Cerebral revascularization for the management of complex middle cerebral artery aneurysm: A case series

xlomafota13 shared this article with you from Inoreader Cerebral revascularization for the management of complex middle cerebral artery aneurysm: A case series Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):883. doi: 10.3892/etm.2021.10315. Epub 2021 Jun 15. ABSTRACT Complex middle cerebral artery (MCA) aneurysms, including aneurysms that are sizeable (large or giant), fusiform, wide-necked or calcified, remain a significant challenge during microsurgical clipping or endovascular coiling as treatment strategies. In the present study, a retrospective analysis of cases of this type of aneurysm treated between August 2012 and December 2019 was performed. From the hospital's database, a total of 13 patients (7 males and 6 females) with a mean age of 39.0 years (range, 13-65 years) were identified. The mean size of the aneurysms was 17.5 mm (range, 3.9-35.0 mm). A total of four patients (30.8%) had ruptured aneurysms and nine (69.2%) had unruptured aneurysms. All aneurysms were treated by proximal occlusion of the parent artery, trapping or excision combined with cerebral revascularization. The bypasses performed i ncluded 10 extracranial-intracranial bypasses and 3 intracranial-intracranial bypasses (1 end-to-end re-anastomosis, 1 interpositional graft and 1 end-to-side reimplantation). Postoperative angiography confirmed that the bypass patency was 92.3% and the clinical outcomes were indicated to be favorable, with a modified Rankin Scale score ≤2 in 12 out of 13 patients (92.3%) at the last follow-up. Taken together, the results of the present analysis suggested that treatment strategies for complex MCA aneurysms should depend on the status and characteristics of the aneurysm, including aneurysm size, location and morphology. For aneurysms that lack perforating arteries in the aneurysm dome, clip trapping or aneurysm excision with or without bypass are preferred as treatment strategies. When there are perforating arteries (particularly the lenticulostriate artery) arising from the aneurysm dome, however, the aneurysms should be treated with bypass followed by proximal occlusion of the pa rent artery or clip reconstruction. PMID:34194561 | PMC:PMC8237261 | DOI:10.3892/etm.2021.10315 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Curcumin inhibits the viability, migration and invasion of papillary thyroid cancer cells by regulating the miR-301a-3p/STAT3 axis

xlomafota13 shared this article with you from Inoreader Curcumin inhibits the viability, migration and invasion of papillary thyroid cancer cells by regulating the miR-301a-3p/STAT3 axis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):875. doi: 10.3892/etm.2021.10307. Epub 2021 Jun 14. ABSTRACT Thyroid cancer is one of the most common malignant tumors, and the mortality rate associated with thyroid cancer has been increasing annually. Curcumin has been reported to exert an antitumor effect on papillary thyroid cancer (PTC), and the identification of additional mechanisms underlying the anticancer effect of curcumin on PTC requires further investigation. The present study aimed to explore the effects of curcumin on the viability, migration and invasion of PTC cells. TPC-1 cells were incubated with different concentrations of curcumin, and then, cell viability, migration and invasion, and wound healing were examined by CCK-8, Transwell and wound healing assays, respectively. Subsequently, microRNA (miR)-301a-3p mimics, miR-301a-3p inhibitors and signal transducer and activator of transcription (STAT)3 overexpression vector were transfected into TPC-1 cells, and cell viability, migration, and invasion were reassessed in these transfected cells. Matrix metallopeptidase (MMP)-2, MMP-9, epithelial-mesenchymal transition (EMT)-related markers, and Janus kinase (JAK)/STAT signaling pathway components were assessed by western blot analysis. Curcumin significantly inhibited cell viability, migration and invasion and downregulated MMP-2, MMP-9 and EMT marker expression. Additionally, curcumin decreased STAT3 expression by upregulating miR-301a-3p expression, and the inhibition of miR-301a-3p and the overexpression of STAT3 reversed the effects of curcumin on cell viability, migration and invasion, and MMP-2, MMP-9 and EMT marker expression in TPC-1 cells. Furthermore, curcumin suppressed the JAK/STAT signaling pathway through the miR-301a-3p/STAT3 axis. The data of the present study indicated that curcumin could inhibit the viability, migration and invasion of TPC-1 cells by regulating the miR-301a-3p/STAT3 axis. These findin gs may provide a possible strategy for the clinical treatment of PTC. PMID:34194553 | PMC:PMC8237388 | DOI:10.3892/etm.2021.10307 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Long non-coding RNA RP11-81H3.2 suppresses apoptosis by targeting microRNA-1539/COL2A1 in human nucleus pulposus cells

