Journal of Receptors and Signal Transduction最新文献_第9页

Silencing of circular RNA PUM1 inhibits clear cell renal cell carcinoma progression through the miR-340-5p/FABP7 axis. 沉默环状RNA PUM1通过miR-340-5p/FABP7轴抑制透明细胞肾细胞癌的进展。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-01-20 DOI: 10.1080/10799893.2020.1870494

Fanchang Zeng, Liumei Luo, Mi Song, Daoyuan Li

{"title":"Silencing of circular RNA PUM1 inhibits clear cell renal cell carcinoma progression through the miR-340-5p/FABP7 axis.","authors":"Fanchang Zeng, Liumei Luo, Mi Song, Daoyuan Li","doi":"10.1080/10799893.2020.1870494","DOIUrl":"https://doi.org/10.1080/10799893.2020.1870494","url":null,"abstract":"Circular RNAs (circRNAs) monitor the development of clear cell renal cell carcinoma (ccRCC). However, the role of CircPUM1 in ccRCC malignancy is not studied. We estimated the mechanism of CircPUM1 in ccRCC progression in this study. CircPUM1 expression in ccRCC tissues and cells was detected. The expression of CircPUM1 was interfered in ccRCC cells, and its effects on the growth of ccRCC cells were studied. Nuclear/cytosol fractionation assay was performed for the location of CircPUM1, and the downstream miR, gene, and pathway involved in ccRCC progression were explored through gain- and loss-of-function experiments. CircPUM1 was highly expressed in ccRCC samples and cells. Inhibition of CircPUM1 prevented the growth ccRCC cells. CircPUM1 was localized in the cytoplasm and bound to miR-340-5p. Overexpression of miR-340-5p inhibited the growth of ccRCC cells. miR-340-5p targeted FABP7, and CircPUM1 induced FABP7 expression and the activation of MEK/ERK pathway through competitively binding to miR-340-5p. Overexpression of FABP7 attenuated the inhibitory effect of CircPUM1 silencing on the growth of ccRCC cells. Overall, CircPUM1 upregulates FABP7 expression by competitively binding to miR-340-5p, and then activates the MEK/ERK pathway, thus promoting ccRCC progression.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"141-150"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1870494","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38842066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 9

miR-183/TMSB4Y, a new potential signaling axis, involving in the progression of laryngeal cancer via modulating cell adhesion. miR-183/TMSB4Y，一个新的潜在信号轴，通过调节细胞粘附参与喉癌的进展。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2020-12-27 DOI: 10.1080/10799893.2020.1863987

Bin Lu, Ying Yu, Xiao-Ling Xing, Rui-Yue Liu

{"title":"miR-183/TMSB4Y, a new potential signaling axis, involving in the progression of laryngeal cancer via modulating cell adhesion.","authors":"Bin Lu, Ying Yu, Xiao-Ling Xing, Rui-Yue Liu","doi":"10.1080/10799893.2020.1863987","DOIUrl":"https://doi.org/10.1080/10799893.2020.1863987","url":null,"abstract":"Laryngeal cancer (LCa) is a prevalent malignant head and neck cancer with relatively unclear pathogenesis. A prior study has suggested that miR-183 differentially expressed in laryngeal-related malignancies, but its accurate role has not been fully ascertained in LCa. miR-183 expression in LCa tissues and cells was detected assisted by TCGA/GEO databases or qRT-PCR assay, relatively. Target genes of miR-183 were predicted via accessing to TargetScan website. Luciferase activity analysis was conducted to determine the relationship between miR-183 and its possible target. CCK-8, colony formation and transwell invasion and migration experiments were implemented to measure LCa cell viability, invasion and migration. Western blot assay was utilized to evaluate cell adhesion and EMT-related proteins expressions. The expression of miR-183 was expressed in LCa tissue samples and cells at higher levels than normal controls. Upregulation of miR-183 facilitated Hep-2 and TU212 cells viability, while miR-183 reduction inhibited the proliferative potential of Hep-2 and TU212 cells. TMSB4Y was determined as a possible target of miR-183, and its expression was decreased in LCa. LCa patients with low TMSB4Y expression had poorer outcomes relative to that with high TMSB4Y expression. TMSB4Y overturned the promoting impacts of miR-183 on the LCa cellular malignant behaviors, including cell proliferation, colonogenicity, invasion and migration. miR-183 overexpression inhibited cell adhesion through inhibiting TMSB4Y expression. Overall, all results elucidated that miR-183, as an oncogenic molecule in LCa, may be used to predict the prognosis of LCa patients by targeting TMSB4Y.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"133-140"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1863987","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38745399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Plantamajoside protects H9c2 cells against hypoxia/reoxygenation-induced injury through regulating the akt/Nrf2/HO-1 and NF-κB signaling pathways. 车前草皂苷通过调节akt/Nrf2/HO-1和NF-κB信号通路，保护H9c2细胞免受缺氧/再氧化诱导的损伤。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2020-12-22 DOI: 10.1080/10799893.2020.1859534

