Guillain-Barré syndrome associated with Covid-19: A close relationship or just a coincidence? (Review)

xlomafota13 shared this article with you from Inoreader Guillain-Barré syndrome associated with Covid-19: A close relationship or just a coincidence? (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):916. doi: 10.3892/etm.2021.10348. Epub 2021 Jun 29. ABSTRACT Several neurological complications affecting the central and peripheral nervous system were described secondary to COVID-19 infection such as hyposmia, headache, nausea, impaired consciousness, psychosis, neurocognitive syndromes and even cerebrovascular accidents. The mechanism of these complications is not fully understood, but heterogenous mechanisms such as cytokine storm, secondary hypercoagulability and direct neurotropism of the virus are thought to be involved. Guillain-Barré syndrome is a heterogeneous disease that frequently follows a bacterial or viral infection. During the ongoing SARS-CoV-2 pandemic, several isolated case reports and case series have suggested an association between this viral infection and the occurrence of Guillain-Barré syndrome. The main mechanism of Guillain-Barré syndrome is probably post-viral dysregulation of the immune system generated by SARS-CoV-2. The clinical characteristics and disease evolution seem to be similar to those observed in Guillain-Barré syndrome secondary to other etiologies. The aim of the present review is to summarize the relevant literature regarding SARS-CoV-2-related Guillain-Barré syndrome. PMID:34306190 | PMC:PMC8281479 | DOI:10.3892/etm.20 21.10348 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Icariin inhibits oral squamous cell carcinoma cell proliferation and induces apoptosis via inhibiting the NF-κB and PI3K/AKT pathways

xlomafota13 shared this article with you from Inoreader Icariin inhibits oral squamous cell carcinoma cell proliferation and induces apoptosis via inhibiting the NF-κB and PI3K/AKT pathways Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):942. doi: 10.3892/etm.2021.10374. Epub 2021 Jul 1. ABSTRACT Oral squamous cell carcinoma (OSCC), one of the most common types of human cancer, has a high mortality rate and a poor prognosis due to its high rates of recurrence and metastasis. In recent years, icariin (ICA) has been reported to play an important role in a variety of malignancies, such as gastric, colorectal, pancreatic and ovarian cancer. However, its role and mechanism in OSCC remains to be elucidated. The present study aimed to investigate the effect of ICA in OSCC cells and to reveal its underlying mechanisms. The OSCC cell lines SCC9 and Cal 27 were used to explore the effect of different concentrations of ICA on the biological behavior of OSCC cells. The effect of ICA on OSCC cell proliferation and apoptosis was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide and flow cytometric assays, respectively. Sub sequently, the protein expression levels of caspase-3 and cleaved-caspase-3 were detected using western blot analysis. Additionally, the protein and mRNA expression levels of nuclear factor-κB (NF-κB) and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway-related factors were determined using western blot analysis and reverse transcription-quantitative PCR, respectively. The results demonstrated that ICA inhibited OSCC cell proliferation and significantly increased the apoptosis rate in a dose-dependent manner. In addition, treatment of OSCC cells with ICA upregulated the protein expression of cleaved-caspase-3 and increased the cleaved-caspase-3/caspase-3 ratio. The protein expression levels of phosphorylated (p)-p65, p-PI3K and p-AKT were decreased in OSCC cells treated with ICA. The aforementioned findings revealed that ICA could attenuate the proliferation of OSCC cells and induce apoptosis via inhibiting the NF-κB and PI3K/AKT signaling pathways. T herefore, the current study provided a new insight into the clinical treatment of OSCC. PMID:34306206 | PMC:PMC8281471 | DOI:10.3892/etm.2021.10374 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Clinical characteristics and survival of patients with three major connective tissue diseases associated with pulmonary hypertension: A study from China

