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miR-3648 promotes lung adenocarcinoma-genesis by inhibiting SOCS2 (suppressor of cytokine signaling 2)

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ABSTRACT Lung adenocarcinoma (LUAD) is the most common histologic subtype of lung cancer and is associated with high morbidity and mortality. We aimed to study the effects of microRNA-3648 (miR-3648)… Click to show full abstract

ABSTRACT Lung adenocarcinoma (LUAD) is the most common histologic subtype of lung cancer and is associated with high morbidity and mortality. We aimed to study the effects of microRNA-3648 (miR-3648) on LUAD by inhibiting its downstream target suppressor of cytokine signaling 2 (SOCS2) mRNA. miR-3648 expression was measured by real-time quantitative PCR in LUAD and normal lung epithelial cell lines. The direct interaction between miR-3648 and SOCS2 mRNA was identified through luciferase reporter and RNA pull-down assays. Cell viability, migration, and invasion were examined using cell functional assays. MiR-3648 was found to be overexpressed in LUAD cells and tissues. Overexpression of miR-3648 significantly enhanced cell proliferation, migration, and invasion abilities in LUAD cells. Furthermore, SOCS2 was targeted by miR-3648, and co-transfection of a miR-3648 inhibitor or si-SOCS2 reversed the suppressive effects of SOCS2 in PC9 and A549 cells. miR-3648 enhanced the proliferation and promoted migration and invasion of LUAD by inhibiting SOCS2. In conclusion, our results indicate that miR-3648 plays a pivotal role in LUADe progression and might thus provide a novel therapeutic strategy for patients with LUAD.

Keywords: socs2; suppressor cytokine; mir; mir 3648; lung adenocarcinoma

Journal Title: Bioengineered
Year Published: 2022

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