Suppressive effect of Hsa-miR-125a-5p on cervical cancer proliferation and invasion via regulation of Rab25- PI3K/AKT pathway
Abstract
Purpose: To study the suppressive effect of Hsa-miR-125a-5p on the proliferation and invasion of cervical cancer (CC) cells through the modulation of the Rab25-PI3K/AKT pathway.
Methods: 66 pairs of CC and neighboring cell samples were harvested from patients who underwent surgical resection in the Oncology Department from August 2017 to December 2018. The expression levels of Hsa-miR-125a-5p in CC and neighboring cell samples were assessed by quantitative polymerase chain reaction (qPCR). The overexpression vector was transfected into CC cells (siHa cell line), and the proliferation, invasion, migration, and apoptosis of siHa cells were determined. The regulatory role of Hsa-miR-125a-5p in PI3K/AKT pathway was determined using Western blotting.
Results: CC tissues, relative to the neighboring tissues, exhibited remarkably lower Hsa-miR-125a-5p levels (p < 0.05), and their upregulation significantly inhibited the growth, migration, and intrusion of siHa cells while repressing apoptosis (p < 0.05). Dual-luciferase reporter assay (DLRA) data indicate that luciferase activity decreased when Hsa-miR-125a-5p was bound to Rab25 (p < 0.05). The HsamiR-125a-5p mimics group had significantly lower PI3K/AKT levels, relative to the negative control mimics group (p < 0.05).
Conclusion: Hsa-miR-125a-5p represses CC cell proliferation and invasion through the modulation of Rab25-PI3K/AKT pathway, thus suggesting that this pathway is a target for drug development
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.