Analytical Cellular Pathology最新文献

{"title":"Fetal and Postnatal Nicotine Exposure Modifies Maturation of Gonocytes to Spermatogonia in Mice.","authors":"Rosa María Vigueras-Villaseñor,&nbsp;Martín Alejandro Fuentes-Cano,&nbsp;Margarita Chávez Saldaña,&nbsp;Liliana Rivera Espinosa,&nbsp;Rafael Reynoso-Robles,&nbsp;Patricia Rojas,&nbsp;Pilar Durán,&nbsp;Julio César Rojas-Castañeda","doi":"10.1155/2020/8892217","DOIUrl":"https://doi.org/10.1155/2020/8892217","url":null,"abstract":"<p><p>Studies in laboratory animals have shown that male offspring from dams, exposed to nicotine during pregnancy and postnatal periods, show alterations in fertility, although the origin of this is still uncertain. In this study, we examined in a mouse model if the process of gonocyte maturation to spermatogonia was affected in male offspring from dams with nicotine administration during pregnancy and postnatal periods. BALB/C mice, with and without nicotine administrations in pregnancy and postnatal periods, were studied. The animals were euthanized at 3, 7, 10, 16, and 35 days postpartum (dpp). Testicular tissue samples were processed for histological, ultrastructural, and immunohistochemical studies; and testicular lipoperoxidation was determined. It was observed that in the nicotine-exposed animals, there was increased apoptosis and a reduction in the number of gonocytes that matured to spermatogonia. This gonocyte-spermatogonia maturation reduction was associated with a greater immunoreactivity to nicotinic acetylcholine receptors in the germ cells. Lipoperoxidation was similar in both groups until 16 dpp, with significant reduction at 35 dpp. Our findings suggest that nicotine intake during pregnancy and postnatal periods can affect the process of maturation of gonocytes to spermatogonia and the pool of available spermatogonia for spermatogenesis.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2020 ","pages":"8892217"},"PeriodicalIF":3.2,"publicationDate":"2020-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7758125/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38768119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory Effects of Genistein on Vascular Smooth Muscle Cell Proliferation Induced by Ox-LDL: Role of BKCa Channels.","authors":"Bing Bai,&nbsp;Nanjuan Lu,&nbsp;Wei Zhang,&nbsp;Jinghan Lin,&nbsp;Tingting Zhao,&nbsp;Shanshan Zhou,&nbsp;Elona Khasanova,&nbsp;Liming Zhang","doi":"10.1155/2020/8895449","DOIUrl":"https://doi.org/10.1155/2020/8895449","url":null,"abstract":"<p><strong>Background: </strong>Oxidized low-density lipoprotein (Ox-LDL) is a crucial pathogenic factor for vascular diseases, which can induce the proliferation of vascular smooth muscle cells (VSMCs). Genistein is the main component of soybean isoflavone. Genistein has a variety of pharmacological properties in the treatment of vascular diseases and a promising clinical application. Large-conductance calcium-activated potassium (BKCa) channels are the primary type of potassium channels in VSMCs, which regulate various biological functions of VSMCs. However, whether genistein exerts an antiproliferation effect on Ox-LDL-stimulated VSMCs remains unclear. The current study is aimed at elucidating the effect of genistein on the Ox-LDL-stimulated proliferation of VSMCs and its possible molecular mechanism, especially the electrophysiological mechanism related to BKCa channels.</p><p><strong>Methods: </strong>Monoculture VSMC was obtained by an acute enzyme-dispersing method. The proliferation of cells was measured by CCK-8, cell cycle, and proliferating cell nuclear antigen (PCNA) expression. The BKCa whole-cell currents were measured by patch-clamp.</p><p><strong>Results: </strong>Ox-LDL treatment induced the proliferation of VSMCs, upregulated the BKCa protein expression, and increased the density of BKCa currents, while genistein significantly inhibited these effects caused by Ox-LDL. BKCa channels exerted a regulatory role in the proliferation of VSMCs in response to Ox-LDL. The inhibition of BKCa channels suppressed Ox-LDL-stimulated VSMC proliferation, while the activation of BKCa channels showed the opposite effect. Moreover, genistein suppressed the activity of BKCa, including protein expression and current density in a protein tyrosine kinase- (PTK-) dependent manner.