論文 - 詳細
| RRC ID | 69855 |
|---|---|
| 著者 | Qian Y, Liu X, Feng Y, Li X, Xuan Y. |
| タイトル | Tenascin C regulates cancer cell glycolysis and tumor progression in prostate cancer. |
| ジャーナル | Int J Urol |
| Abstract |
OBJECTIVES:Tenascin C is a potential biomarker of cancer-associated fibroblasts and has been significantly associated with poor prognosis in patients with prostate cancer. However, the effects of Tenascin C in prostate cancer cell glycolysis largely remain unclear. Thus, this study aimed to investigate the Tenascin C expression in prostate cancer and its correlation to glycolysis-related protein and gene expression, clinicopathological parameters, and survival of patients. METHODS:We performed immunohistochemical staining for Tenascin C in 141 cases of primary prostate cancer. Based on public data sets, we explored the association of Tenascin C with angiogenesis-related genes, M2 macrophage-related gene, androgen receptor levels, PI3K/AKT/NF-κB pathway genes, and glycolytic enzyme expression. The glucose uptake, lactate production, and glycolytic enzyme levels were detected by glycolysis assay and western blotting. RESULTS:Our results showed that Tenascin C expression is upregulated in prostate cancer tissues compared with benign prostatic hyperplasia tissues. High Tenascin C expression in prostate cancer cells was positively associated with lymph node metastasis, advanced clinical stage, the expression of CD105, CD206, and androgen receptor levels. The Kaplan-Meier curves showed a significant association of Tenascin C expression with the patient's overall survival. Tenascin C expression was positively associated with PI3K p85, pAKT-ser308, and NF-κB p65 protein expression in prostate cancer samples. Moreover, siRNA-mediated knockdown of Tenascin C expression inhibited cell glucose uptake, lactate production, and glycolytic-enzyme expression in prostate cancer cells in vitro. CONCLUSIONS:Together, our findings suggest that Tenascin C is a prognostic marker for patients with prostate cancer and that its effects might be mediated via regulation of the glycolysis process of prostate cancer cells. |
| 巻・号 | 29(6) |
| ページ | 578-585 |
| 公開日 | 2022-6-1 |
| DOI | 10.1111/iju.14830 |
| PMID | 35218089 |
| MeSH | Cell Line, Tumor Glucose Glycolysis Humans Lactates Male NF-kappa B / metabolism Phosphatidylinositol 3-Kinases / metabolism Prostatic Neoplasms* / pathology Receptors, Androgen / metabolism Tenascin / genetics Tenascin / metabolism* |
| IF | 2.445 |
| リソース情報 | |
| ヒト・動物細胞 | PC-3(RCB2145) DU145(RCB2143) |