Melanoma is one of the severe skin cancers, accounting for three fourths of all deaths caused by skin cancers and gathering attention from researchers. Previous studies have elucidated that long noncoding RNAs (lncRNA) engage actively in tissue physiology and disease development, especially in tumorigenesis. LncRNA LHFPL3 antisense RNA 1 (LHFPL3-AS1) has rarely been mentioned in researches regarding cancers; therefore, the underlying role and function of LHFPL3-AS1 in melanoma arouse our interest. Data from our work suggested that LHFPL3-AS1 expression was markedly elevated in melanoma tissues and cells. Of note, patients with melanoma with high level of LHFPL3-AS1 were burdened with unfavorable prognosis. Functionally, it has been revealed that LHFPL3-AS1 exerted pro-growth, pro-invasion, and pro-EMT functions in melanoma. Mechanistically, it was figured out that LHFPL3-AS1 could be transcriptionally activated by STAT3. In turn, LHFPL3-AS1 served as a sponge of miR-580-3p to augment STAT3 expression, resulting in activated JAK2/STAT3 signaling pathway in melanoma. Implications: Our study revealed a novel positive feedback loop LHFPL3-AS1/miR-580-3p/STAT3 in melanoma, which might contribute to finding potential therapeutic targets for melanoma.

中文翻译：

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LHFPL3-AS1/miR-580-3p/STAT3 反馈回路通过激活 JAK2/STAT3 信号促进黑色素瘤的恶性程度

黑色素瘤是严重的皮肤癌之一，占皮肤癌导致的所有死亡人数的四分之三，引起了研究人员的关注。先前的研究已经阐明，长链非编码 RNA (lncRNA) 积极参与组织生理学和疾病发展，尤其是在肿瘤发生中。LncRNA LHFPL3反义RNA 1（LHFPL3-AS1）在癌症研究中很少被提及；因此，LHFPL3-AS1 在黑色素瘤中的潜在作用和功能引起了我们的兴趣。我们的工作数据表明，LHFPL3-AS1 表达在黑色素瘤组织和细胞中显着升高。值得注意的是，具有高水平 LHFPL3-AS1 的黑色素瘤患者预后不良。在功能上，已经表明 LHFPL3-AS1 在黑色素瘤中发挥促生长、促侵袭和促 EMT 功能。从机制上讲，研究表明 LHFPL3-AS1 可以被 STAT3 转录激活。反过来，LHFPL3-AS1 充当 miR-580-3p 的海绵以增加 STAT3 表达，导致黑色素瘤中激活的 JAK2/STAT3 信号通路。启示：我们的研究揭示了黑色素瘤中一个新的正反馈回路 LHFPL3-AS1/miR-580-3p/STAT3，这可能有助于寻找黑色素瘤的潜在治疗靶点。