Translational cancer research · 2026
Lnc-TIM3 promotes acute lymphoblastic leukemia progression through miR-5094-mediated regulation of TIM3.
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Sun Jing, Zhao Jiou, Fu Wenfeng, Li Huimin, Kang Meiyun, Fang Yongjun, Wang Yaping
Аннотация
BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most common hematologic malignancy in children and is associated with dysregulated long non-coding RNAs (lncRNAs), some of which may serve as potential biomarkers and therapeutic targets. However, the expression pattern and biological role of Lnc-TIM3 in pediatric ALL remain poorly understood. This study aimed to characterize Lnc-TIM3 expression in pediatric ALL and investigate its functional role and underlying regulatory mechanism, with a particular focus on the Lnc-TIM3/miR-5094/TIM3 axis.
METHODS: The expression levels of lncRNAs, microRNAs (miRNAs), and messenger RNAs (mRNAs) were measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, DNA synthesis, migration, and invasion capabilities were assessed using Cell Counting Kit-8 (CCK-8) assays, soft-agar colony assays, flow cytometry, and in vitro transduction experiments, respectively. In vivo validation was conducted using a zebrafish model. The competitive endogenous RNA (ceRNA) regulatory mechanism was examined using dual-luciferase reporter assays, whereas protein expression was assessed by Western blotting.
RESULTS: Lnc-TIM3 was highly expressed in primary bone marrow samples from patients with ALL and in ALL cell lines. Lnc-TIM3 knockdown reduced TIM3 expression and significantly inhibited ALL progression in both in vitro and in vivo models. Furthermore, inhibition of miR-5094 partially reversed the phenotypic effects of Lnc-TIM3 knockdown. Changes in GAL9 and downstream signaling components suggested, but did not establish, the involvement of TIM3/GAL9-related signaling.
CONCLUSIONS: Lnc-TIM3 promotes the progression of ALL by binding to miR-5094 and upregulating TIM3 expression.
METHODS: The expression levels of lncRNAs, microRNAs (miRNAs), and messenger RNAs (mRNAs) were measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, DNA synthesis, migration, and invasion capabilities were assessed using Cell Counting Kit-8 (CCK-8) assays, soft-agar colony assays, flow cytometry, and in vitro transduction experiments, respectively. In vivo validation was conducted using a zebrafish model. The competitive endogenous RNA (ceRNA) regulatory mechanism was examined using dual-luciferase reporter assays, whereas protein expression was assessed by Western blotting.
RESULTS: Lnc-TIM3 was highly expressed in primary bone marrow samples from patients with ALL and in ALL cell lines. Lnc-TIM3 knockdown reduced TIM3 expression and significantly inhibited ALL progression in both in vitro and in vivo models. Furthermore, inhibition of miR-5094 partially reversed the phenotypic effects of Lnc-TIM3 knockdown. Changes in GAL9 and downstream signaling components suggested, but did not establish, the involvement of TIM3/GAL9-related signaling.
CONCLUSIONS: Lnc-TIM3 promotes the progression of ALL by binding to miR-5094 and upregulating TIM3 expression.