xlomafota13 shared this article with you from Inoreader Clinical characteristics and survival of patients with three major connective tissue diseases associated with pulmonary hypertension: A study from China Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):925. doi: 10.3892/etm.2021.10357. Epub 2021 Jun 30. ABSTRACT The present cross-sectional study investigated the clinical characteristics and survival of patients with three types of connective tissue disease associated with pulmonary hypertension (CTD-PH) diagnosed early by echocardiography. A total of 218 patients with CTD-PH were included in the present study. Patients with the three major types of CTD, namely systemic lupus erythematosus (SLE), systemic sclerosis (SSc) and primary Sjögren's syndrome (pSS), were included. PH was diagnosed based on pulmonary arterial systolic pressure >35 mmHg, as measured by Doppler echocardiography. Demographic data, clinical features, laboratory results and echocardiographic parameters were collected and analyzed. The Kaplan-Meier method was used to calculate survival rates. Multivariate analysis was used to identify independent factors affecting mortality. Compared with patients with CTD with pSS (6.5%) or SLE (3.8%), those with SSc had a higher prevalance of PH (12.9%). Patients with SSc-PH had the highest rate of lung involvement (81.2%) and 42.2% of patients were classified as World Health Organization-function class III/IV at the time of diagnosis with PH. The overall survival rate among patients with CTD-PH at 1, 3 and 5 years was 81.4, 72.4 and 56.9%, respectively. Patients with SLE-PH appeared to have the most favorable prognosis and patients with SSc-PH had the poorest relative outcomes. Multivariate analysis revealed that age ≥50 years was the only independent risk factor for mortality. In conclusion, among the patients with CTDs investigated, the prevalence of PH was highest among those with SSc. Patients with SSc-PH had the highest prevalence of pulmonary involvement, the lowest survival rate and the worst prognosis. PMID:34306194 | PMC:PMC8280713 | DOI:10.3892/etm.2021.10357 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

miR-374a-5p inhibits non-small cell lung cancer cell proliferation and migration via targeting NCK1

xlomafota13 shared this article with you from Inoreader miR-374a-5p inhibits non-small cell lung cancer cell proliferation and migration via targeting NCK1 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):943. doi: 10.3892/etm.2021.10375. Epub 2021 Jul 1. ABSTRACT Emerging studies have indicated that microRNAs (miRNAs/miRs) are involved in regulating non-small cell lung cancer (NSCLC)-associated processes. The present study aimed to evaluate the biological roles of miR-374a-5p in NSCLC. Using reverse transcription-quantitative PCR, the expression levels of miR-374a-5p were determined in NSCLC cells and a normal cell line. Functional experiments were performed to investigate the functions of miR-374a-5p in NSCLC. A luciferase activity reporter assay and rescue experiments were performed to validate NCK adaptor protein 1 (NCK1) as a functional target of miR-374a-5p. It was demonstrated that miR-374a-5p levels were decreased in NSCLC cell lines compared with those in a normal cell line. Furthermore, overexpression of miR-374a-5p inhibited NSCLC cell proliferation and migration in vitro. Of note, NCK1 ove rexpression reversed the effects of miR-375a-5p on NSCLC cell proliferation and migration. The present results confirmed the tumor suppressor role of miR-374a-5p via targeting NCK1 in NSCLC, indicating the importance of the miR-374a-5p/NCK1 axis in NSCLC. PMID:34306207 | PMC:PMC8281440 | DOI:10.3892/etm.2021.10375 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

miR-374a-5p inhibits non-small cell lung cancer cell proliferation and migration via targeting NCK1

