The emerging role of long non‐coding <scp>RNA</scp>s in cutaneous melanoma

Leucci, Eleonora; Coe, Elizabeth A.; Marine, Jean–Christophe; Vance, Keith W.

doi:10.1111/pcmr.12537

Cited by 57 publications

(43 citation statements)

References 65 publications

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“…The incidence of MM is rising more rapidly than any other prevalent cancers [2]. MM accounts for the vast majority of skin cancer patient deaths [3]. MM has proclivity to metastasize, and patients with metastatic MM has a poor prognosis [4].…”

Section: Introductionmentioning

confidence: 99%

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

Xue

Chen²,

Chen

et al. 2020

Bioscience Reports

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The present study aimed to investigate the effects of lncRNA FENDRR on the migration and invasion of malignant melanoma (MM) cells. The expression levels of FENDRR in MM tissues and MM cell lines were detected using qRT-PCR, followed by construction of FENDRR-knocked down and overexpressed stable cells. Then the effects of FENDRR on cell proliferation, migration and invasion were detected using MTT assay and Transwell assay. The protein expression levels of matrix metallopeptidase 2 (MMP2), MMP9, and related factors in JNK/c-Jun pathway were detected using Western blot. FENDRR was down-regulated in MM tissues and cell lines. Besides, its expression levels in different MM cells were diverse. Knockdown of FENDRR facilitated MM cells proliferation, migration and invasion in A375 cells, while overexpressing FENDRR had reverse results. In addition, MMPs and JNK/c-Jun pathway involved in the FENDRR-mediated regulation of MM cell proliferation, migration and invasion. Our results demonstrated that FENDRR mediated the metastasis phenotype of MM cells by inhibiting the expressions of MMP2 and MMP9 and antagonizing the JNK/c-Jun pathway.

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Section: Introductionmentioning

confidence: 99%

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

Xue

Chen²,

Chen

et al. 2020

Bioscience Reports

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“…BRAF-activated non-coding RNA (BANCR), a 693-bp lncRNA on chromosome 9, has been reported to exert oncogenic acvities in many cancers under some specific conditions, such as non-small cell lung cancer, papillary thyroid carcinoma and colorectal cancer (14)(15)(16). Recent studies reported that BANCR is abnormally overexpressed in human malignant melanoma cell lines and tissues, and promotes proliferation and migration in malignant melanoma (17,18). These results suggest the oncogenic role and potential of BANCR as a therapeutic target for melanoma.…”

Section: Introductionmentioning

confidence: 99%

BANCR contributes to the growth and invasion of melanoma by functioning as a competing endogenous RNA to upregulate Notch2 expression by sponging miR-204

Cai

Zheng

et al. 2017

International Journal of Oncology

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BRAF-activated non-coding RNA (BANCR) is a long non-coding RNA (lncRNA) that contributes to the initiation and development of many solid tumors, including melanoma. However, the BANCR functions and downstream mechanisms are largely unknown. In this study, we aim to investigate how BANCR participates in the proliferation and migration of malignant melanoma and elucidate the underlying mechanism in this process. We found that the expression of the BANCR was low in melanocytic nevus and human melanocytes but high in melanoma tissues and cell lines. Knockdown of BANCR inhibited melanoma cell proliferation and invasion, and induced cell apoptosis. The decreased expression of relative marker proteins further demonstrated the inhibitory effect of BANCR siRNA in cell growth and migration. Then, we detected downregulation of microRNA-204 (miR‑204), a suppressor of melanoma growth, in melanoma tissues and cell lines. We identified that miR‑204 was a direct target of BANCR and neurogenic locus notch homolog protein 2 (Notch2) was a direct target of miR‑204. BANCR may promote melanoma cell growth through inhibition of miR‑204, leading to the activation of Notch2 pathway. By tumorigenicity assay in BALB/c nude mice, we further demonstrated that BANCR knockdown inhibited tumor growth in vivo. Our results suggest the BANCR/miR‑204/Notch2 axis mediates melanoma cell proliferation and tumor progression.

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“…Genomewide association studies have recently mapped a large proportion of disease‐ or trait‐associated single nucleotide polymorphisms outside the protein coding regions of the genome, often in or near genes transcribed into lncRNAs (Bartonicek et al, ; Gong, Liu, Zhang, Miao, & Guo, ). There are bona fide examples of lncRNA linked to one or multiple hallmarks of cancer in a variety of cancers, including melanoma, in which many emerge as regulators of the MAPK and PI3K pathways (for review, Huang et al, ; Leucci, Coe, Marine, & Vance, ; Schmitt & Chang, ; Tasharrofi & Ghafouri‐Fard, ).…”

Section: Introductionmentioning

confidence: 99%

“…There are bona fide examples of lncRNA linked to one or multiple hallmarks of cancer in a variety of cancers, including melanoma, in which many emerge as regulators of the MAPK and PI3K pathways (for review, Huang et al, 2018;Leucci, Coe, Marine, & Vance, 2016;Schmitt & Chang, 2016;Tasharrofi & Ghafouri-Fard, 2018).…”

Section: Introductionmentioning

confidence: 99%

The lncRNA RMEL3 protects immortalized cells from serum withdrawal‐induced growth arrest and promotes melanoma cell proliferation and tumor growth

Cardoso

Serafim

Kawakami

et al. 2018

Pigment Cell Melanoma Res

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RMEL3 is a recently identified lncRNA associated with BRAFV600E mutation and melanoma cell survival. Here, we demonstrate strong and moderate RMEL3 upregulation in BRAF and NRAS mutant melanoma cells, respectively, compared to melanocytes. High expression is also more frequent in cutaneous than in acral/mucosal melanomas, and analysis of an ICGC melanoma dataset showed that mutations in RMEL3 locus are preponderantly C > T substitutions at dipyrimidine sites including CC > TT, typical of UV signature. RMEL3 mutation does not correlate with RMEL3 levels, but does with poor patient survival, in TCGA melanoma dataset. Accordingly, RMEL3 lncRNA levels were significantly reduced in BRAFV600E melanoma cells upon treatment with BRAF or MEK inhibitors, supporting the notion that BRAFMEK- ERK pathway plays a role to activate RMEL3 gene transcription. RMEL3 overexpression, in immortalized fibroblasts and melanoma cells, increased proliferation and survival under serum starvation, clonogenic ability, and xenografted melanoma tumor growth. Although future studies will be needed to elucidate the mechanistic activities of RMEL3, our data demonstrate that its overexpression bypasses the need of mitogen activation to sustain proliferation/survival of non-transformed cells and suggest an oncogenic role for RMEL3.

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The emerging role of long non‐coding RNAs in cutaneous melanoma

Cited by 57 publications

References 65 publications

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

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

BANCR contributes to the growth and invasion of melanoma by functioning as a competing endogenous RNA to upregulate Notch2 expression by sponging miR-204

The lncRNA RMEL3 protects immortalized cells from serum withdrawal‐induced growth arrest and promotes melanoma cell proliferation and tumor growth

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