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

. 2020 Oct 5;11:4980. doi: 10.1038/s41467-020-18735-8

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

© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 1 — a c-Myc bound to MILIP promoter in A549 and MCF-7 cells. An E-box motif, not associated with MYC target genes on Chr22, was used as a negative control. Data shown represent three independent experiments. ChIP, chromatin immunoprecipitation. b c-Myc silencing downregulated MILIP expression in A549 and MCF-7 cells. c-Myc responsive lncRNA OVAAL was used as a positive control. Data are mean ± s.d.; n = 3 independent experiments, one-way ANOVA followed by Tukey’s multiple comparisons test. c c-Myc silencing reduced the activity of reporters with intact c-Myc binding region (BR) of MILIP promoter but not that with the c-Myc-BR deleted (ΔBR) in A549 and MCF-7 cells. Data are mean ± s.d.; n = 3 independent experiments, two-tailed Student’s t test. d Representative microscopic photographs of in situ hybridization (ISH) analysis of MILIP expression in formalin-fixed paraffin-embedded (FFPE) lung adenocarcinoma (LUAD; n = 88 biologically independent samples) compared with paired adjacent normal tissues. Scale bar, 5 µm. e Quantitation of MILIP expression as detected in (d) in FFPE LUAD in comparison with paired adjacent normal tissues. RS, reactive score. Two-tailed Student’s t test. f Ingenuity Pathway Analysis (IPA) of RNA-seq data showing that p53 signaling was the most enriched pathway in A549 cells transfected with a MILIP siRNA (si-MILIP.2) relative to those introduced with the control siRNA. Orange bars represent pathways that were activated, and blue bars, inactivated. DEGs differentially expressed genes. g c-Myc knockdown upregulated p53 expression, which was diminished by MILIP overexpression in A549 and MCF-7 cells. Data are representatives or mean ± s.d.; n = 3 independent experiments, One-way ANOVA followed by Tukey’s multiple comparisons test. h c-Myc overexpression downregulated p53 expression, which was abolished by knockdown of MILIP in A549 and MCF-7 cells. Data shown represent three independent experiments. DOX, doxycycline, 200 ng/mL. Source data of Fig. 1a–c, e–h are provided as a Source Data file.