xlomafota13 shared this article with you from Inoreader miR-374a-5p inhibits non-small cell lung cancer cell proliferation and migration via targeting NCK1 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):943. doi: 10.3892/etm.2021.10375. Epub 2021 Jul 1. ABSTRACT Emerging studies have indicated that microRNAs (miRNAs/miRs) are involved in regulating non-small cell lung cancer (NSCLC)-associated processes. The present study aimed to evaluate the biological roles of miR-374a-5p in NSCLC. Using reverse transcription-quantitative PCR, the expression levels of miR-374a-5p were determined in NSCLC cells and a normal cell line. Functional experiments were performed to investigate the functions of miR-374a-5p in NSCLC. A luciferase activity reporter assay and rescue experiments were performed to validate NCK adaptor protein 1 (NCK1) as a functional target of miR-374a-5p. It was demonstrated that miR-374a-5p levels were decreased in NSCLC cell lines compared with those in a normal cell line. Furthermore, overexpression of miR-374a-5p inhibited NSCLC cell proliferation and migration in vitro. Of note, NCK1 ove rexpression reversed the effects of miR-375a-5p on NSCLC cell proliferation and migration. The present results confirmed the tumor suppressor role of miR-374a-5p via targeting NCK1 in NSCLC, indicating the importance of the miR-374a-5p/NCK1 axis in NSCLC. PMID:34306207 | PMC:PMC8281440 | DOI:10.3892/etm.2021.10375 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Macrophages induce the expression of lncRNA ATB via the secretion of TGF-β to relieve ischemia-reperfusion injury in cardiomyocytes

xlomafota13 shared this article with you from Inoreader Macrophages induce the expression of lncRNA ATB via the secretion of TGF-β to relieve ischemia-reperfusion injury in cardiomyocytes Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):910. doi: 10.3892/etm.2021.10342. Epub 2021 Jun 29. ABSTRACT Cardiac ischemia-reperfusion can cause severe damage to cardiomyocytes. Previous studies have revealed that TGF-β can alleviate ischemia-reperfusion injury in cardiomyocytes by inducing the expression of long non-coding RNA (lncRNA) activated by TGF-β (ATB). However, M2 macrophages can secrete a large amount of TGF-β. However, whether M2 macrophages alleviate the ischemia-reperfusion-induced injury of cardiomyocytes by secreting TGF-β is unclear. In the present study, macrophages and cardiomyocytes were cultured under oxygen-glucose deprivation/reoxygenation (OGD/R) conditions to simulate ischemia-reperfusion injury. M2-type macrophage markers (IL-10, Arginase-1 and IL-13) were validated using reverse transcription-quantitative PCR and western blotting. Subsequently, the culture medium of M2-type macrophages was collected for the treatment of cardiomyocytes, which were cultured under OGD/R conditions. The levels of inflammatory factors and oxidase enzymes were detected with ELISA. The apoptotic rates of cardiomyocytes were detected by flow cytometry. The expression of cell apoptosis-related proteins and the phosphorylation levels of NF-κB were analyzed by western blotting. The expression levels of specific inflammatory cytokines and the levels of malondialdehyde and lactate dehydrogenase were suppressed in cardiomyocytes following treatment with culture medium derived from M2-type macrophages, which were cultured under OGD/R conditions. Furthermore, OGD/R-induced apoptosis of cardiomyocytes was also relieved following treatment of the cells with macrophage medium. It was found that M2-type macrophages could secrete TGF-β and that the culture medium of M2-type macrophages could activate the expression of lncRNA ATB in cardiomyocytes. TGF-β secreted by M2 macrophages relieved the inflammatory response, oxidative stress and apoptosis of cardiomyocytes by inducing the expression of lncRNA ATB. PMID:34306184 | PMC:PMC8281357 | DOI:10.3892/etm.2021.10342 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress

