LncRNA HAGLR May Aggravate Melanoma Malignancy Via miR-4644/ASB11 Pathway

In this study, we aimed to assess the biological functions of HAGLR and its underlying mechanisms in melanoma. HAGLR and ASB11 were knocked down by transfection with the corresponding siRNAs. Meanwhile, miR-4644 was downregulated using the miR-4644 inhibitor treatment. The target interactions among the three molecules were demonstrated using dual-luciferase reporter and RNA immunoprecipitation assays. The levels of HAGLR, miR-4644, and ASB11 in melanoma cells and tissues were assessed using quantitative real‑time PCR and western blotting. The functions and mechanisms underlying HAGLR action in melanoma progression were examined using Cell Counting Kit-8, Transwell, Caspase-3 activity, and xenograft tumor formation assays. HAGLR and ASB11 expression were elevated, whereas that of miR-4644 was downregulated in melanoma cells and tissues. The viability and migration of melanoma cells (A875 and A375) were markedly suppressed by the knockdown of HAGLR and ASB11 but promoted following miR-4644 inhibitor transfection. In contrast, apoptosis showed the opposite trend. In vivo, tumor weight declined considerably with downregulation of HAGLR. Mechanistically, HAGLR sponges miR-4644, increasing the levels of ASB11 and further aggravating melanoma. It latter negatively targets ASB11 in melanoma cells. Hence, the HAGLR-miR-4644-ASB11 axis may be a promising target for melanoma treatment.