MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.

摘要: HOTAIR (homeobox transcript antisense RNA), one of the prototypical long non-coding RNAs, has been verified overexpressed in multiple carcinomas and emerged as a promising novel anticancer target. Its well-established role is acting predictor poor prognosis promoting cancer cell metastasis. Recently, another important mission was uncovered that targeting caused apoptosis. Nevertheless, so far there no published data elaborating mechanism. Here, we report microRNA miR-125a-5p decreases releases caspase 2 to promote apoptosis after knockdown. We applied siRNAs various cells, observed all these lines. RNA sequencing detected decreased knockdown mimics could rescue induced by deficiency. Luciferase assays identified 2, an initiator caspase, be new target miR-125a-5p. Elevated expression subsequent cleavage or inhibition RNAi attenuate In 80 clinical colon tissues, levels were higher than adjacent whereas lower. MiR-125a-5p level significantly correlated with tumor size, lymph node metastasis stage. These findings indicate releasing 2. Our work reveals previously unidentified apoptotic mechanism, which might exploitable drug development.