ArticleOpen medicine (Warsaw, Poland)2025
Peptide CCAT1-70aa promotes hepatocellular carcinoma proliferation and invasion via the MAPK/ERK pathway.
Article in Open medicine (Warsaw, Poland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Peptide-encoding roles of lncRNAs are emerging in cancer biology. This study explores the function of the CCAT1-70aa peptide in hepatocellular carcinoma (HCC) and its underlying mechanisms. Methods: Immunohistochemistry was used to detect CCAT1-70aa expression in HCC and adjacent tissues. An expression vector verified CCAT1's role in encoding CCAT1-70aa. Cell counting kit-8 and Transwell assays assessed the effects of CCAT1-70aa on HCC cell proliferation and invasion. Small-interfering RNAs (siRNAs) targeting CCAT1 were transfected into HCC cells to examine CCAT1-70aa expression. The role of the MAPK/ERK pathway was confirmed via Western blot and the ERK inhibitor FR180204. Results: CCAT1-70aa was significantly upregulated in HCC tissues, correlating with tumor stage, serum alpha-fetoprotein levels, and vascular invasion. siRNA-mediated CCAT1 silencing reduced CCAT1-70aa expression, supporting that CCAT1-70aa is translated from lncRNA CCAT1. CCAT1-70aa, a 70-amino acid peptide, enhanced proliferation and invasion, activating the MAPK/ERK pathway, with its effects mitigated by ERK inhibition. Conclusion: The CCAT1-70aa peptide is overexpressed in HCC and linked to aggressive tumor characteristics. It promotes proliferation and invasion via the MAPK/ERK pathway, providing insights for HCC diagnosis and treatment strategies.
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