xlomafota13 shared this article with you from Inoreader Long non-coding RNA RP11-81H3.2 suppresses apoptosis by targeting microRNA-1539/COL2A1 in human nucleus pulposus cells Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):884. doi: 10.3892/etm.2021.10316. Epub 2021 Jun 16. ABSTRACT Intervertebral disk degeneration (IDD) is a severe health problem that results in lower back pain and disability. Previous evidence has indicated that excessive apoptosis of nucleus pulposus (NP) cell is involved in the occurrence and development of IDD. However, the underlying mechanisms regulating NP cell apoptosis are unclear. The present study aimed to investigate the function of a novel long non-coding RNA RP11-81H3.2 in modulating NP cell apoptosis and the potential underlying mechanisms. The results demonstrated that the RP11-81H3.2 expression levels were significantly decreased in NP tissues from patients with IDD compared with those from healthy controls, and that lower expression levels were associated with higher-grade disk degeneration. Functionally, RP11-81H3.2 silencing promoted apoptosis and decreased the viability of NP cells deriv ed from tissue samples of patients with IDD, whereas RP11-81H3.2 overexpression induced opposite effects. Bioinformatics analysis, luciferase assays and reverse transcription-quantitative PCR revealed that microRNA (miR)-1539 was a direct target of RP11-81H3.2. A mechanistic analysis demonstrated that RP11-81H3.2 functioned as an RNA sink to downregulate miR-1539, which led to the upregulation of collagen type 2 α 1 chain (COL2A1), a target of miR-1539. Collectively, the present results suggested that lower RP11-81H3.2 expression levels were associated with higher-grade IDD, and that RP11-81H3.2 inhibited NP cell apoptosis by decreasing the levels of miR-1539 to increase COL2A1 expression levels. The present study identified a beneficial role of RP11-81H3.2 against NP cell apoptosis. PMID:34194562 | PMC:PMC8237274 | DOI:10.3892/etm.2021.10316 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Mediators of extracellular matrix degradation and inflammation: A new team of possible biomarkers for oral squamous cell carcinoma stage

xlomafota13 shared this article with you from Inoreader Mediators of extracellular matrix degradation and inflammation: A new team of possible biomarkers for oral squamous cell carcinoma stage Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):877. doi: 10.3892/etm.2021.10309. Epub 2021 Jun 15. ABSTRACT Oral cancer represents one of the most common types of cancer worldwide, with oral squamous cell carcinoma (OSCC) being the most frequently diagnosed. Cytokines play a crucial role in inflammation, apoptosis and metastasis. Interleukin (IL)-8 promotes the direct migration of inflammatory cells. IL-6 induces tumor cell proliferation, increases expression of invasiveness and angiogenetic factors or matrix metalloproteinases (MMPs), promoting metastasis. Tissue inhibitor of metalloproteinases (TIMPs) blocks the action of MMPs controlling extracellular matrix degradation and inhibiting metastasis. The aim of our study was to analyze the existence of correlations between inflammation markers (IL-6 and IL-8) and extracellular degradation protection markers such as TIMP-1 in OSCC tumors. Our study included 20 patients (12 females and 8 males) diagnosed w ith OSCC, recruited from January to April, 2020. IL-8, IL-6 and TIMP-1 levels were measured in the tumor cell lysates by ELISA technique, using relevant assay kits. Our results showed a positive and significant correlation between IL-6 and IL-8 (P=0.005, R=0.517) indicating that high IL-8 levels can be associated with high IL-6 levels. We also found a significant and high negative correlation (P<0.001, R=-0.673) between IL-6 and TIMP-1 and a significant and high negative correlation (P<0.001, R=-0.684) between IL-8 and TIMP-1 indicating that high levels of IL-8 and IL-6 are significantly associated with lower levels of TIMP-1. In conclusion, our study confirms the available literature data on IL-6 and IL-8 as potential markers for oral cancers such as OSCC and affect the tumor microenvironment by decreasing TIMPs. All three biomarkers included in this study have the potential to be used as detection or prognostic factors for oral cancer. PMID:34194555 | PMC:PMC8237384 | DOI:10.3892/etm.2021.10309 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Advanced oxidation protein products trigger apoptosis and block epithelial-to-mesenchymal transition in crypt epithelial cells

