ArticleThe Kaohsiung journal of medical sciences2013
Hepatocellular carcinoma cells cause different responses in expressions of cancer-promoting genes in different cancer-associated fibroblasts.
Article in The Kaohsiung journal of medical sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Hotspots and frontiers of the relationship between hepatocellular carcinoma and cancer-associated fibroblasts: a bibliometric analysis and review.Discover oncology · 2025Article
- MicroRNA as Key Players in Hepatocellular Carcinoma: Insights into Their Role in Metastasis.Biochemical genetics · 2025Review
- The impact of apelin on polarization of macrophages in the microenvironment of colon cancer.Central-European journal of immunology · 2025Article
- Prediction of CAF-related genes in immunotherapy and drug sensitivity in hepatocellular carcinoma: a multi-database analysis.Genes and immunity · 2024Article
- The LINC00152/miR-205-5p/CXCL11 axis in hepatocellular carcinoma cancer-associated fibroblasts affects cancer cell phenotypes and tumor growth.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Three-Dimensional Cell Culture Models of Hepatocellular Carcinoma - a Review.Journal of gastrointestinal cancer · 2021Review
- Cancer-associated fibroblast-derived CXCL11 modulates hepatocellular carcinoma cell migration and tumor metastasis through the circUBAP2/miR-4756/IFIT1/3 axis.Cell death & disease · 2021Article
- Study Progression of Apelin/APJ Signaling and Apela in Different Types of Cancer.Frontiers in oncology · 2021Review
- Primary cultures of aspiration residual specimens predict outcomes of hepatocellular carcinoma patients receiving curative treatment.The Kaohsiung journal of medical sciences · 2020Article
- Primary culture of aspiration residual specimens improves the diagnostic accuracy between hepatocellular carcinoma and benign nodules.The Kaohsiung journal of medical sciences · 2020Article
- MicroRNA-195 suppresses the progression of lung adenocarcinoma by directly targeting apelin.Thoracic cancer · 2019Article
- Multiple Functions of Lysyl Oxidase Like-2 in Oral Fibroproliferative Processes.Journal of dental research · 2018Article
- Article
- Nab-paclitaxel interrupts cancer-stromal interaction through C-X-C motif chemokine 10-mediated interleukin-6 downregulation in vitro.Cancer science · 2018Article
- The Role of Apelin in Cardiovascular Diseases, Obesity and Cancer.Frontiers in physiology · 2018Review
- Resistance a major hindrance to chemotherapy in hepatocellular carcinoma: an insight.Cancer cell international · 2018Review
- Circulating LOXLPathogens & immunity · 2017Article
- Cancer-associated fibroblasts in hepatocellular carcinoma.World journal of gastroenterology · 2016Review
- CAF cellular glycolysis: linking cancer cells with the microenvironment.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Hepatoprotective and anti-tumor effects of targeting MMP-9 in hepatocellular carcinoma and its relation to vascular invasion markers.Clinical & experimental metastasis · 2015Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-associated fibroblast (CAF) is one of the most crucial components of the tumor microenvironment to promote the invasiveness of cancer cells. The interactions between cancer cells and CAFs are bidirectional. Our recent study showed that up-regulations of chemokine (C-C motif) ligand 2 (CCL2), chemokine (C-C motif) ligand 26 (CCL26), interleukin 6 (IL6), and lysyl oxidase-like 2 (LOXL2) genes in cancer cells were parts of the common effects of CAFs on hepatocellular carcinoma (HCC) cells to promote proliferation, migration and invasion of cancer cells. However, the subject of how HCC cells to influence the gene expressions of CAFs still needs to be clarified. The purpose of this study was to investigate this issue. Two human HCC (HCC24/KMUH, HCC38/KMUH) and two human CAF cell lines (F26/KMUH, F28/KMUH) were studied. Influence of HCC38/KMUH cancer cells on differential expressions of genes in F28/KMUH CAFs was detected by microarray to select target genes for further analysis. Both HCC cell lines increased proliferation (all p < 0.005) and migration (all p < 0.0001) of two CAF cell lines. HCC24/KMUH cancer cells had stronger ability to promote migration of F26/KMUH CAFs than HCC38/KMUH cancer cells did (p < 0.0001). Eleven up-regulated cancer-promoting genes, including apelin (APLN), CCL2, CCL26, fibroblast growth factor 1 (FGF1), fibroblast growth factor 2 (FGF2), IL6, mucin 1 (MUC1), LOXL2, platelet-derived growth factor alpha polypeptide (PDGFA), phosphoglycerate kinase 1 (PGK1), and vascular endothelial growth factor A (VEGFA) detected by microarray showed good correlation with results of quantitative reverse transcriptase-polymerase chain reaction study. Among these genes, HCC24/KMUH cancer cells had same tendency of effects on differential expressions of genes in F28/KMUH CAFs as HCC38/KMUH cancer cells did. However, the responses of F26/KMUH CAFs to different HCC cell lines were variable. Only PGK1 gene was consistently up-regulated and PDGFA gene was consistently down-regulated caused by both HCC cell lines in F26/KMUH CAFs. Besides PGK1 gene, HCC38/KMUH cancer cells only up-regulated APLN, LOXL2, and VEGFA genes and HCC24/KMUH cancer cells only up-regulated FGF2 gene in F26/KMUH CAFs. In conclusion, HCC cells can promote proliferation and migration of CAFs. However, the impact of HCC cells on differential expressions of cancer-promoting genes in CAFs is influenced by the characteristics of CAFs. This implies that blocking single or several particular cancer-promoting genes in CAFs is unable to become a common stratagem for the treatment of HCC.
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