</p><p><strong>Conclusion: </strong>This study demonstrated that genistein inhibited the Ox-LDL-mediated proliferation of VSMCs by blocking the cell cycle progression; the possible molecular mechanism may be related to PTK-dependent suppression of BKCa channels. Our results provided novel ideas for the application of genistein in the treatment of vascular diseases and proposed a unique insight into the antiproliferative molecular mechanism of genistein.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2020 ","pages":"8895449"},"PeriodicalIF":3.2,"publicationDate":"2020-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7752275/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38795409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"eIF4E Overexpression Is Associated with Poor Prognoses of Ovarian Cancer.","authors":"Jun Zheng,&nbsp;Xueqing Li,&nbsp;Chunyan Zhang,&nbsp;Yiqiang Zhang","doi":"10.1155/2020/8984526","DOIUrl":"https://doi.org/10.1155/2020/8984526","url":null,"abstract":"<p><strong>Aim: </strong>Ovarian cancer is a common malignant tumor of the gynecological oncology worldwide, with a high incidence and mortality rate and poor prognosis. Searching for new diagnostic molecular biomarkers for ovarian cancer is extremely significant.</p><p><strong>Methods: </strong>Here, we analyzed the expression rates of eIF4E and cyclin D1 proteins in 123 cases of cancer tissue samples and 38 cases of paracancerous tissue samples and studied the connection between the expression rates of eIF4E and cyclin D1 proteins by immunohistochemistry and statistically correlated with clinicopathological features in ovarian cancer.</p><p><strong>Results: </strong>The results showed that the expression rates of eIF4E and cyclin D1 proteins in ovarian cancer tissues were significantly higher than those in noncancerous epithelial ovarian tissues (<i>P</i> = 0.001 and <i>P</i> = 0.032, respectively). Additionally, the results revealed that a higher expression rate of eIF4E (<i>P</i> = 0.008) was found in the advanced stage (stage III/IV), and also patients with cervical lymph node metastasis displayed higher expression of eIF4E (<i>P</i> < 0.001) and cyclin D1 (<i>P</i> = 0.033) than those without lymph node metastasis. Spearman's rank correlation test showed that there was a significant positive correlation between the eIF4E and cyclin D1 proteins in ovarian cancer. The Kaplan-Meier method showed that patients with lower expression of eIF4E had marginally better survival than those with high expression of eIF4E (<i>P</i> = 0.012). Multivariate Cox regression analysis further identified that positive expression of eIF4E was an independent prognostic factor.</p><p><strong>Conclusion: </strong>In ovarian cancer, eIF4E might be a valuable biomarker to predict poor prognoses and a potential therapeutic target to develop valid treatment strategies.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2020 ","pages":"8984526"},"PeriodicalIF":3.2,"publicationDate":"2020-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7787841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38855387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Expression and Prognostic Value of FGF2, FGFR3, and FGFBP1 in Esophageal Squamous Cell Carcinoma.","authors":"Wenjing Zhang,&nbsp;Yaxing Zhou,&nbsp;Chao Li,&nbsp;Shanshan Xu,&nbsp;Mengyan Li,&nbsp;Wenying Liu,&nbsp;Yuqing Ma,&nbsp;Hui Wang","doi":"10.1155/2020/2872479","DOIUrl":"https://doi.org/10.1155/2020/2872479","url":null,"abstract":"Background Esophageal squamous cell carcinoma was treated by operation and chemoradiotherapy. However, the prognosis of most patients is poor after treatment, and most studies have shown that FGF2 and its receptor (FGFR) are involved in the development of various malignant tumors. FGF2 plays an important role in tumor progression and malignancy. In this study, the immunohistochemistry of FGF2, FGFR3, and FGFBP1 was used to further verify the expression of the three proteins in 172 patients with esophageal squamous cell carcinoma (ESCC) who had not received preoperative chemoradiotherapy and its effect on the prognosis of ESCC. Methods (1) χ2 test was used to analyze the relationship between proteins and clinicopathological parameters. Survival analysis was used to investigate the effect of three proteins on prognosis. (2) Paired sample t-test was used to analyze the