Histology and histopathology Vol.37,nº12 (2022)
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- PublicationOpen AccessHsa_circ_0048674 facilitates hepatocellular carcinoma progression and natural killer cell exhaustion depending on the regulation of miR-223-3p/PDL1(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Li, Suihui; Chen, Zhuangzhong; Zhou, Ruisheng; Wang, Sisi; Wang, Wenping; Liu, De; Li, Mengquan; Guo, TianshengBackground. Circular RNAs (circRNAs) play vital regulatory roles in human cancers, including hepatocellular carcinoma (HCC). In this study, we aimed to explore the functions of hsa_circ_0048674 in HCC development. Methods. Quantitative real-time polymerase chain reaction (qRT-PCR) assay was used to detect hsa_circ_0048674, ubiquitin-like with PHD and RING finger domains 1 (UHRF1), microRNA-223-3p (miR223-3p) and programmed death ligand 1 (PDL1). RNase R assay and Actinomycin D assay were employed to analyze the stability of hsa_circ_0048674. Cell Counting Kit-8 (CCK-8) assay, colony formation assay and 5- ethynyl-2'- deoxyuridine (EdU) assay were conducted to assess cell proliferation. Flow cytometry analysis, transwell assay and tube formation assay were carried out for cell apoptosis, migration, invasion and angiogenesis, respectively. Western blot assay was adopted for protein levels. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were used to analyze the relationship between miR-223-3p and hsa_circ_0048674 or PDL1. Murine xenograft model assay was conducted for the function of hsa_circ_0048674 in vivo. Immunohistochemistry (IHC) assay was used to detect Ki-67 level in tumor tissues. Enzyme linked immunosorbent assay (ELISA) kits were employed for the concentrations of inflammatory factors. Results. Hsa_circ_0048674 was highly expressed in HCC tissues and cells. Silencing of hsa_circ_0048674 repressed cell growth, migration, invasion and angiogenesis and promoted apoptosis in HCC cells in vitro and hampered tumor growth in vivo. Hsa_circ_0048674 served as an miR-223-3p sponge to alter PDL1 expression. MiR-223-3p inhibition or PDL1 overexpression restored the impacts of hsa_circ_ 0048674 silencing on HCC malignant behaviors. In addition, hsa_circ_0048674 knockdown promoted natural killer (NK) cell-mediated cytotoxicity to HCC cells. Conclusion. Hsa_circ_0048674 knockdown decelerated HCC progression through the mediation of the miR-223-3p/PDL1 axis.
- PublicationOpen AccessState-of-the-art review on the correlations between pathological and magnetic resonance features of cirrhotic nodules(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Renzulli, Matteo; Braccischi, Lorenzo; D’Errico, Antonietta; Pecorelli, Anna; Brandi, Nicolò; Golfieri, Rita; Albertini, Elisa; Vasuri, FrancescoHepatocellular carcinoma (HCC) has become the second greatest cause of cancer-related mortality worldwide and the newest advancements in liver imaging have improved the diagnosis of both overt malignancies and premalignant lesions, such as cirrhotic or dysplastic nodules, which is crucial to improve overall patient survival rate and to choose the best treatment options. The role of Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) has grown in the last 20 years. In particular, the introduction of hepatospecific contrast agents has strongly increased the definition of precursor nodules and detection of highgrade dysplastic nodules and early HCCs. Nevertheless, the diagnosis of liver tumours in cirrhotic patients sometimes remains challenging for radiologists, thus, in doubtful cases, biopsy and histological analysis become critical in clinical practice. This current review briefly summarizes the history of imaging and histology for HCC, covering the newest techniques and their limits. Then, the article discusses the links between radiological and pathological characteristics of liver lesions in cirrhotic patients, by describing the multistep process of hepato carcinogenesis. Explaining the evolution of pathologic change from cirrhotic nodules to malignancy, the list of analyzed lesions provides regenerative nodules, lowgrade and high-grade dysplastic nodules, small HCC and progressed HCC, including common subtypes (steatohepatitic HCC, scirrhous HCC, macrotrabecular massive HCC) and more rare forms (clear cell HCC, chromophobe HCC, neutrophil-rich HCC, lymphocyterich HCC, fibrolamellar HCC). The last chapter covers the importance of the new integrated morphologicalmolecular classification and its association with radiological features
- PublicationOpen AccessHigh expression of the phosphoinositide 3-kinase p110γ isoform can predict poor prognosis of non-small cell lung cancer(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Jung, Ina; Lee, Hyoun Wook; Roh, Mee Sook; Lee, Jae Seok; Kim, Kisu; Kim, Kyungeun; Kim, Tae Gyu; Nam, Hyun-YeolThe protein p110γ is an isoform of the catalytic subunit of class I phosphoinositide 3-kinases (PI3Ks). PI3Ks are involved in the regulation of cell survival, growth, proliferation, and migration and have been implicated in the oncogenesis of various cancers. In this study, p110γ expression in non-small cell lung cancer (NSCLC) and its association with clinicopathological factors and patient survival were evaluated. A total of 230 NSCLC tumors were immunohistochemically stained for p110γ. Of these, 174 (75.7%) and 56 (24.3%) were placed in the low and high expression groups, respectively. The positive rate of p110γ was significantly higher in adenocarcinoma than in squamous cell carcinoma (p<0.001). Advanced stage NSCLCs showed higher p110γ expression than those at an early stage (p=0.002). Irrespective of the histological tumor type, the patients with high p110γ expression had significantly worse overall survival than those with low p110γ expression (p=0.004). p110γ expression was an independent poor prognostic factor in the multivariate analysis. Our results suggest that p110γ may be involved in the development and progression of NSCLC, and that p110γ has promising potential as a prognostic factor or novel therapeutic target for NSCLC.