Guangwei Zeng, Huixian An, Dong Fang, Wei Wang, Yang Han, Cheng Lian

{"title":"Plantamajoside protects H9c2 cells against hypoxia/reoxygenation-induced injury through regulating the akt/Nrf2/HO-1 and NF-κB signaling pathways.","authors":"Guangwei Zeng, Huixian An, Dong Fang, Wei Wang, Yang Han, Cheng Lian","doi":"10.1080/10799893.2020.1859534","DOIUrl":"https://doi.org/10.1080/10799893.2020.1859534","url":null,"abstract":"Myocardial ischemia/reperfusion (I/R) injury has been found to be associated with oxidative stress. Plantamajoside (PMS) is a major compound of Plantago asiatica that was reported to possess cardioprotective and antioxidant effects. The current study was designed to investigate the effect of PMS on myocardial I/R injury. Rat cardiomyocytes H9c2 cells were exposed to hypoxia/reoxygenation (H/R) to establish in vitro model of myocardial I/R injury. MTT assay proved that H9c2 cells viability was significant reduced under H/R treatment, while the reduction was ameliorated by PMS. H/R-induced ROS production in H9c2 cells was suppressed by PMS. The decreased activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in the H/R group were effectively elevated by PMS. In addition, treatment with PMS attenuated H/R-stimulated production of TNF-α, IL-6 and IL-1β in H9c2 cells. Besides, PMS significantly suppressed bax expression and caspase 3 activity, as well as increased bcl-2 expression in H/R-stimulated H9c2 cells. Furthermore, we also found that PMS significantly enhanced the activation of Akt/Nrf2/HO-1 signaling pathway and suppressed the activation of NF-κB signaling pathway in H/R-stimulated H9c2 cells. These results provided substantial evidence that PMS protected against myocardial I/R injury via attenuating oxidative stress, inflammatory response and apoptosis. The protective effects of PMS were attributed to the Akt/Nrf2/HO-1 and NF-κB signaling pathways.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"125-132"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1859534","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38739873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12

Polygonatum sibiricum polysaccharide inhibits high glucose-induced oxidative stress, inflammatory response, and apoptosis in RPE cells. 黄精多糖抑制高糖诱导的RPE细胞氧化应激、炎症反应和凋亡。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-02-08 DOI: 10.1080/10799893.2021.1883061

Wenjun Wang, Shang Li, Meixia Song

{"title":"Polygonatum sibiricum polysaccharide inhibits high glucose-induced oxidative stress, inflammatory response, and apoptosis in RPE cells.","authors":"Wenjun Wang, Shang Li, Meixia Song","doi":"10.1080/10799893.2021.1883061","DOIUrl":"https://doi.org/10.1080/10799893.2021.1883061","url":null,"abstract":"Diabetic retinopathy is one of the major diabetic complications and remains the most common cause of adult blindness among patients with diabetes mellitus. Polygonatum sibiricum polysaccharides (PSP) are a group important component of Polygonatum sibiricum (PS) with anti-diabetic activity. However, the effect and underlying mechanism of PSP on diabetic retinopathy remains unclear. We used high glucose (HG)-stimulated ARPE-19 cells to establish in vitro diabetic retinopathy model. Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay was performed to evaluate cell viability of ARPE-19 cells. The changes in the ROS production, malondialdehyde (MDA) content, and activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were detected to indicate oxidative stress. The secretion levels of tumor necrosis factor-alpha (TNF-α) and interleukin-8 (IL-8) were detected by ELISA. The protein levels of TNF-α, IL-8, bcl-2, bax, nuclear Nrf2, and anti-hemeoxygenase-1 (HO-1) were detected by western blot analysis. Our results showed that HG treatment caused a significant reduction in cell viability of ARPE-19 cells. PSP treatment improved the reduced cell viability of ARPE-19 cells. PSP also attenuated HG-induced oxidative stress with decreased ROS production and MDA content, as well as increased the activities of SOD and GPx. In addition, HG significantly increased bax expression and caspase-3 activity, and decreased bcl-2 expression. However, these changes were mitigated by PSP treatment. Furthermore, PSP markedly induced the activation of Nrf2/HO-1 pathway in HG-induced ARPE-19 cells. Knockdown of Nrf2 reversed the protective effects of PSP on HG-induced ARPE-19 cells. Taken together, these findings indicated that PSP protects ARPE-19 cells from HG-induced oxidative stress, inflammation, and cell apoptosis through regulation of Nrf2/HO-1 signaling pathway.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"189-196"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1883061","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25345583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 14