mRNA expression of the three proteins in fresh ESCC tissues and adjacent normal tissues. Results FGF2 was correlated with tumor size (p = 0.026), gender (p = 0.047), and lymph metastasis (p = 0.007) in ESCC tissues. The high expression of FGFR3 was associated with tumor differentiation (p = 0.043 and p < 0.05), lymph node metastasis (p = 0.078 and p < 0.1), and race (p = 0.033 and p < 0.05). The high expression of FGFBP1 was significantly associated with the degree of tumor differentiation (p = 0.012), age (p = 0.045), and lymph node metastasis (p = 0.032) of ESCC patients. The expression of FGF2, FGFR3, and FGFBP1-mRNA in ESCC tissues was significantly higher than that in adjacent tissues (p < 0.001, p < 0.001, and p = 0.001). Patients with high expression of FGF2, FGFBP1, and FGFR3 had poor prognosis. There was a weak positive correlation between FGF2 and FGFBP1, as well as FGFR. Conclusion The FGF2-FGFR3 axis may promote the progression of esophageal squamous cell carcinoma. The FGF2-FGFR3 axis may be a new direction of targeted therapy for esophageal squamous cell carcinoma. FGF2 and FGFR3 may be used as prognostic markers of esophageal squamous cell carcinoma.","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2020 ","pages":"2872479"},"PeriodicalIF":3.2,"publicationDate":"2020-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7748917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38768116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"p300-Catalyzed Lysine Crotonylation Promotes the Proliferation, Invasion, and Migration of HeLa Cells via Heterogeneous Nuclear Ribonucleoprotein A1.","authors":"Xuesong Han,&nbsp;Xudong Xiang,&nbsp;Hongying Yang,&nbsp;Hongping Zhang,&nbsp;Shuang Liang,&nbsp;Jie Wei,&nbsp;Jing Yu","doi":"10.1155/2020/5632342","DOIUrl":"https://doi.org/10.1155/2020/5632342","url":null,"abstract":"<p><p>Cervical carcinoma is the third most common cause of cancer in women with a significant challenge in clinical treatment. Human papillomavirus (HPV) is strongly responsible for cervical carcinoma. Here, we show the increased expression level of heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1) in HPV-associated cervical cancer cells including HeLa, Caski, and SiHa cells, especially in HeLa cells. We provide the evidence that the expression of HNRNPA1 is closely related to HeLa cell proliferation, invasion, and migration. Emerging evidence show that histone modifications account for gene expression. Moreover, our results indicate that HNRNPA1 could be regulated by p300 through p300-mediated lysine crotonylation. Inhibition of p300 downregulated both the lysine crotonylation level and the HNRNPA1 expression. And p300-mediated lysine crotonylation participates in the regulation of HNRNPA1 on HeLa cell proliferation, invasion, and migration. Collectively, our study uncovers that p300-mediated lysine crotonylation enhances expression of HNRNPA1 to promote the proliferation, invasion, and migration of HeLa cells.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2020 ","pages":"5632342"},"PeriodicalIF":3.2,"publicationDate":"2020-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7787849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38831838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FKBP4 Accelerates Malignant Progression of Non-Small-Cell Lung Cancer by Activating the Akt/mTOR Signaling Pathway.","authors":"Wen Meng,&nbsp;Jingfei Meng,&nbsp;Hong Jiang,&nbsp;Xing Feng,&nbsp;Dongshan Wei,&nbsp;Qingsong Ding","doi":"10.1155/2020/6021602","DOIUrl":"https://doi.org/10.1155/2020/6021602","url":null,"abstract":"<p><strong>Objective: </strong>To study the expression, biological function, and mechanism of FKBP4 in non-small-cell lung cancer (NSCLC).</p><p><strong>Methods: </strong>First of all, the expression of FKBP4 in NSCLC tissues and cell lines was detected by qRT-PCR; then, the effects of FKBP4 on proliferation, apoptosis, migration, and invasion of NSCLC were studied by CCK-8 assays, flow cytometry assays, wound-healing assays, and Transwell assays. After that, tumor xenografts were used to explore the effect of FKBP4 on NSCLC tumor growth in vivo, and the phosphorylation of Akt and mTOR was measured by western blot.