- PublicationOpen AccessAnesthetic propofol suppresses growth and metastasis of lung adenocarcinoma in vitro through downregulating circ-MEMO1-miR-485-3p-NEK4 ceRNA axis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Chen, Lei; Wu, Guangyi; Li, Yongle; Cai, QiaoyingBackground. Recently, circular RNAs (circRNAs) have been emerging as new regulators in the propofol-induced tumor-suppressive role. Here, we intended to investigate the involvement of circRNAMediator of cell motility 1 (circ-MEMO1; hsa_circ_0007385) in propofol role in cancer hallmarks of lung adenocarcinoma (LUAD). Methods. Real-time quantitative PCR and western blotting examined transcriptional and translational levels of circ-MEMO1, microRNA (miR)-485-3p, and NIMArelated kinase-4 (NEK4), and markers of growth and metastasis including E-cadherin, CyclinD1, and Vimentin. Cancer hallmarks were measured by 3-(4, 5- dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, 5-ethynyl-2-deoxyuridine assay, and transwell assay. The interaction among circMEMO1, miR-485-3p, NEK4 was determined by dualluciferase reporter assay and Pearson’s correlation analysis. Results. Circ-MEMO1 and NEK4 were highexpressed, and miR-485-3p was low-expressed in LUAD patients and cells; moreover, circ-MEMO1 and NEK4 expression in LUAD cells could be suppressed, whereas miR-485-3p could be elevated with propofol anesthesia. Functionally, propofol restrained cell viability, cell cycle entrance, cell proliferation, migration, and invasion of LUAD cells, accompanied by promoted E-cadherin and depressed CyclinD1 and Vimentin. Coincidently, high circ-MEMO1 was associated with low overall survival of LUAD patients, and overexpressing circ-MEMO1 could overall attenuate propofol effects in LUAD cells. Of note, upregulating miR-485-3p and/or interfering NEK4 could partially countermand the adverse impacts of circ-MEMO1 on propofol’s role in LUAD cells. Importantly, circMEMO1 acted as a sponge for miR-485-3p to modulate the expression of miR-485-3p-targeted oncogene NEK4. Conclusion. Promoting the circ-MEMO1-miR-485- 3p-NEK4 axis might halt the tumor-inhibiting role of propofol in LUAD cells in vitro, suggesting a potential epigenetic pathway of propofol.
- PublicationOpen AccessSphingosine Kinase-1 (SPHK1) promotes inflammation in infantile pneumonia by regulating NLRP3 inflammasome and SIRT1 expression(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Ding, Niu; Meng, Yanni; Liu, Lianhong; Ma, Song; Chen, YanpingBackground. Infantile pneumonia is an acute inflammatory disorder of the lung caused by mycoplasma pneumonia. SPHK1 (sphingosine kinase-1) signaling pathway is involved in the process of inflammatory diseases. However, whether SphK1 regulates inflammatory responses in infantile pneumonia remains unclear. In this study, we investigated the role of SPHK1 in infantile pneumonia and its underlying mechanisms. Methods. Serum samples of 12 patients with infantile pneumonia and healthy controls were obtained from Hunan Children's Hospital. To induce pneumonia, mice were administrated with LPS (lipopolysaccharide) into the lung. RAW264.7 cells were used as an in vitro macrophage model stimulated with LPS or PBS for 4 h. Results. SPHK1 mRNA level and protein level in the LPS-treated mice and patients with infantile pneumonia were significantly increased. SPHK1 promoted inflammation and lung injury in mice with infantile pneumonia. The knockdown of SPHK1 expression inhibited inflammation and restrained lung injury in mice with infantile pneumonia. SPHK1 overexpression also exacerbated inflammation in RAW264.7 cells stimulated by LPS, and SPHK1 silencing reduced inflammatory responses. We further showed that SPHK1 induced NLRP3 (NLR Family Pyrin Domain Containing 3) activity by inhibiting SIRT1 expression. Conclusion. Our study demonstrated that SPHK1 promotes inflammation of infantile pneumonia by modulating NLRP3 inflammasome via the regulation of SIRT1 expression and mitochondrial permeability transition