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      KCI등재 SCIE SCOPUS

      Molecular mechanism of long non-coding RNA SNHG12 regulating bladder cancer cell activities

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      https://www.riss.kr/link?id=A109283588

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      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.
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      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 ...

      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.

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