</p><p><strong>Results: </strong>FKBP4 was highly expressed in NSCLC tissues and cells, and its expression was closely related to NSCLC tumor size, lymph node metastasis, and patient prognosis. In vitro, FKBP4 can promote NSCLC cell proliferation, migration, and invasion and inhibit NSCLC cell apoptosis. In vivo, FKBP4 can promote NSCLC tumor growth. Furthermore, FKBP4 can promote Akt and mTOR phosphorylation and activate the Akt/mTOR signaling pathway and an mTOR inhibitor can neutralize the functions of FKBP4 in NSCLC cells.</p><p><strong>Conclusion: </strong>FKBP4 serves as an oncogene to promote malignant processes in NSCLC, and it has the potential to be used as a biological marker and therapeutic target for NSCLC.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2020 ","pages":"6021602"},"PeriodicalIF":3.2,"publicationDate":"2020-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/6021602","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38744391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ABCG1 Attenuates Oxidative Stress Induced by H₂O₂ through the Inhibition of NADPH Oxidase and the Upregulation of Nrf2-Mediated Antioxidant Defense in Endothelial Cells.","authors":"Jiahong Xue,&nbsp;Jiali Fan,&nbsp;Yuan Li,&nbsp;Wenhuan Wu,&nbsp;Qing Yan,&nbsp;Qiangsun Zheng","doi":"10.1155/2020/2095645","DOIUrl":"https://doi.org/10.1155/2020/2095645","url":null,"abstract":"<p><p><i>Summary</i>. Oxidative stress is an important factor that is related to endothelial dysfunction. ATP-binding cassette transporter G1 (ABCG1), a regulator of intracellular cholesterol efflux, has been found to prevent endothelial activation in vessel walls. To explore the role of ABCG1 in oxidative stress production in endothelial cells, HUAECs were exposed to H₂O₂ and transfected with the specific ABCG1 siRNA or ABCG1 overexpression plasmid. The results showed that overexpression of ABCG1 by ABCG1 plasmid or liver X receptor (LXR) agonist T0901317 treatment inhibited ROS production and MDA content induced by H₂O₂ in HUAECs. Furthermore, ABCG1 upregulation blunted the activity of prooxidant NADPH oxidase and the expression of Nox4, one of the NADPH oxidase subunits. Moreover, the increased migration of Nrf2 from the cytoplasm to the nucleus and antioxidant HO-1 expression were detected in HUAECs with upregulation of ABCG1. Conversely, ABCG1 downregulation by ABCG1 siRNA increased NADPH oxidase activity and Nox4 expression and abrogated the increase at Nrf2 nuclear protein levels. In addition, intracellular cholesterol load interfered with the balance between NADPH oxidase activity and HO-1 expression. It was suggested that ABCG1 attenuated oxidative stress induced by H₂O₂ in endothelial cells, which might be involved in the balance between decreased NADPH oxidase activity and increased Nrf2/OH-1 antioxidant defense signaling via its regulation for intracellular cholesterol accumulation.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2020 ","pages":"2095645"},"PeriodicalIF":3.2,"publicationDate":"2020-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/2095645","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38394414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PKM2 Promotes Breast Cancer Progression by Regulating Epithelial Mesenchymal Transition.","authors":"Hui Xiao, Longxiao Zhang, Yuan Chen, Chengjun Zhou, Xiao Wang, Dehai Wang, Zhenzhong Liu","doi":"10.1155/2020/8396023","DOIUrl":"10.1155/2020/8396023","url":null,"abstract":"<p><p>Breast cancer is the leading cause of females characterized by high invasive potential. It is necessary to explore the underlying mechanism of breast cancer metastases and to find specific therapeutic targets. PKM2 is considered a new biomarker of cancer with upregulated expression in tumor tissue. PKM2 participates in the cancer-specific Warburg effect to regulate fast glucose intake consumption. Besides, PKM2 also contributes to cancer progression, especially tumor metastasis. In this study, we showed that PKM2 is upregulated in breast cancer tissues and the upregulating of PKM2 in breast cancer correlates with poor prognosis. PKM2 can regulate tumor progression by promoting tumor cell viability and mobility. Furthermore, overexpression of PKM2 can promote EMT to encourage tumor metastasis. These findings indicate PKM2 is a potentially useful diagnostic biomarker and therapeutic target in breast cancer.