Article Sidebar
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
Shikonin suppresses the proliferation and colony formation of gastric cancer cells by regulating miR96/SOCS4 pathway
Abstract
Purpose: To investigate whether shikonin is able to inhibit cell proliferation and colony formation in gastric cancer (GC) cells and to elucidate the molecular mechanism.
Methods: Gastric cancer (GC) cell line SGC-7901 was used. The effects of shikonin on SGC-7901 cells were evaluated using Cell Counting Kit-8 (CCK-8) and soft-agar colony formation assays, respectively. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was employed to measure miR-96 expression levels. The regulatory effect of miR-96 on SOCS4 was determined by luciferase activity assay, while the effect of shikonin and miR-96 overexpression on proliferating cell nuclear antigen (PCNA), cyclin D1, suppressor of cytokine signaling 4 (SOCS4), and JAK/STAT pathwayrelated protein expression levels were analyzed by western blots.
Results: The results show that shikonin dose-dependently suppressed the proliferation and colony formation of SGC-7901 cells. Western blot analysis revealed that PCNA and cyclin D1 were downregulated by shikonin treatment. Luciferase activity assay demonstrated that miR-96 is directly bound to SOCS4. Further results showed that miR-96 mimics reversed the effects of shikonin on SOCS4 and JAK/STAT pathway-related protein expression levels.
Conclusion: Shikonin suppresses proliferation and colony formation by regulating miR-96/SOCS4 pathway in SGC-7901 cells, providing a potential therapeutic target for GC.
