Cell Proliferation
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2022 ◽  
Vol 52 (4) ◽  
Renato Luiz Silveira ◽  
Ana Claudia de Menezes Cruz ◽  
Phillipe Bauer de Araújo Doria ◽  
Joao Marcelo Silva Silveira ◽  
Carlos Otávio de Paula Vasconcelos ◽  

ABSTRACT: Tumors are rarely diagnosed in swine specie because of the short lifespan of production animals. Normally, these tumors do not present any clinical signs and are often detected at the time of slaughter. A 2-year-old Large White boar, used in the reproductive management of a farm and without a history of pre-existing problems, was examined for skin lesions on the scrotum. Samples were collected from skin segments containing lesions for histopathological and immunohistochemical diagnosis. Microscopically, the nodes in the scrotum pouch consisted of poorly demarcated, highly cellular, expansile, and multifocally invasive neoplasms, composed of immature endotheliocytes organized into neovascular formations. The tumor cells were pleomorphic, slightly oval to spindle-shaped, with eosinophilic cytoplasm and hyperchromatic nuclei with one to three nucleoli. All the nodules analyzed were compatible with hemangiosarcoma. After immunohistochemical evaluation, for the quantification of tissue angiogenesis the neoplastic cells immunoexpressed the CD31 monoclonal antibodies and factor VIII, through the identification of proteins expressed on the surface of endothelial cells. The Ki67 cell proliferation marker was positive in approximately 10% of the neoplastic cells, demonstrating a high degree of malignancy. Hemangiosarcoma in swine species has already been identified in several organs and tissues; however, to date, no study has demonstrated the diagnosis of this condition on the skin of the scrotum, as reported in this study. Therefore, it is expected that this report will contribute to the knowledge of the frequency of neoplasms in swine species.

Mohamad Zahid Kasiram ◽  
Hermizi Hapidin ◽  
Hasmah Abdullah ◽  
Nor Munira Hashim ◽  
Ahmad Azlina ◽  

2021 ◽  
Vol 13 (1) ◽  
Li Zhao ◽  
Huaqian Chen ◽  
Lin Wu ◽  
Zhengdong Li ◽  
Ren Zhang ◽  

Abstract Background Long non-coding RNAs (lncRNAs) have been reported to play vital roles in diabetic nephropathy (DN). The aim of this study was to explore the function of mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in DN. Methods DN cell models were established using high glucose (HG) treatment in human glomerular mesangial cells (HGMC) and human renal glomerular endothelial cells (HRGEC). The expression levels of KCNQ1OT1, microRNA-93-5p (miR-93-5p), and Rho associated coiled-coil containing protein kinase 2 (ROCK2) mRNA was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. ROCK2 and apoptosis/fibrosis-related protein levels were examined by western blot. The predicted interaction between miR-93-5p and KCNQ1OT1 or ROCK2 was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results KCNQ1OT1 was upregulated in DN patients and DN cell models. KCNQ1OT1 knockdown inhibited cell proliferation and fibrosis and induced apoptosis in DN cell models. MiR-93-5p was a direct target of KCNQ1OT1, and miR-93-5p inhibition restored the KCNQ1OT1 knockdown-mediated effects on cell proliferation, fibrosis and apoptosis in DN cell models. In addition, ROCK2 was identified as a target of miR-93-5p, and miR-93-5p overexpression suppressed cell proliferation and fibrosis and accelerated apoptosis by targeting ROCK2 in DN cell models. Moreover, KCNQ1OT1 regulated ROCK2 expression by binding to miR-93-5p. Conclusion KCNQ1OT1 knockdown inhibited cell proliferation and fibrosis and induced apoptosis in DN by regulating miR-93-5p/ROCK2 axis, providing potential value for the treatment of DN.

