Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Oct 10;114(12):4747–4762. doi: 10.1111/cas.15989

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2023 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

PMC Copyright notice

DLGAP1‐AS2 upregulates HK2 expression by sponging miR‐451a. (A, B) Cellular localization of DLGAP1‐AS2 determined by subcellular fractionation assay and FISH. (C) A Venn diagram of the intersection of miRNAs predicted by the targetScan and lncRNASNIP2 databases. (D) RT‐qPCR analysis of miR‐451a expression in osteosarcoma (OS) cell lines and hFOB 1.19 cells. (E) Overexpression efficiency of miR‐451a shown by RT‐qPCR. (F) Possible binding site of DLGAP1‐AS2/HK2 to miR‐451a. (G) Luciferase reporter assay for validation of the interaction between DLGAP1‐AS2 and miR‐451a. (H) The interactions among DLGAP1‐AS2, miR‐451a, and HK2 were verified by luciferase reporter assay. (I) The impact of miR‐451a overexpression and silenced DLGAP1‐AS2 on HK2 protein level shown by western blotting. **p < 0.01, ***p < 0.001.