We have located links that may give you full text access.
Geniposide suppresses growth, migration and invasion of MKN45 cells by down-regulation of lncRNA HULC.
Experimental and Molecular Pathology 2018 August 32
Gastric cancer (GC) is a serious disease with high incidence rate and high mortality. Geniposide (GEN) exhibits multiple biological properties including anti-tumor function. However, effect of GEN on GC is not well studied. Hence, the effects of GEN on GC were investigated in our study. HULC expression in GC tissue and GC cell lines (MKN45, SGC-7901, MKN28, AGS) was detected by qRT-PCR. Cell viability, colony formation, migration, invasion and cell apoptosis were examined by CCK-8 assay, survival fraction assay, modified two-chamber migration assay, Millicell Hanging Cell Culture and flow cytometry analysis, respectively. The expression of matrix metalloproteinase (MMP)-2/9 and vimentin was detected by qRT-PCR and western blot, respectively. The expression of PI3K/AKT and JNK was measured by western blot. The expression of HULC was up-regulated both in GC tissue and cell lines (P < .05, P < .01 or P < .001). GEN negatively regulated the expression of HULC in MKN45 cells (P < .05 or P < .01). GEN decreased cell viability (P < .05), colony formation (P < .01), migration (P < .05) and invasion (P < .05) while HULC overexpression led to the opposite results in GEN-treated cells. The expression of phosphatidylinositol 3' -kinase (PI3K)/ protein kinase B (AKT) and c-Jun N-terminal kinase (JNK) was down-regulated by GEN (all P < .05) while reversed by HULC overexpression. HULC was up-regulated in GC. GEN inhibited MNK45 cell viability, colony formation, migration and invasion while induced cell apoptosis by down-regulation of HULC in MKN45 cells. GEN inactivated PI3K/AKT and JNK signal pathways through down-regulation of HULC.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app