{"title":"Overexpression of miR-100-5p inhibits papillary thyroid cancer progression via targeting FZD8.","authors":"Peng Ma, Jianli Han","doi":"10.1515/med-2022-0490","DOIUrl":"https://doi.org/10.1515/med-2022-0490","url":null,"abstract":"<p><p>Papillary thyroid cancer (PTC) is the most prevalent type of TC worldwide; however, its pathological process remains unclear at the molecular level. In the current study, we analyzed the microarray data of PTC tissues and non-neoplastic thyroid tissues, and confirmed miR-100-5p as a downregulated miRNA in PTC. Via bioinformatic approach, western blotting, and TOP/FOP-flash assay, miR-100-5p was observed to be involved in the inactivation of Wnt/β-catenin signaling in TPC-1 and KTC-1. Frizzled Class Receptor 8 (FZD8), the coupled receptor for canonical Wnt/β-catenin signaling, was verified to be targeted and inhibited by miR-100-5p in TPC-1 and KTC-1. In the function assay, miR-100-5p mimic repressed PTC cell proliferation and induced cell apoptosis of TPC-1 and KTC-1; meanwhile, transfection of full-length FZD8 attenuated the effect of miR-100-5p mimic. Moreover, in the collected samples, miR-100-5p was lowly expressed in PTC tissues compared with normal tissues, especially in those of advanced stage (Stage III/IV vs Stage I/II), while FZD8 was highly expressed in PTC tissues, which in PTC tissues was inversely correlated to miR-100-5p. Thus, we suggest that overexpression of miR-100-5p inhibits the development of PTC by targeting FZD8.</p>","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1172-1182"},"PeriodicalIF":2.1,"publicationDate":"2022-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9263890/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40540548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Antitumor activity of recombinant oncolytic vaccinia virus with human IL2.","authors":"Liqiong Liu, Huiqun Li, Qinggang Xu, Yan Wu, Dongfeng Chen, Feng Yu","doi":"10.1515/med-2022-0496","DOIUrl":"https://doi.org/10.1515/med-2022-0496","url":null,"abstract":"<p><p>The tumor microenvironment is highly immunosuppressive. The genetically modified oncolytic vaccinia virus (OVV) is a promising vector for cancer immunotherapy. The aim of the present study was to assess the antitumor effects of human interleukin-2 (hIL2)-armed OVV <i>in vitro</i>. The hIL2 gene was inserted into a thymidine kinase and the viral growth factor double deleted oncolytic VV (VVDD) to generate recombinant hIL2-armed OVV (rVVDD-hIL2). Viral replication capacity in A549 cells was quantified by plaque titration on CV-1 cells. Production of hIL2 in cancer cells infected by rVVDD-hIL2 was measured by enzyme-linked immunosorbent assay. Finally, 3-(4,5-dimethylthiazol-2-yl)-5-(3-arboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt (MTS) assay was performed to assess the antitumor effects of rVVDD-hIL2. The results showed that rVVDD-hIL2 viral particles expressed increasing levels of hIL2 in human and murine cancer cell lines with growing multiplicities of infection (MOIs). The insertion of the hIL2 gene did not impair the replication capacity of VV, and the rVVDD-hIL2 virus killed cancer cells efficaciously. The lytic effects of the recombinant oncolytic virus on tumor cells increased with the growing MOIs. In conclusion, these findings suggest that hIL2-armed VVDD effectively infects and lyses tumor cells, with high expression of hIL2.</p>","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1084-1091"},"PeriodicalIF":2.1,"publicationDate":"2022-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9206501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40571032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Risk prediction of cardiovascular disease using machine learning classifiers.","authors":"Madhumita Pal, Smita Parija, Ganapati Panda, Kuldeep Dhama, Ranjan K Mohapatra","doi":"10.1515/med-2022-0508","DOIUrl":"https://doi.org/10.1515/med-2022-0508","url":null,"abstract":"<p><p>Cardiovascular disease (CVD) makes our heart and blood