xlomafota13 shared this article with you from Inoreader Advanced oxidation protein products trigger apoptosis and block epithelial-to-mesenchymal transition in crypt epithelial cells Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):885. doi: 10.3892/etm.2021.10317. Epub 2021 Jun 16. ABSTRACT Advanced oxidation protein products (AOPPs) are uremic toxins. The present study aimed to investigate the effects of AOPPs on the epithelial mesenchymal transition (EMT) and apoptosis of rat crypt epithelial cells, and to assess the signaling pathways involved. The oxidized rat serum albumin was obtained by sodium hypochlorite modification as AOPPs, and the rat serum albumin (RSA) without sodium hypochlorite modification was set as the control. Different concentrations of AOPPs or RSA were incubated with rat crypt epithelial cells (IEC-6 cells). After culturing for 48 and 72 h, apoptosis was detected by flow cytometry. IEC-6 cells were divided into three groups: A normal group, an AOPPs group and an RSA group. Three groups of cells were collected following treatment for 2 h, and the phosphorylation levels of Akt and p65 NF-κB were detected by wes tern blotting. After 72 h of treatment, the cells were collected and the apoptotic rate was detected by flow cytometry. The expression of EMT-related proteins was detected by reverse transcription-quantitative polymerase chain reaction and western blotting. The apoptotic rate of IEC-6 cells increased with the concentration of AOPPs, and the apoptotic rate of the AOPPs group was higher than that of the RSA group. The expression of fibronectin, snail, slug and collagen I in the AOPPs group was lower than that in the RSA group, while the expression of E-cadherin was not significantly different between the two groups. In addition, the expression of fibronectin, snail, slug and collagen I genes in the AOPPs-treated group was equal to or lower than that in the normal group. Compared with the normal group, the Akt phosphorylation level was decreased and the p65 phosphorylation level was increased in the AOPPs- or RSA-treated groups. Compared with the AOPPs-treated group, Akt and p65 phosph orylation levels in RSA-treated group were slightly higher. In conclusion, AOPPs trigger apoptosis and inhibit the EMT of rat crypt epithelial cells, which may be associated with the inhibition of Akt phosphorylation and the promotion of p65 phosphorylation. PMID:34194563 | PMC:PMC8237260 | DOI:10.3892/etm.2021.10317 < /div> View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Interference of long non-coding RNA HAGLROS inhibits the proliferation and promotes the apoptosis of ovarian cancer cells by targeting miR-26b-5p

xlomafota13 shared this article with you from Inoreader Interference of long non-coding RNA HAGLROS inhibits the proliferation and promotes the apoptosis of ovarian cancer cells by targeting miR-26b-5p Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):879. doi: 10.3892/etm.2021.10311. Epub 2021 Jun 15. ABSTRACT Ovarian cancer (OV) is the fifth most common type of cancer affecting women worldwide. Long non-coding RNAs (lncRNAs) serve essential roles in the progression of OV. As such, the present study aimed to investigate the specific role of HAGLR opposite strand lncRNA (HAGLROS) in OV and the underlying mechanism of action through which HAGLROS exerts its effects on OV cells. In the present study, the expression of HAGLROS in several OV cell lines was first detected using reverse transcription-quantitative PCR. HAGLROS was then silenced to evaluate cell viability, proliferation and apoptosis, which were determined using Cell Counting Kit-8, colony formation and TUNEL assays, respectively. Additionally, immunofluorescence staining and western blotting were used to confirm the expression profile of proliferation- and apoptosis-related proteins. Moreover, a dual luciferase reporter assay was used to verify the potential interactions between HAGLROS and microRNA (miR)-26b-5p. Subsequently, rescue assays were performed to investigate the effects of HAGLROS and miR-26b-5p on OV progression. The results indicated that HAGLROS was highly expressed in OV cells. Interference of HAGLROS led to a decrease in the proliferation, but an increase in the apoptosis of OV cells, accompanied by downregulated expression levels of Ki67 and Bcl-2, and upregulated expression levels of Bax and cleaved caspase-3. Further study revealed that HAGLROS acted as a sponge for miR-26b-5p and positively regulated its expression. miR-26b-5p inhibitor transfection partially reversed the effects of HAGLROS knockdown on the proliferation and apoptosis of OV cells. In conclusion, the results of the present study suggested that interference of HAGLROS suppressed the proliferation and promoted the apoptosis of OV cells through regulating miR-26b-5p, indicating that HAGLR OS may be a promising biomarker in OV diagnosis and treatment. PMID:34194557 | PMC:PMC8237406 | DOI:10.3892/etm.2021.10311 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Oridonin improves the therapeutic effect of lentinan on lung cancer