JAK2/STAT3 inhibitor reduced 5-FU resistance and autophagy through ATF6-mediated ER stress. JAK2/STAT3抑制剂通过atf6介导的内质网应激降低5-FU耐药和自噬。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-02-18 DOI: 10.1080/10799893.2021.1887219

Lijuan Ma, Youhui Wang

{"title":"JAK2/STAT3 inhibitor reduced 5-FU resistance and autophagy through ATF6-mediated ER stress.","authors":"Lijuan Ma, Youhui Wang","doi":"10.1080/10799893.2021.1887219","DOIUrl":"https://doi.org/10.1080/10799893.2021.1887219","url":null,"abstract":"Drug resistance seriously limits the efficacy of chemotherapy drugs and hinders successful treatment in patients with gastric cancer. Endoplasmic reticulum (ER) and autophagy are recognized to be one of the mechanisms involving the drug resistance of gastric cancer. The mechanisms of action of JAK2/STAT3 pathway were investigated in AGS cells with drug resistance of 5-fluorouracil (5-FU) by corresponding inhibitors. We firstly analyzed the effects of JAK2/STAT3 inhibitor on the expression of drug resistance genes, autophagy markers, and ER stress-related markers on AGS/5-FU cells by Western blot. Whether JAK2/STAT3 pathway regulated the transcription of ATF6 was investigated through luciferase reporter assay. The expression of LC3B was detected by immunofluorescence assay. Next, ER stress inhibitor and ATF6 overexpression plasmid were respectively used to treat AGS/5-FU cells for analyzing whether JAK2/STAT3 pathway regulated ER stress. The results showed that JAK2 inhibitor or STAT3 inhibitor significantly altered the expression of these proteins and suppressed the activities of ATF6 promoter. Intriguingly, ATP6 overexpression could markedly reverse their effects. Moreover, similar effects to JAK2 inhibitor or STAT3 inhibitor appeared in ER stress inhibitor-treated group. These findings indicated that the involvement of JAK2/STAT3 pathway in regulating ER stress affected the 5-FU resistance of AGS cells and autophagy, which was mediated by ATF6. Targeting JAK2/STAT3 pathway could be a potential approach to decrease the 5-FU resistance of gastric cancer and enhance the sensitivity of gastric cancer to 5-FU. Additionally, our study offers new insights into the molecular mechanisms underlying the resistance of gastric cancer to 5-FU.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"206-213"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1887219","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25378962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Inhibition of TGF-β1 on Gli2 expression was promoted by TNF-α in primary leukemia cells. TNF-α可促进原发性白血病细胞TGF-β1对Gli2表达的抑制作用。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-02-22 DOI: 10.1080/10799893.2021.1881555

Zhe Li, Shudan Mao, Ning Zhang

引用次数: 0

The protective effects of simvastatin in Cadmium-Induced preosteoblast injury through Nox4. 辛伐他汀对镉诱导的成骨前细胞损伤的保护作用。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2020-12-22 DOI: 10.1080/10799893.2020.1859533

