ArticleArchives of pharmacal research2021
Chemerin reverses the malignant phenotype and induces differentiation of human hepatoma SMMC7721 cells.
Article in Archives of pharmacal research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 9 citations in OpenAlex.
- Chemerin and the Gut: From Inflammation to Cancer.Biomedicines · 2025Review
- Exploring the role of adipokines in exercise-induced inhibition of tumor growth.Sports medicine and health science · 2025Article
- Anti-Tumoral Effect of Chemerin on Ovarian Cancer Cell Lines Mediated by Activation of Interferon Alpha Response.Cancers · 2022Article
- Chemerin enhances mesenchymal features of glioblastoma by establishing autocrine and paracrine networks in a CMKLR1-dependent manner.Oncogene · 2022Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Chemerin exhibits an inhibitory effect on hepatocellular carcinoma; however, the underlying mechanism is unclear. Here, low chemerin expression was confirmed in samples of liver cancer patients and hepatoma cells. Chemerin altered hepatoma cell morphology but had no effect on normal hepatocytes. Chemerin inhibited proliferation of several human hepatoma cell lines. Real-time PCR detection of hepatocellular carcinoma markers showed that mRNA levels of albumin and A-type gamma-glutamyl transferase increased whereas those of alpha-fetoprotein, alkaline phosphatase, B-type gamma-glutamyl transferase, insulin-like growth factor II, and human telomerase reverse transcriptase decreased in chemerin-treated SMMC7721 cells. Western blotting revealed that chemerin up-regulated albumin and vimentin expressions, and downregulated alpha-fetoprotein expression. Phosphorylated STAT3 was significantly up-regulated, whereas phosphorylated ERK and AKT were significantly downregulated by chemerin. Chemerin decreased phosphorylated ERK and AKT expression and the cell proliferation induced by PI3K activator 740 Y-P but could not significantly alter phosphorylated STAT3 expression and the cell growth induced by STAT3 inhibitor NSC74859. In conclusion, chemerin reversed the malignant phenotype and induced SMMC7721 cell differentiation by inhibiting MAPK/ERK and PI3K/AKT signaling; growth inhibition by chemerin is not directly related to the JAK/STAT signaling pathway. Our study provides novel evidence that chemerin could be utilized for liver cancer treatment.
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