2021 ◽  
Vol 46 (6) ◽  
Li-Ya Ji ◽  
Ming Wei ◽  
Yuan-Yuan Liu ◽  
Zheng-Li Di ◽  
San-Zhong Li

2021 ◽  
Vol 12 (1) ◽  
Hongda Wang ◽  
Yiming Zhao ◽  
Bingbing Ren ◽  
Yafei Qin ◽  
Guangming Li ◽  

Abstract Background Autoimmune hepatitis (AIH) is a T cell-mediated immune disease that activates abnormally against hepatic antigens. We have previously reported that endometrial regenerative cells (ERCs) were a novel source of adult stem cells, which exhibiting with powerful immunomodulatory effects. Galectin-9 (Gal-9) is expressed in ERCs and plays an important role in regulating T cell response. This study aims to explore the role of ERCs in attenuation of AIH and to determine the potential mechanism of Gal-9 in ERC-mediated immune regulation. Methods ERCs were obtained from menstrual blood of healthy female volunteers. In vitro, ERCs were transfected with lentivirus vectors carrying LGALS9 gene and encoding green fluoresce protein (GFP-Gal-9-LVs) at a MOI 50, Gal-9 expression in ERCs was detected by ELISA and Q-PCR. CD4+ T cells isolated from C57BL/6 mouse spleen were co-cultured with ERCs. The proliferation of CD4+ T cells was detected by CCK-8 kit and the level of Lck/zap-70/LAT protein was measured by western blot. Furthermore, AIH was induced by ConA in C57BL/6 mice which were randomly assigned to untreated, unmodified ERC-treated and Gal-9 high-expressing ERC-treated groups. Histopathological score, liver function, CD4+/CD8+ cell infiltration in liver tissues, the proportion of immune cells in the spleen and liver, and ERC tracking were performed accordingly to assess the progression degree of AIH. Results After transfecting with GFP-Gal-9-LVs, Gal-9 expression in ERCs was significantly increased. Additionally, Gal-9 high-expressing ERCs effectively inhibited CD4+ T cell proliferation and downregulated CD4+ T cell active related proteins p-Lck/p-ZAP70/p-LAT in vitro. Furthermore, treatment with Gal-9 high-expressing ERCs restored liver function, ameliorated liver pathological damage, inhibit CD4+ and CD8+ T cell proliferation and suppress Th1 and Th17 cell response in the hepatitis mice. In addition, Gal-9 high-expressing ERCs further markedly enhanced the level of IL-10 but reduced the levels of IFN-γ, TNF-α, and IL-4 in mouse sera and liver. Cell tracking also showed that ERCs could migrate to the damaged liver organs. Conclusions The results suggested that Gal-9 was an essential modulator, which was required by ERCs in regulating T cell response and attenuating ConA-induced experimental hepatitis. And also, it provides a novel idea for the clinical treatment of AIH.

2021 ◽  
Vol 22 (6) ◽  
Shaoqiang Liang ◽  
Ning Zhang ◽  
Yanming Deng ◽  
Lusi Chen ◽  
Yang Zhang ◽  

Yating Xu ◽  
Xiao Yu ◽  
Menggang Zhang ◽  
Qingyuan Zheng ◽  
Zongzong Sun ◽  

Long non-coding RNAs (lncRNAs) are RNAs with a length of no less than 200 nucleotides that are not translated into proteins. Accumulating evidence indicates that lncRNAs are pivotal regulators of biological processes in several diseases, particularly in several malignant tumors. Long intergenic non-protein coding RNA 1116 (LINC01116) is a lncRNA, whose aberrant expression is correlated with a variety of cancers, including lung cancer, gastric cancer, colorectal cancer, glioma, and osteosarcoma. LINC01116 plays a crucial role in facilitating cell proliferation, invasion, migration, and apoptosis. In addition, numerous studies have recently suggested that LINC01116 has emerged as a novel biomarker for prognosis and therapy in malignant tumors. Consequently, we summarize the clinical significance of LINC01116 associated with biological processes in various tumors and provide a hopeful orientation to guide clinical treatment of various cancers in future studies.