xlomafota13 shared this article with you from Inoreader Oridonin improves the therapeutic effect of lentinan on lung cancer Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):886. doi: 10.3892/etm.2021.10318. Epub 2021 Jun 16. ABSTRACT Oridonin, a compound from Rabdosia rubescens, has been shown to exhibit a potent ability to improve the antitumor effects of lentinan (LNT). In the present study, the effects of oridonin, LNT, and the combination of these treatments were assessed on the normal human fetal lung fibroblast cell line MRC-5, as well as the non-small cell lung cancer cell line A549. Next, their effects on metastasis and survival in vivo were assessed in a mouse model of lung cancer. The effects of the treatments on the mRNA and protein expression levels of several regulatory factors in A549 cells and lung tissues were determined using reverse transcription-quantitative PCR and western blotting. The results showed that the viability of MRC-5 and A549 cells were not affected by 0-20 µg/ml oridonin; 0-300 µg/ml LNT did not affect the viability of MRC-5 cel ls, but 50-400 µg/ml LNT reduced the viability of A549 cells. Thus, 20 µg/ml oridonin and 100 or 300 µg/ml LNT were used in the subsequent experiments. Treatment with oridonin and LNT, alone or combined, had no effect on MRC-5 cell viability. Oridonin treatment had no effect on A549 cell viability; however, LNT suppressed A549 cell viability, and oridonin promoted the suppressive effects of LNT on A549 cells. In vivo analysis showed that oridonin alone had no effect on metastasis and survival, but LNT decreased metastasis and survival in mice. Oridonin augmented the effects of LNT against metastasis and further improved the survival rates of mice. In both A549 cells and lung tissues, LNT increased the mRNA and protein expression levels of caspase-3, caspase-8, caspase-9, Bax, p53, p21 and inhibitor of nuclear factor-κB (NF-κB)-α, and reduced the mRNA and protein expression levels of Bcl-2 and NF-κB. Oridonin augmented all the effects of LNT on expression of these prote ins in the cells. Together, the results showed that oridonin enhanced the antitumor effects of LNT, and may thus serve as an adjuvant alongside LNT as a novel anticancer regimen for treatment of lung cancer. PMID:34194564 | PMC:PMC8237276 | DOI:10.3892/etm.2021.10318 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

MicroRNA-29b participates in the epithelial-mesenchymal transition of retinal pigment epithelial cells through p-p65

xlomafota13 shared this article with you from Inoreader MicroRNA-29b participates in the epithelial-mesenchymal transition of retinal pigment epithelial cells through p-p65 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):868. doi: 10.3892/etm.2021.10300. Epub 2021 Jun 13. ABSTRACT Epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells is considered to be the main mechanism of proliferative vitreoretinopathy (PVR). Our previous study demonstrated that microRNA-29b (miR-29b) and its target protein kinase B (Akt2) played vital roles in this process. miR-29b, a mesenchymal marker α-smooth muscle actin (α-SMA) and the epithelial marker E-cadherin were assessed in epiretinal membranes of patients with PVR. The potential mechanism of miR-29b and EMT was also investigated. The expression levels of miR-29b, E-cadherin, and α-SMA in PVR epiretinal membranes were measured using quantitative PCR. The expression levels of Akt2, phosphorylated (p)-Akt2, p65, p-p65, and Snail in ARPE-19 cells were assessed using western blotting. The expression levels of miR-29b were positively correlated with E-cadherin mRNA expression, while an inverse correlation was observed between miR-29b and α-SMA mRNA expression in epiretinal membranes of patients with PVR. When miR-29b was transfected into ARPE-19 cells, the expression levels of Akt2, p-Akt2, p-p65 and Snail were downregulated. shRNA-Akt2 inhibited p-p65 and Snail expression, while the NF-κB inhibitor BAY11-7082 reduced Snail expression. The Akt2/p-p65/Snail pathway may be the underlying mechanism of miR-29b in EMT of RPE cells. The results of the present study may provide a new strategy for prevention and therapy of PVR. PMID:34194546 | PMC:PMC8237392 | DOI:10.3892/etm.2021.10300 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Disruption of anchoring junctions in the testes of experimental varicocele rats

