Background

Bladder cancer (BC) originating from the bladder mucosa is a malignant tumor of the genitourinary system. Long non-coding RNAs (lncRNAs) can participate in cell proliferation and differentiation at multiple levels, and lncRNA dysregulation involves in the processes of malignant tumors.

Methods

Focused on lncRNA small nucleolar RNA host gene 12 (SNHG12) and its target miR-143-3p, the specific mechanism related to BC was discovered. SNHG12 and miR-143-3p expression in BC samples was checked, together with the association with the malignant activities of BC cells.

Results

As texted, SNHG12 expression went upward and miR-143-3p expression went downward in BC. SNHG12 depletion or miR-143-3p over-expression was causal for the suppression of BC cell activities. SNHG12 expression was directly associated with miR-143-3p expression. Ablating miR-143-3p abrogated changes in BC cell function induced by SNHG12 depletion.

Conclusions

Generally, SNHG12/miR-143-3p induces the malignant activities of BC cells.

中文翻译：

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长链非编码RNA SNHG12调控膀胱癌细胞活性的分子机制

背景

膀胱癌（BC）是起源于膀胱粘膜的泌尿生殖系统恶性肿瘤。长链非编码RNA（lncRNA）可在多个水平参与细胞增殖和分化，lncRNA失调参与恶性肿瘤的发生过程。

方法

重点关注lncRNA小核仁RNA宿主基因12（SNHG12）及其靶标miR-143-3p，发现了与BC相关的具体机制。检查 BC 样本中的 SNHG12 和 miR-143-3p 表达，以及与 BC 细胞恶性活动的关联。

结果

正如文本所述，BC 中 SNHG12 表达上升，miR-143-3p 表达下降。SNHG12 缺失或 miR-143-3p 过表达是 BC 细胞活性抑制的原因。SNHG12 表达与 miR-143-3p 表达直接相关。消除 miR-143-3p 消除了 SNHG12 耗竭引起的 BC 细胞功能变化。

结论

一般来说，SNHG12/miR-143-3p会诱导BC细胞的恶性活动。