2021 ◽  
Lev Brio ◽  
Danit Wasserman ◽  
Efrat Michaely-Barbiro ◽  
Doron Gerber ◽  
Amit Tzur

Protein degradation mediated by the ubiquitin-proteasome pathway regulates signaling events in all eukaryotic cells, with implications in pathological conditions such as cancer and neurodegenerative diseases. Detection of protein degradation is an elementary need in basic and translational research. In vitro degradation assays, in particular, have been instrumental in the understanding of how cell proliferation and other fundamental cellular processes are regulated. These assays are direct, quantitative and highly informative but also laborious, typically relying on low-throughput polyacrylamide gel-electrophoresis followed by autoradiography or immunoblotting. We present protein degradation on chip (pDOC), a MITOMI-based integrated microfluidic device for discovery and analysis of ubiquitin mediated proteolysis. The platform accommodates microchambers on which protein degradation is assayed quickly and simultaneously in physiologically relevant environments, using minute amount of reagents. Essentially, pDOC provides a multiplexed, sensitive and colorimetric alternative to the conventional degradation assays, with relevance to biomedical and translational research.

2021 ◽  
Suli Wang ◽  
Yingchun Wang ◽  
Jin Lu ◽  
Jinhua Wang

Abstract Objective: Previous reports indicate that long intergenic non-coding RNA LINC00665 naturally occurred vital effect in various cancers. Herein, the role of LINC00665 in ovarian cancer progress was explored.Methods: We found that LINC00665 was upregulated in ovarian cancer cell lines. Besides that, A series of assays including flow cytometry, wound-healing, Transwell, Cell Counting Kit-8 (CCK-8), and EdU assay confirmed that the knockdown of LINC00665 could reduce the viability, proliferation and migration of SKOV-3 and OVCAR-3 cells. Accumulating evidence indicates that many lncRNAs can function as endogenous miRNA sponges by competitively binding common miRNAs. In this study, the bioinformatics analysis suggested that LNC00665 specifically binds to miR-181a-5p.Results: LINC00665 downregulated the miR-181a-5p in SKOV-3 and OVCAR-3 cells. The knockdown of miR-181a-5p evidently reverses the inhibitory effect of sh-LINC00662. Besides, FH2 Domain Containing 1 (FHDC1) has been proved to deed as an effective target of miR-181a-5p.Conclusion: Our results reveal the knockdown of LINC00665 facilitates ovarian cancer via development by sponging miR-181a-5p and upregulating FHDC1 expression; these may contribute to ovarian cancer therapy.

Cancers ◽  
2021 ◽  
Vol 13 (20) ◽  
pp. 5160
Thomas J. Kalantzakos ◽  
Travis B. Sullivan ◽  
Thales Gloria ◽  
David Canes ◽  
Alireza Moinzadeh ◽  

MicroRNAs (miRNAs) are non-coding post-transcriptional regulators of gene expression that are dysregulated in clear cell renal cell carcinoma (ccRCC) and play an important role in tumor progression. Our prior work identified a subset of miRNAs in pT1 ccRCC tumors, including miR-424-5p, that are associated with an aggressive phenotype. We investigate the impact of this dysregulated miRNA and its protein target O-GlcNAc-transferase (OGT) to better understand the mechanisms behind aggressive stage I ccRCC. The ccRCC cell lines 786-O and Caki-1 were used to assess the impact of miR-424-5p and OGT. Cells were transfected with pre-miR-424-5p, a lentiviral anti-OGT shRNA, or were treated with the demethylating agent 5-Aza-2′-deoxycytidine. Cell proliferation was measured via MT cell viability assay. Cell migration and invasion were analyzed using Transwell assays. The expression of miR-424-5p was determined through qRT-PCR, while OGT protein expression was evaluated through Western blotting. The interaction between miR-424-5p and OGT was confirmed via luciferase reporter assay. The transfection of ccRCC cells with pre-miR-424-5p or anti-OGT shRNA significantly inhibited cell proliferation, migration, and OGT expression, while miR-424-5p also attenuated cell invasion. Addition of the demethylating agent significantly reduced cell proliferation, migration, invasion, and OGT expression, while significantly increasing the expression of miR-424-5p. Altogether, these findings suggest that epigenetic downregulation of miR-424-5p, which in turn augments OGT expression, contributes to the creation of aggressive forms of stage I ccRCC.

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