vessels dysfunctional and often leads to death or physical paralysis. Therefore, early and automatic detection of CVD can save many human lives. Multiple investigations have been carried out to achieve this objective, but there is still room for improvement in performance and reliability. This study is yet another step in this direction. In this study, two reliable machine learning techniques, multi-layer perceptron (MLP), and <i>K</i>-nearest neighbour (K-NN) have been employed for CVD detection using publicly available University of California Irvine repository data. The performances of the models are optimally increased by removing outliers and attributes having null values. Experimental-based results demonstrate that a higher accuracy in detection of 82.47% and an area-under-the-curve value of 86.41% are obtained using the MLP model, unlike the K-NN model. Therefore, the proposed MLP model was recommended for automatic CVD detection. The proposed methodology can also be employed in detecting other diseases. In addition, the performance of the proposed model can be assessed via other standard data sets.</p>","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1100-1113"},"PeriodicalIF":2.1,"publicationDate":"2022-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9206502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40569096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiaoshan Zhang, ShiBing Deng, Yang Peng, Han Wei, Zhiming Tian
{"title":"ALKBH5 inhibits TNF-α-induced apoptosis of HUVECs through Bcl-2 pathway.","authors":"Xiaoshan Zhang, ShiBing Deng, Yang Peng, Han Wei, Zhiming Tian","doi":"10.1515/med-2022-0484","DOIUrl":"https://doi.org/10.1515/med-2022-0484","url":null,"abstract":"<p><p>The dysfunction and apoptosis of vascular endothelial cells are the initiating links in the formation of atherosclerosis. N6-methyladenosine (m6A) is an extremely extensive RNA methylation modification and its abnormality leads to the occurrence of various human diseases. In this study, we explored the effects of demethylase <i>α</i>-ketoglutarate-dependent dioxygenase ALKB homolog 5 (ALKBH5) on TNF-α-induced apoptosis of human umbilical vein endothelial cells (HUVECs). In TNF-α-treated HUVECs, the expression of ALKBH5 was significantly decreased. ALKBH5 overexpression promoted the proliferation and inhibited the apoptosis in TNF-α-treated HUVECs, suggesting that ALKBH5 had a protective effect on cell damage induced by TNF-α. Importantly, ALKBH5 promoted the expression of Bcl-2 in HUVECs. Bcl2 overexpression reduced the expression of Gadd45, Bax, and p21, which are transcriptionally activated by p53. But the expression of p53 has not been significantly affected, indicating that Bcl2 might regulate the apoptosis by inhibiting p53 downstream targets. In addition, ALKBH5 overexpression significantly increased the level of pri-miR-7 and decreased the level of miR-7. In conclusion, ALKBH5 attenuated the TNF-α-induced cell injury via promoting Bcl2 expression. Our research expands the understanding of the progression mechanism of atherosclerosis and provides a potential strategy for the protection of vascular endothelial injury.</p>","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1092-1099"},"PeriodicalIF":2.1,"publicationDate":"2022-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9202073/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40569094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Expression and role of ABIN1 in sepsis: <i>In vitro</i> and <i>in vivo</i> studies.","authors":"Haolan Li, Aichen Sun, Taocheng Meng, Yan Zhu","doi":"10.1515/med-2022-0503","DOIUrl":"https://doi.org/10.1515/med-2022-0503","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1515/med-2021-0008.].