Chongxia Huang, Du Liang, Chongbo Huang, Baolin Li, Jiandong He, Ximou Huang

{"title":"The protective effects of simvastatin in Cadmium-Induced preosteoblast injury through Nox4.","authors":"Chongxia Huang, Du Liang, Chongbo Huang, Baolin Li, Jiandong He, Ximou Huang","doi":"10.1080/10799893.2020.1859533","DOIUrl":"https://doi.org/10.1080/10799893.2020.1859533","url":null,"abstract":"Cadmium (Cd) has a direct toxic effect on bones. Statins such as simvastatin have protective effects on various diseases, including on tissue injury. The current study revealed the efficacy of simvastatin on Cd-induced preosteoblast injury. Preosteoblast MC3T3-E1 cells were incubated with various doses of CdCl2 for 12 h, 24 h and 48 h, and then the cell cytotoxicity was assessed using MTT assay and flow cytometry, respectively. The expression level of Nox4 was assessed by Western blot and qRT-PCR. The morphological appearance of MC3T3-E1 cells was observed under a microscope. Cells exposed to CdCl2 (5 µM) were further treated by simvastatin at various doses, subsequently cell viability, apoptosis and the expression of Nox4 were measured. Furthermore, to confirm the protective effects of simvastatin on Cd-induced pre-osteoblast injury, functional rescue assays were performed after corresponding cell treatment by simvastatin (10-8 M), CdCl2 (5 µM), and overexpression of Nox4. Expressions of cell apoptosis-related markers were measured by Western blot and qRT-PCR. The results revealed that CdCl2 caused MC3T3-E1 cell injury because the cell viability was decreased and the apoptosis was increased. Nox4 expression was up-regulated with the increase of CdCl2 concentrations. Simvastatin increased the cell viability, relieved the cell apoptosis and Nox4 expression previously increased by CdCl2. The effects of CdCl2 on MC3T3-E1 cells and Nox4 expression could be attenuated by simvastatin, and promoted by Nox4 overexpression. The current study found that simvastatin protects Cd-induced preosteoblast injury via Nox4, thus, it can be used as a potential drug for treating cadmium-induced bone injury.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"117-124"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1859533","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39087751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Sauchinone inhibits hypoxia-induced invasion and epithelial-mesenchymal transition in osteosarcoma cells via inactivation of the sonic hedgehog pathway. 苏奇诺酮通过灭活sonic hedgehog通路抑制缺氧诱导的骨肉瘤细胞侵袭和上皮-间质转化。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-02-09 DOI: 10.1080/10799893.2021.1881556

Dan Zhou, Ling He

{"title":"Sauchinone inhibits hypoxia-induced invasion and epithelial-mesenchymal transition in osteosarcoma cells via inactivation of the sonic hedgehog pathway.","authors":"Dan Zhou, Ling He","doi":"10.1080/10799893.2021.1881556","DOIUrl":"https://doi.org/10.1080/10799893.2021.1881556","url":null,"abstract":"Hypoxia is a typical feature of solid tumors and is closely associated with tumor progression. Sauchinone, a biologically diastereomeric lignan, is isolated from the root of Saururus chinensis and has been widely used for the treatment of various diseases. Recently, sauchinone has been reported to play an anti-cancer role in cancer development under normoxia or hypoxia. However, the specific effects of sauchinone on osteosarcoma (OS) remain unclear. The aim of the present study was to investigate the role of sauchinone in OS progression under hypoxic conditions. The human OS cell lines U2OS and MG-63 were exposed to hypoxia followed by treatment with sauchinone. Cell viability was assessed by the CCK-8 assay. Cell migration and invasion were detected by transwell assays. The expression levels of VEGF, HIF-1α, E-cadherin and N-cadherin were examined by the western blot analysis. Our study showed that OS cell migration and invasion were significantly enhanced by hypoxia. Besides, hypoxic conditions resulted in a remarkable change in the expression of EMT markers. All these effects induced by hypoxia were abrogated by sauchinone treatment. Moreover, sauchinone inhibited hypoxia-induced activation of the sonic hedgehog (Shh) pathway. Additionally, the Shh agonist reversed the inhibitory effect of sauchinone on hypoxia-induced invasion and EMT of OS cells. In conclusion, these findings demonstrated that sauchinone inhibits hypoxia-induced invasion and EMT in OS cells via inactivation of the Shh pathway. We provided a novel insight for understanding the mechanisms underlying the anti-cancer effect of sauchinone and suggested sauchinone as a promising agent for OS treatment.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"173-179"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1881556","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25350353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Glaucocalyxin a prevents hypoxia-induced epithelial-mesenchymal transition in human gastric cancer cells through the PI3K/Akt signaling pathway. 青萼藻素a通过PI3K/Akt信号通路阻止缺氧诱导的人胃癌细胞上皮-间质转化。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2020-12-13 DOI: 10.1080/10799893.2020.1853160

