Article Sidebar
Published:
Oct 21, 2021Keywords:
Article Details
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.
Main Article Content
MiR-331-5p suppresses gastric cancer cell proliferation, migration, invasion, and glycolysis via targeting PFKFB3
Abstract
Purpose: To examine the role of microRNAs (miRNAs), miR-331-5p, in gastric cancer (GC).
Methods: The mRNA level of miR-331-5p and protein level of 6-phosphofructo-2-kinase/fructose-2,6- bisphosphatase-3 (PFKFB3) were determined using quantitative real-time reverse transcription– polymerase chain reaction (qRT–PCR) and western blotting, respectively. The cell viability and proliferation of the two GC cell lines (AGS and MKN45) were evaluated using Cell Counting Kit-8 (CCK8) and bromodeoxyuridine (BrdU) ssays. Cell migration and invasion of AGS and MKN45 were evaluated using wound healing and invasion assays, respectively. Potential interactions between miR331-5p and PFKFB3 were assessed by luciferase activity assay, while the effects of the interactions on cell physiology and metabolism were investigated in cells verexpressing both miR-331-5p and PFKFB3.
Results: MiR-331-5p overexpression inhibited cell proliferation, suppressed migration and invasion, and inhibited glycolysis in AGS and MKN45 cells. The mRNA for the glycolytic regulatory enzyme PFKFB3 was shown to be a direct target of miR-331-5p and modulated by miR-331-5p. In rescue experiments, PFKFB3 reversed the miR-331-5p-induced inhibition of proliferation, migration, invasion, and glycolysis in AGS cells.
Conclusion: This work supports a role for miR-331-5p through the modulation of PFKFB3 activity in GC in vivo, thus providing insight into novel potential therapies for the treatment of GC.