</p>","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1064"},"PeriodicalIF":2.1,"publicationDate":"2022-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9191561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40569093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A low serum uric acid concentration predicts a poor prognosis in adult patients with candidemia.","authors":"Yuqi Zhou, Wenjuan Li, Yubo Huang","doi":"10.1515/med-2022-0511","DOIUrl":"https://doi.org/10.1515/med-2022-0511","url":null,"abstract":"<p><p>This study aimed to determine the relation of serum uric acid (UA) level with outcomes in adults with candidemia. Medical records of patients with candidemia treated from 2014 to 2017 were retrospectively reviewed. Patients were age- and sex-matched with healthy control subjects. The associations of UA and cystatin C (CysC) levels with diagnosis and prognosis of candidemia were determined. Sixty-four patients with candidemia (13 females and 51 males; mean age 48.5 years) and 64 matched control subjects were included. The median UA level of patients with candidemia was 255 μmol/L (range, 158-395 μmol/L), and of healthy controls was 398 μmol/L (range, 345-450 μmol/L) (<i>P</i> < 0.001). The median CysC level of patients with candidemia was 1.07 mg/L (range, 0.89-1.59 mg/L), and of the healthy controls was 0.82 mg/L (range, 0.74-0.95 mg/L) (<i>P</i> < 0.001). Patients with a favorable prognosis had significantly higher serum UA levels than those with a poor prognosis (181 μmol/L vs 344 μmol/L; <i>P</i> = 0.001). It was indicated that the estimated OR for UA was significantly > 1 (<i>P</i> = 0.009), and the AUC was 0.734. In summary, a lower serum UA level is associated with a diagnosis of candidemia, and a poor outcome.</p>","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1077-1083"},"PeriodicalIF":2.1,"publicationDate":"2022-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9186511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40477048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lanzhi Zheng, Zhuoyi Zhang, Kang Song, Xiaoyang Xu, Yixin Tong, Jinling Wei, Lu Jiang
{"title":"Potential biomarkers for inflammatory response in acute lung injury.","authors":"Lanzhi Zheng, Zhuoyi Zhang, Kang Song, Xiaoyang Xu, Yixin Tong, Jinling Wei, Lu Jiang","doi":"10.1515/med-2022-0491","DOIUrl":"https://doi.org/10.1515/med-2022-0491","url":null,"abstract":"<p><p>Acute lung injury (ALI) is a severe respiratory disorder occurring in critical care medicine, with high rates of mortality and morbidity. This study aims to screen the potential biomarkers for ALI. Microarray data of lung tissues from lung-specific geranylgeranyl pyrophosphate synthase large subunit 1 knockout and wild-type mice treated with lipopolysaccharide were downloaded. Differentially expressed genes (DEGs) between ALI and wild-type mice were screened. Functional analysis and the protein-protein interaction (PPI) modules were analyzed. Finally, a miRNA-transcription factor (TF)-target regulation network was constructed. Totally, 421 DEGs between ALI and wild-type mice were identified. The upregulated DEGs were mainly enriched in the peroxisome proliferator-activated receptor signaling pathway, and fatty acid metabolic process, while downregulated DEGs were related to cytokine-cytokine receptor interaction and regulation of cytokine production. <i>Cxcl5</i>, <i>Cxcl9</i>, <i>Ccr5</i>, and <i>Cxcr4</i> were key nodes in the PPI network. In addition, three miRNAs (miR505, miR23A, and miR23B) and three TFs (PU1, CEBPA, and CEBPB) were key molecules in the miRNA-TF-target network. Nine genes including <i>ADRA2A</i>, <i>P2RY12</i>, <i>ADORA1</i>, <i>CXCR1</i>, and <i>CXCR4</i> were predicted as potential druggable genes. As a conclusion, <i>ADRA2A</i>, <i>P2RY12</i>, <i>ADORA1</i>, <i>CXCL5</i>, <i>CXCL9</i>, <i>CXCR1</i>, and <i>CXCR4</i> might be novel markers and potential druggable genes in ALI by regulating inflammatory response.