Abstract
Hepatic metastasis is a major cause of colorectal cancer (CRC)-related deaths. Presently, the role of long non-coding RNAs (lncRNAs) in hepatic metastases from CRC is elusive. We dissected possible interplay between LINC00858/miR-132-3p/IGF2BP1 via bioinformatics approaches. Subsequently we analyzed mRNA expression of LINC00858, miR-132-3p and IGF2BP1 through qRT-PCR. Western blot was used to detect protein expression of IGF2BP1. RNA immunoprecipitation chip and dual-luciferase assay validated interaction between LINC00858 and miR-132-3p, as well as miR-132-3p and IGF2BP1. Cell viability, invasion, and migration were examined via CCK-8, colony formation, transwell and wound healing assays. Effect of LINC00858 on CRC hepatic metastases was validated via in vivo assay. Upregulated LINC00858 and IGF2BP1, and downregulated miR-132-3p were predicted in tumor tissues of patients with hepatic metastases from CRC. There were targeting relationships between LINC00858 and miR-132-3p, as well as miR-132-3p and IGF2BP1. Besides, LINC00858 facilitated progression of CRC cells. Rescue assay suggested that silencing LINC00858 suppressed CRC cell progression, while further silencing miR-132-3p or overexpressing IGF2BP1 reversed such effects. LINC00858 could facilitate CRC tumor growth and hepatic metastases. LINC00858 induced CRC hepatic metastases via regulating miR-132-3p/ IGF2BP1, and this study may deliver a new diagnostic marker for the disease.
Funding source: Sanming Project of Medicine in Shenzhen
Award Identifier / Grant number: SZSM201911012
Funding source: Shenzhen High-level Hospital Construction Fund
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Research funding: This work was supported by Sanming Project of Medicine in Shenzhen (grant number: SZSM201911012) and Shenzhen High-level Hospital Construction Fund. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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Author contributions: Conception and design: Peng Sun, Yusong Luan. Administrative support: Yinggang Chen, Peide Ren, Peng Sun. Provision of study materials: Xuhao Cai, Qi Liu, Peide Ren, Pengpan Xin. Collection and assembly of data: Yonggang Yu, Bolun Song, Yangyang Wang. Data analysis and interpretation: Huijing Chang, Haoyue Ma, Peng Sun, Yusong Luan. Manuscript writing: All authors. Final approval of manuscript: All authors
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Conflict of interest statement: The authors declare that they have no competing interests.
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Ethical approval: This study protocol was reviewed and approved by [Cancer Hospital, Chinese Academy of Medical Science], approval number [NCC2016JZ-06].
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Data availability: Data cannot be shared for confidentiality reasons. Queries about the data should be directed to the corresponding author.
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© 2023 Walter de Gruyter GmbH, Berlin/Boston
Articles in the same Issue
- Frontmatter
- Research Articles/Short Communications
- Protein Structure and Function
- Stoichiometry and architecture of the platelet membrane complex glycoprotein Ib-IX-V
- Characterization of the active site in the thiocyanate-forming protein from Thlaspi arvense (TaTFP) using EPR spectroscopy
- Molecular Medicine
- Salvia miltiorrhiza augments endothelial cell function for ischemic hindlimb recovery
- Cell Biology and Signaling
- LINC00858 facilitates formation of hepatic metastases from colorectal cancer via regulating the miR-132-3p/IGF2BP1 axis
- Mechanism of hypoxia-induced exosome circ_0051799 regulating the progression of lung adenocarcinoma
Articles in the same Issue
- Frontmatter
- Research Articles/Short Communications
- Protein Structure and Function
- Stoichiometry and architecture of the platelet membrane complex glycoprotein Ib-IX-V
- Characterization of the active site in the thiocyanate-forming protein from Thlaspi arvense (TaTFP) using EPR spectroscopy
- Molecular Medicine
- Salvia miltiorrhiza augments endothelial cell function for ischemic hindlimb recovery
- Cell Biology and Signaling
- LINC00858 facilitates formation of hepatic metastases from colorectal cancer via regulating the miR-132-3p/IGF2BP1 axis
- Mechanism of hypoxia-induced exosome circ_0051799 regulating the progression of lung adenocarcinoma