xlomafota13 shared this article with you from Inoreader Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):944. doi: 10.3892/etm.2021.10376. Epub 2021 Jul 1. ABSTRACT Diabetic cardiomyopathy is a common complication of diabetes, in which endoplasmic reticulum stress (ERS) serves an important role. Rutin can treat the myocardial dysfunction of diabetic rats. However, to the best of our knowledge, studies on the effects of Rutin on myocardial injury caused by diabetes from the perspective of ERS have not previously been reported. In the present study, the role of rutin in the regulation of ERS in myocardial injury was assessed. Different high glucose concentrations were used to treat H9C2 myoblast cells to establish a myocardial damage model. A cell counting kit-8 assay was used to determine cell viability. A lactate dehydrogenase kit was used to detect cytotoxicity. Apoptosis levels were determined using a TUNEL assay. Western blotting was used to determine the expression levels of apoptosis-related proteins and ERS-related proteins, including heat shock protein A family member 5, inositol-requiring enzyme-1α, X-box binding protein 1, activating transcription factor 6, C/EBP-homologous protein (CHOP), cleaved caspase-12 and caspase-12. The anti-apoptotic and anti-ERS effects of Rutin on H9C2 cardiac cells induced by high glucose were examined after the administration of the ERS activator thapsigargin (TG). The results indicated that rutin could dose-dependently inhibit the level of apoptosis and ERS induced by high glucose in H9C2 cells. After administration of the ERS activator TG, it was demonstrated that TG could reverse the anti-apoptotic and anti-ERS effects of rutin on H9C2 cells stimulated with high glucose. Collectively, the present results suggested that rutin may alleviate cardiomyocyte model cell injury induced by high glucose through the inhibition of apoptosis and ERS. PMID:34306208 | PMC:PMC8281503 | DOI:10.3892/etm.2021.10376 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Increased SPC24 in prostatic diseases and diagnostic value of SPC24 and its interacting partners in prostate cancer

xlomafota13 shared this article with you from Inoreader Increased SPC24 in prostatic diseases and diagnostic value of SPC24 and its interacting partners in prostate cancer Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):923. doi: 10.3892/etm.2021.10355. Epub 2021 Jun 30. ABSTRACT SPC24 is a crucial component of the mitotic checkpoint machinery in tumorigenesis. High levels of SPC24 have been found in various cancers, including breast cancer, lung cancer, liver cancer, osteosarcoma and thyroid cancer. However, to the best of our knowledge, the impact of SPC24 on prostate cancer (PCa) and other prostate diseases remains unclear. In the present study expression of global SPC24 messenger RNA (mRNA) was assessed in a subset of patients with PCa included in The Cancer Genome Atlas (TCGA) database. Increased levels of SPC24 expression were found in PCa patients >60 years old compared to patients <60 and increased SPC24 expression was also associated with higher levels of prostate specific antigen (P<0.05) and lymph node metastasis (P<0.05). Higher levels of SPC24 expression were associated with negative outcomes in PC a patients (P<0.05). Furthermore, in Chinese patients with prostatitis, benign prostatic hypertrophy (BPH) and PCa, SPC24 was expressed at significantly higher levels than that in adjacent/normal tissues, as assessed by reverse transcription-quantitative polymerase chain reaction, immunohistochemistry and western blotting. High expression of SPC24 was associated with high Gleason stages (IV and V; P<0.05). Further analysis, based on Gene Ontology and pathway functional enrichment analysis, suggested that nuclear division cycle 80 (NDC80), an SPC24 protein interaction partner, and mitotic spindle checkpoint serine/threonine-protein kinase BUB1 (BUB1), a core subunit of the spindle assembly checkpoint, may be associated with SPC24 in PCa development. Finally, using binary logistic regression, algorithms combining the receiver operating characteristic between SPC24 and BUB1 or NDC80 indicated that a combination of these markers may provide better PCa diagnosis ability than other PCa diagnosis markers. Taken together, these findings suggest that SPC24 may be a promising prostate disease biomarker. PMID:34306192 | PMC:PMC8281004 | DOI:10.3892/etm.2021.10355 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

MicroRNA-301a-3p promotes triple-negative breast cancer progression through downregulating MEOX2