</p>","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1066-1076"},"PeriodicalIF":2.1,"publicationDate":"2022-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9186513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40477050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Let-7i-3p inhibits the cell cycle, proliferation, invasion, and migration of colorectal cancer cells via downregulating CCND1.","authors":"Fei Tu, Mengfan Li, Yinyu Chen, Huiru Chu, Shujie Wang, Lun Hai, Ting Xie, Fangfang Geng, Tiesuo Zhao, Qingzhi Wang, Zhiwei Feng","doi":"10.1515/med-2022-0499","DOIUrl":"https://doi.org/10.1515/med-2022-0499","url":null,"abstract":"<p><p>Dysregulated microRNAs are closely related to the malignant progression of colorectal cancer (CRC). Although abnormal let-7i-3p expression has been reported in various human cancers, its biological role and potential mechanism in CRC remain unclear. Therefore, the purpose of this study was to investigate the expression and regulation of let-7i-3p in CRC. Here, we demonstrated that let-7i-3p expression was significantly downregulated in three CRC cell lines while CyclinD1 (CCND1) was upregulated compared with the normal colon epithelial FHC cells. Moreover, bioinformatics and luciferase reporter assays revealed that CCND1 was a direct functional target of let-7i-3p. In addition, let-7i-3p overexpression or CCND1 silencing inhibited cell cycle, proliferation, invasion, and migration and diminished the activation of p-ERK in HCT116 cells. However, exogenously expressing CCND1 alleviated these effects. Taken together, our findings may provide new insight into the pathogenesis of CRC and let-7i-3p/CCND1 might function as new therapeutic targets for CRC.</p>","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1019-1030"},"PeriodicalIF":2.1,"publicationDate":"2022-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9175015/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40487299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiaochun Yang, Xuegang Liang, Haohui Guo, Long Ma, Li Jian, Xin Zhao, Jian Wang, Lvlin Yang, Zhiqiang Meng, Qunhua Jin
{"title":"β2-Adrenergic receptor expression in subchondral bone of patients with varus knee osteoarthritis.","authors":"Xiaochun Yang, Xuegang Liang, Haohui Guo, Long Ma, Li Jian, Xin Zhao, Jian Wang, Lvlin Yang, Zhiqiang Meng, Qunhua Jin","doi":"10.1515/med-2022-0498","DOIUrl":"https://doi.org/10.1515/med-2022-0498","url":null,"abstract":"<p><p>An important causative factor in osteoarthritis (OA) is the abnormal mechanical stress-induced bone remodeling of the subchondral bone. β2-adrenergic receptor (Adrb2) plays a major role in mechanical stresses that induce bone remodeling. The medial tibial plateau (MTP) and lateral tibial plateau (LTP) of patients with varus Knee osteoarthritis (KO) bear different mechanical stresses. The present study aimed to investigate the expression of Adrb2 in medial tibial plateau subchondral bone (MTPSB) and lateral tibial plateau subchondral bone (LTPSB) in patients with varus KO. A total of 30 tibial plateau samples from patients undergoing total knee arthroplasty for varus KO and MTPSB and LTPSB were studied. Statistical analysis was performed using paired sample <i>t</i>-tests. Safranin O-Fast Green staining and Micro-computed tomography showed significant differences in the bone structure between MTPSB and LTPSB. Tartrate-resistant acid phosphatase (TRAP)-positive cell density in MTPSB was higher than that in LTPSB. Immunohistochemistry, reverse transcription-quantitative polymerase chain reaction, and Western blot analysis revealed that compared to LTPSB, the levels of Adrb2, tyrosine hydroxylase (TH), and osteocalcin increased significantly in MTPSB. Double-labeling immunofluorescence showed Adrb2 was present in the majority of TRAP-positive multinuclear cells of the MTPSB. The expression of Adrb2 and TH was significantly higher in MTPSB than in LTPSB, confirming the involvement of these molecules in the development of OA.</p>","PeriodicalId":520729,"journal":{"name":"Open medicine (Warsaw, Poland)","volume":" ","pages":"1031-1044"},"PeriodicalIF":2.1,"publicationDate":"2022-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9175016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40477047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}