RESUMEN
Nucleobindin2 (NUCB2) is a member of nucleobindin family which was first found in the nucleus of the hypothalamus, and had a relationship in diet and energy homeostasis. Its location in normal tissues such as stomach and islet further confirms that it plays a vital role in the regulation of physiological functions of the body. Besides, NUCB2 participates in tumorigenesis through activating various signal-pathways, more and more studies indicate that NUCB2 might impact tumor progression by promoting or inhibiting proliferation, apoptosis, autophagy, metastasis, and invasion of tumor cells. In this review, we comprehensively stated NUCB2's expression and functions, and introduced the role of NUCB2 in physiology and pathology and its mechanism. What is more, pointed out the potential direction of future research.
Asunto(s)
Proteínas de Unión al Calcio , Proteínas del Tejido Nervioso , Proteínas de Unión al Calcio/metabolismo , Proteínas de Unión al ADN/metabolismo , Hipotálamo/metabolismo , Proteínas del Tejido Nervioso/genética , Proteínas del Tejido Nervioso/metabolismo , NucleobindinasRESUMEN
Sorafenib is a multikinase inhibitor capable of facilitating apoptosis, mitigating angiogenesis and suppressing tumor cell proliferation. In late-stage hepatocellular carcinoma (HCC), sorafenib is currently an effective first-line therapy. Unfortunately, the development of drug resistance to sorafenib is becoming increasingly common. This study aims to identify factors contributing to resistance and ways to mitigate resistance. Recent studies have shown that epigenetics, transport processes, regulated cell death, and the tumor microenvironment are involved in the development of sorafenib resistance in HCC and subsequent HCC progression. This study summarizes discoveries achieved recently in terms of the principles of sorafenib resistance and outlines approaches suitable for improving therapeutic outcomes for HCC patients.
Asunto(s)
Carcinoma Hepatocelular/tratamiento farmacológico , Resistencia a Antineoplásicos/genética , Neoplasias Hepáticas/tratamiento farmacológico , Sorafenib/uso terapéutico , Apoptosis/efectos de los fármacos , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patología , Proliferación Celular/efectos de los fármacos , Resistencia a Antineoplásicos/efectos de los fármacos , Humanos , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patología , Sorafenib/efectos adversos , Microambiente Tumoral/efectos de los fármacosRESUMEN
OBJECTIVE: The aim of this study was to investigate the role of LONP1 in the progression of pancreatic cancer. METHODS: Lentivirus was used to silence LONP1 in PANC-1 cells. Colony formation assay, cell counting kit (CCK8) assay, cell scratch-wound assay, and transwell assay were used to assess the effects of our strategy on inhibiting cancer growth, migration, and invasion. Protein expression was detected by Western blot analysis. RESULTS: The expression of LONP1 in pancreatic carcinoma tissues was higher than that in adjacent normal pancreatic tissues. Downregulation of LONP1 suppressed the proliferation, migration, and invasion of PANC-1 cells. Knockdown of LONP1 in PANC-1 cells inhibited epithelial-mesenchymal transition and matrix metalloprotein (MMP) 2/9 by downregulation of vimentin, snail, slug, MMP2, and MMP9 and upregulation of claudin-1. The c-Jun N-terminal kinase pathway was inactivated in LONP1 knockdown PANC-1 cells. Activation of the c-Jun N-terminal kinase pathway by anisomycin treatment significantly reversed the changes in epithelial-mesenchymal transition markers and MMP2/9 induced by ablation of LONP1 in PANC-1 cells. CONCLUSIONS: LONP1 plays a vital role in the proliferation and metastasis of pancreatic cancer, which provides a potential therapeutic target for the treatment of pancreatic cancer.