xlomafota13 shared this article with you from Inoreader MicroRNA-301a-3p promotes triple-negative breast cancer progression through downregulating MEOX2 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):945. doi: 10.3892/etm.2021.10377. Epub 2021 Jul 1. ABSTRACT Breast cancer is one of the most frequently diagnosed malignancies among women. Triple-negative breast cancer (TNBC) represents a significant challenge for breast oncologists, as the availability of effective therapies for this aggressive disease is limited. The molecular mechanisms underlying TNBC development are not fully understood. Previous studies have demonstrated that microRNAs (miRNAs/miRs) play important roles in the development of various types of cancer, including breast cancer; however, the role of miRNAs in TNBC remains undetermined. The results of the present study revealed that miR-301a-3p may function as an oncogenic miRNA in TNBC. Based on The Cancer Genome Atlas data, miR-301a-3p expression levels were found to be upregulated in breast cancer tissues. Reverse transcription-quantitative PCR analysis demonstrated that the expression levels of miR-301a-3p were upregulated in TNBC tissues compared with non-TNBC tissues, and in MDA-MB-231 cells compared with normal MCF-10A breast cells. miR-301a-3p mimics and inhibitors were subsequently used to overexpress and knock down miR-301a-3p expression, respectively, in MDA-MB-231 cells. Biological functional experiments demonstrated that miR-301a-3p overexpression increased the viability, and the migratory and invasive abilities of MDA-MB-231 cells. By contrast, miR-301a-3p knockdown exerted the opposite effects on MDA-MB-231 cells. Cell apoptosis was negatively regulated by miR-301a-3p. Moreover, overexpression of miR-301a-3p was found to downregulate the expression levels of mesenchyme homeobox 2 (MEOX2). The expression levels of miR-301a-3p were negatively correlated with the expression levels of MEOX2 in clinical tissue specimens from patients with TNBC. Subsequently, the knockdown of MEOX2 expression promoted the viability of MDA-MB-231 cells. In conclusion, the re sults of the present study suggested that miR-301a-3p may serve as an oncogenic miRNA in TNBC by regulating MEOX2 expression. PMID:34306209 | PMC:PMC8281382 | DOI:10.3892/etm.2021.10377 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

ZFAS1 knockdown inhibits fibroblast-like synoviocyte proliferation, migration, invasion and inflammation, and promotes apoptosis via miR-3926/FSTL1 in rheumatoid arthritis

xlomafota13 shared this article with you from Inoreader ZFAS1 knockdown inhibits fibroblast-like synoviocyte proliferation, migration, invasion and inflammation, and promotes apoptosis via miR-3926/FSTL1 in rheumatoid arthritis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):914. doi: 10.3892/etm.2021.10346. Epub 2021 Jun 29. ABSTRACT Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by joint disorders. Long non-coding RNA zinc finger antisense 1 (ZFAS1) is aberrantly expressed in numerous human diseases, including RA. The present study aimed to investigate the functions and underlying mechanisms of ZFAS1 in RA. Reverse transcription-quantitative PCR was performed to determine the expression levels of ZFAS1, microRNA (miR)-3926 and follistatin-like protein 1 (FSTL1). MTT assay, flow cytometric analysis and Transwell assay were performed to examine the proliferation, apoptosis, migration and invasion of fibroblast-like synoviocytes (FLSs), respectively. Western blotting was employed to measure the protein expression levels of cleaved caspase-3, interleukin (IL)-6, IL-1β, tumor necrosis factor-α and FSTL1. Dual-luciferase reporter assay was perfo rmed to verify the interaction between miR-3926 and ZFAS1 or FSTL1. The results demonstrated that ZFAS1 and FSTL1 were upregulated, and miR-3926 was downregulated in RA synovial tissues and RA-FLSs. ZFAS1 knockdown suppressed cell proliferation, migration, invasion and inflammatory cytokine production, and induced apoptosis in RA-FLSs. ZFAS1 acted as a sponge for miR-3926, and ZFAS1 overexpression abolished the impact of miR-3926 on the development of RA-FLSs. FSTL1 was a direct target of miR-3926, and the effect of FSTL1 knockdown on the progression of RA-FLSs was rescued by miR-3926 inhibition. Furthermore, ZFAS1 regulated FSTL1 expression levels via sponging miR-3926 in RA-FLSs. In conclusion, ZFAS1 knockdown inhibited RA-FLS proliferation, migration, invasion and inflammatory cytokine production, and induced apoptosis in RA via the miR-3926/FSTL1 axis. PMID:34306188 | PMC:PMC8281480 | DOI:10.3892/etm.2021.10346 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.