The calcimedin annexin A3 displays tumor-promoting effect in esophageal squamous cell carcinoma by activating NF-κB signaling
Autor: | Fengjin Liu, Xiaozhe Liu, Zhangzhan Wang, Shihao Gao, Bing Xu |
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Rok vydání: | 2021 |
Předmět: |
Esophageal Neoplasms
Mice Nude Biology 03 medical and health sciences Mice 0302 clinical medicine Downregulation and upregulation Western blot In vivo Cell Line Tumor Genetics medicine Animals Humans neoplasms Annexin A3 030304 developmental biology 0303 health sciences Mice Inbred BALB C Oncogene medicine.diagnostic_test Cell growth NF-kappa B digestive system diseases In vitro Cell culture 030220 oncology & carcinogenesis Cancer research Esophageal Squamous Cell Carcinoma Signal Transduction |
Zdroj: | Mammalian genome : official journal of the International Mammalian Genome Society. 32(5) |
ISSN: | 1432-1777 |
Popis: | Esophageal squamous cell carcinoma (ESCC) is one of the lethal malignancies commonly found in the eastern world, with overall five-year survival rates less than 25%. The present study aimed to investigate the biological function of annexin A3 (ANXA3) in ESCC cell proliferation. The mRNA and protein levels of ANXA3 in ESCC tissues and cell lines were determined by real-time PCR and Western blot, respectively. Lentiviral transduction was applied to overexpress or reduce ANXA3 expression in ESCC cell lines. The effect of ANXA3 on ESCC cell proliferation was evaluated by cell-counting kit-8 assay in vitro and tumor-bearing animal model in vivo. We found that ANXA3 was substantially upregulated in ESCC tissues compared to adjacent normal tissues as well as ESCC cell lines compared to normal esophageal endothelial cells. Suppression of ANXA3 significantly inhibited ESCC cell proliferation in vitro and tumor growth in vivo. We further revealed that NF-κB was involved in ANXA3-mediated ESCC cell proliferation. Our results suggest that ANXA3 acts as an oncogene in ESCC, and targeting ANXA3 or NF-κB may serve as potential therapeutic strategies for patients with ESCC. |
Databáze: | OpenAIRE |
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