xlomafota13 shared this article with you from Inoreader Disruption of anchoring junctions in the testes of experimental varicocele rats Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):887. doi: 10.3892/etm.2021.10319. Epub 2021 Jun 16. ABSTRACT Varicocele is a common disease of the male reproductive system and is the main cause of male infertility; however, the pathological mechanisms of varicocele remain unclear. The anchoring junctions (AJs) in the testies are located between Sertoli cells, or between Sertoli cells and germ cells. Intact and functional AJs are crucial for spermatogenesis. In the present study, the histomorphology, ultrastructure of AJ, cell cycle, expression of AJ structural proteins, and the level of AJ-associated signaling molecules were investigated in the left testes of experimental varicocele rats at 8 and 12 weeks after surgery. The results revealed that varicocele induced the loss of premature germ cells from the seminiferous epithelium. Furthermore, the results of the present study also revealed damage to the AJ ultrastructure, disorientation of the spermatid h ead, deregulation of the cell cycle, downregulation of AJ structural proteins, enhanced phosphorylation of focal adhesion kinase (FAK) at Tyr397 and its downstream adapter Src at Tyr416, and activation of the extracellular signal-regulated protein kinase 1 (ERK1) signaling pathway. Thus, the present study demonstrated that varicocele disrupted the structure and function of AJs in the left testes of rats, and that enhancement of FAK phosphorylation may contribute to AJ damage by activating ERK1 signaling, disrupting actin-based filament networks, and altering the balance of the apical ectoplasmic specialization-blood testis barrier functional axis. These findings provide important insights into the pathological mechanisms through which varicocele contributes to male infertility and could help to identify new therapeutic targets for varicocele. PMID:34194565 | PMC:PMC8237278 | DOI:10.3892/etm.2021.10319 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Curcumin sensitizes Epstein-Barr-immortalized lymphoblastoid cell lines to inorganic arsenic toxicity

xlomafota13 shared this article with you from Inoreader Curcumin sensitizes Epstein-Barr-immortalized lymphoblastoid cell lines to inorganic arsenic toxicity Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):872. doi: 10.3892/etm.2021.10304. Epub 2021 Jun 14. ABSTRACT Chronic exposure to inorganic arsenic (iAs) through contaminated drinking water is an important health problem in certain countries. The use of phytochemicals such as curcumin has recently emerged as an alternative strategy for preventing cellular damage caused by iAs. The Epstein-Barr virus (EBV) affects ~90% of the population and experimental evidence suggested that curcumin mediates cytotoxicity against EBV-infected cells. Due to the potential for an interaction of these factors, the aim of the present study was to evaluate the effect of this phytochemical on iAs-related toxicity in EBV-infected cells. Two independent EBV-immortalized human lymphoblastoid cell lines (LCLs) were used as the model. The cell lines were first incubated with increasing concentrations of curcumin or iAs for 24 and 15 h, respectively, to determine the individual effec ts of each exposure on cell death. In the next experiment, cell cultures were pre-incubated with 5 µM curcumin for 9 h prior to treatment with 10 µM iAs for 15 h, followed by evaluation of cell death and the cell cycle profile via flow cytometry. The results indicated that individual treatment with either curcumin or iAs induced cell death in a concentration-dependent manner. Furthermore, curcumin pre-treatment enhanced iAs-induced cell death and promoted cell cycle arrest in G1 phase. Taken together, these results suggested that curcumin sensitizes EBV-positive LCLs to the cytotoxic effects of iAs. PMID:34194550 | PMC:PMC8237405 | DOI:10.3892/etm.2021.10304 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.