.

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Section: Discussionmentioning

confidence: 99%

Section: Sfpq Knockdown Decelerates Cancer Cell Phenotype In Melanomamentioning

confidence: 99%

SFPQ promotes an oncogenic transcriptomic state in melanoma

Anene

Nsengimana

et al. 2021

Oncogene

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“…FENDRR is a long noncoding RNA located on chr3q13.31. Studies have shown that FENDRR is low expressed in a variety of tumor tissues and can inhibit tumor progression ( 26 , 27 ). However, the role of FENDRR in the development of OSCC is still unknown.…”

Section: Discussionmentioning

confidence: 99%

LncRNA FENDRR in Carcinoma-Associated Fibroblasts Regulates the Angiogenesis of Oral Squamous Cell Carcinoma Through the PI3K/AKT Pathway

Jiang

Shao

et al. 2021

Front. Oncol.

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Angiogenesis is essential for the development of tumors. Studies have shown that carcinoma-associated fibroblasts (CAFs) are involved in regulating tumor angiogenesis, but the mechanism remains unclear. Recently, long noncoding RNAs (lncRNAs) have been proved to play an important role in the angiogenesis of various tumors. However, there is currently no research involving the regulation of CAFs on the angiogenesis of oral squamous cell carcinoma (OSCC) mediated by lncRNAs. By analyzing microarray data, we identified that the expression of lncRNA FOXF1 adjacent noncoding developmental regulatory RNA (FENDRR) in OSCC patients is downregulated, compared to that in normal tissues. Quantitative polymerase chain reaction (qPCR) results demonstrated that FENDRR expression is lower in CAFs compared to normal fibroblasts (NFs) of OSCC patients. KEGG pathway analysis revealed that some genes differentially expressed between CAFs and NFs of HNSCC patients are enriched to the PI3K/AKT pathway. Further experiments confirmed that the downregulation of FENDRR can activate the PI3K/AKT pathway in NFs and enhances the expression of matrix metalloproteinase 9 (MMP9). The overexpression of FENDRR had the opposite effect. Besides, we co-cultured human umbilical vein endothelial cells (HUVECs) with CAFs, and the tube-forming ability of HUVECs co-cultured with CAFs overexpressing FENDRR decreased significantly. However, activation of the AKT pathway of CAFs overexpressing FENDRR can weaken the inhibitory effect of FENDRR on angiogenesis. In summary, our experiments are focused on the influence of lncRNAs in CAFs on OSCC angiogenesis for the first time and prove that FENDRR mediates CAFs’ regulation of OSCC angiogenesis through the PI3K/AKT pathway.

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“…For example, lncRNA forkhead box D3 antisense RNA 1 was previously discovered to increase CMM cell proliferation, invasion and migration by regulating the miR-325/mitogen-activated protein kinase kinase kinase 2 axis ( 11 ). In addition, the lncRNA FOXF1 adjacent non-coding developmental regulatory RNA was reported to inhibit the migration and invasion of CMM cells ( 12 ). The lncRNA TINCR ubiquitin domain containing (TINCR) was also found to function as a tumor suppressor in various types of cancer.…”

Section: Introductionmentioning

confidence: 99%

lncRNA TINCR attenuates the proliferation and invasion, and enhances the apoptosis of cutaneous malignant melanoma cells by regulating the miR‑424‑5p/LATS1 axis

et al. 2021

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Cutaneous malignant melanoma (CMM) is responsible for ≥1/2 of skin cancer-related mortalities. The aberrant expression of long non-coding RNAs (lncRNAs) has been associated with the development of CMM. However, to the best of our knowledge, the role of the lncRNA TINCR ubiquitin domain containing (TINCR) in CMM has not been previously investigated, and thus, the current study aimed to evaluate this in vitro and in vivo . Reverse transcription-quantitative PCR (RT-qPCR) was used to analyze microRNA (miR)-424-5p expression, and RT-qPCR and western blotting were used to measure TINCR, large tumor suppressor kinase 1 (LATS1), cellular communication network factor 2 (CTGF), cellular communication network factor 1 (CCN1) and AXL receptor tyrosine kinase (AXL) mRNA and protein expression levels, respectively. Cell Counting Kit-8, flow cytometry and Transwell assays were used to detect the proliferation, apoptosis and invasion of CMM cell lines, respectively. The binding sites between TINCR and miR-424-5p were predicted using the miRDB database. A dual luciferase reporter assay and RT-qPCR were used to identify the relationship between TINCR and miR-424-5p in CMM cell lines. The bioinformatics analysis revealed that TINCR was one of the most significantly downregulated lncRNAs in CMM, and advanced stage CMM tissues showed the greatest decrease in TINCR expression. Moreover, in the collected CMM tissues and tested cell lines of the current study, TINCR expression was found to be downregulated compared with the respective controls. Notably, TINCR overexpression inhibited the expression levels of CTGF, CCN1 and AXL, decreased the proliferation and invasion, and induced the apoptosis of CMM cell lines. In addition, a mutual binding association was identified between miR-424-5p and TINCR in CMM cells. LATS1, a target of miR-424-5p, was found to be positively regulated by TINCR. TINCR activated Hippo signaling and repressed the activity of Yes 1 associated transcriptional regulator by regulating LATS1 expression, while LATS1 knockdown reversed the effect of TINCR overexpression on CMM cells. Collectively, the findings of the present study suggested that TINCR may attenuate the progression of CMM by regulating the miR-424-5p/LATS1 signaling axis. These results indicated that TINCR may play a tumor suppressive role in CMM.

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Long non-coding RNA FENDRR inhibits migration and invasion of cutaneous malignant melanoma cells

Cited by 14 publications

References 29 publications

SFPQ promotes an oncogenic transcriptomic state in melanoma

SFPQ promotes an oncogenic transcriptomic state in melanoma

LncRNA FENDRR in Carcinoma-Associated Fibroblasts Regulates the Angiogenesis of Oral Squamous Cell Carcinoma Through the PI3K/AKT Pathway

lncRNA TINCR attenuates the proliferation and invasion, and enhances the apoptosis of cutaneous malignant melanoma cells by regulating the miR‑424‑5p/LATS1 axis

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