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2020 ","pages":"8396023"},"PeriodicalIF":3.2,"publicationDate":"2020-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/8396023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38351403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic Potential of Mesenchymal Stem Cells and Their Secretome in the Treatment of SARS-CoV-2-Induced Acute Respiratory Distress Syndrome.","authors":"Carl Randall Harrell,&nbsp;Biljana Popovska Jovicic,&nbsp;Valentin Djonov,&nbsp;Vladislav Volarevic","doi":"10.1155/2020/1939768","DOIUrl":"https://doi.org/10.1155/2020/1939768","url":null,"abstract":"<p><p>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent responsible for the development of a new coronavirus disease (COVID-19), is a highly transmittable virus which, in just ten months, infected more than 40 million people in 214 countries worldwide. After inhalation, aerosols containing SARS-CoV-2 penetrate to the depths of the lungs and cause severe pneumonia, alveolar injury, and life-threatening acute respiratory distress syndrome (ARDS). Since there are no specific drugs or vaccines available to cure or prevent COVID-19 infection and COVID-19-related ARDS, a new therapeutic agent which will support oxygen supply and, at the same time, efficiently alleviate SARS-CoV-2-induced lung inflammation is urgently needed. Due to their potent immuno- and angiomodulatory characteristics, mesenchymal stem cells (MSCs) may increase oxygen supply in the lungs and may efficiently alleviate ongoing lung inflammation, including SARS-CoV-2-induced ARDS. In this review article, we described molecular mechanisms that are responsible for MSC-based modulation of immune cells which play a pathogenic role in the development of SARS-CoV-2-induced ARDS and we provided a brief outline of already conducted and ongoing clinical studies that increase our understanding about the therapeutic potential of MSCs and their secretome in the therapy of COVID-19-related ARDS.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2020 ","pages":"1939768"},"PeriodicalIF":3.2,"publicationDate":"2020-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/1939768","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38674128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of <i>Inonotus obliquus</i> Polysaccharides on Proliferation, Invasion, Migration, and Apoptosis of Osteosarcoma Cells.","authors":"Baohui Su,&nbsp;Xuezhi Yan,&nbsp;Yuezhong Li,&nbsp;Junshan Zhang,&nbsp;Xiaoyan Xia","doi":"10.1155/2020/4282036","DOIUrl":"https://doi.org/10.1155/2020/4282036","url":null,"abstract":"<p><strong>Objectives: </strong>To observe the effect of <i>Inonotus obliquus</i> polysaccharide (IOP) on the proliferation, invasion, migration, and apoptosis of osteosarcoma cells and to elucidate its underlying molecular mechanism.</p><p><strong>Methods: </strong>IOP was extracted from <i>Inonotus obliquus</i>, human osteosarcoma MG-63 cells and U2OS cells were cultured in vitro, and the effects of IOP on the proliferation, migration, invasion, and apoptosis of MG-63 cells and U2OS cells were determined by CCK-8 assays, cell scratch assays, transwell assays, and flow cytometry, respectively. Western blot was used to detect the expression of related proteins in the Akt/mTOR and NF-<i>κ</i>B signaling pathways.</p><p><strong>Results: </strong>Compared with the control group, MG-63 cells and U2OS cells treated with IOP of 80 <i>μ</i>g/ml, 160 <i>μ</i>g/ml, and 320 <i>μ</i> g/ml in the experimental group had significantly lower proliferation activity, decreased migration and invasion ability, and increased apoptosis rate (<i>P</i> < 0.05). Furthermore, IOP could significantly inhibit the activation of the Akt/mTOR and NF-<i>κ</i>B signaling pathway (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>IOP can regulate the proliferation, migration, invasion, and apoptosis of osteosarcoma cells by inhibiting the activation of the Akt/mTOR signaling pathway. It has antitumor activity on osteosarcoma and has the potential of clinical application in osteosarcoma treatment.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2020 ","pages":"4282036"},"PeriodicalIF":3.2,"publicationDate":"2020-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/4282036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38683285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}