Xihan Zhou, Weijin Ma, Xiaohui Li, Jiali Xu

{"title":"Glaucocalyxin a prevents hypoxia-induced epithelial-mesenchymal transition in human gastric cancer cells through the PI3K/Akt signaling pathway.","authors":"Xihan Zhou, Weijin Ma, Xiaohui Li, Jiali Xu","doi":"10.1080/10799893.2020.1853160","DOIUrl":"https://doi.org/10.1080/10799893.2020.1853160","url":null,"abstract":"Abstract Hypoxia is a frequent occurrence in most solid tumors and associated with multiple cancer progression. Glaucocalyxin A (GLA) has been found to exhibit anti-tumor effect in several types of cancer, except gastric cancer (GC). The present study aimed to evaluate the function of GLA in GC and explore the underlying mechanism under hypoxia condition. Our results showed that GLA suppressed cell viability of MGC-803 cells in both normoxic or hypoxic conditions. MGC-803 cells were more sensitive to GLA in hypoxic condition. GLA attenuated hypoxia-induced migration and invasion of GC cells. Western blot assay proved that GLA elevated E-cadherin expression, as well reduced N-cadherin and vimentin expressions in hypoxia-induced GC cells. Moreover, we also found that GLA suppressed the expression of HIF-1α in both mRNA and protein levels. Furthermore, GLA blocked hypoxia-induced activation of PI3K/Akt pathway in GC cells. Notably, insulin like growth factor 1 (IGF-1), an activator of PI3K/Akt pathway, reversed the effects of GLA on cell migration, invasion and EMT in hypoxia-treated MGC-803 cells. In conclusion, these findings demonstrated that GLA exerted inhibitory effects on cell migration, invasion and epithelial to mesenchymal transition (EMT) via the PI3K/Akt signaling pathway in GC cells.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"109-116"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1853160","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38702955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Inhibition of TRIM14 protects cerebral ischemia/reperfusion injury through regulating NF-κB/NLRP3 pathway-mediated inflammation and apoptosis. 抑制TRIM14通过调节NF-κB/NLRP3通路介导的炎症和凋亡来保护脑缺血/再灌注损伤。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-03-10 DOI: 10.1080/10799893.2021.1887218

Xianlong Xie, Fan Wang, Xiujuan Li

{"title":"Inhibition of TRIM14 protects cerebral ischemia/reperfusion injury through regulating NF-κB/NLRP3 pathway-mediated inflammation and apoptosis.","authors":"Xianlong Xie, Fan Wang, Xiujuan Li","doi":"10.1080/10799893.2021.1887218","DOIUrl":"https://doi.org/10.1080/10799893.2021.1887218","url":null,"abstract":"Purpose: Many proteins in tripartite motif (TRIM) family have been reported to play an important role in cerebral ischemia/reperfusion (I/R) injury. This study was designed to investigate the effect of TRIM14 on the cerebral I/R injury in rats.Methods: The rat model was constructed through inserting thread into the middle cerebral artery. The expression of TRIM14 was measured by qRT-PCR, immunoblotting, and immunofluorescence. The hippocampal sections were stained with 2,3,5-triphenyltetrazolium chloride (TTC) to determine infarct volume and used for measuring the neurologic deficit score and brain water content. The H&E staining was used for immunohistochemical (IHC) staining. The number of apoptotic cells was measured by fluorescence microscopy. The levels of IL-6, IL-1β, and TNFα were detected by qRT-PCR and ELISA. The swimming speed, latency time, and number of platform crossings were measured by the water maze test.Results: TRIM14 was significantly enhanced in rats with cerebral I/R injury compared to Sham rats, showing its highest level at 24 h after I/R. TRIM14 inhibition reduced ischemic brain injury, suppressed neuron apoptosis, suppressed inflammation, and improved cognitive dysfunction in rats with cerebral I/R injury. TRIM14 inhibition also suppressed the activation of NF-κB/NLRP3 pathway in rats with cerebral I/R injury.Conclusion: In conclusion, the expression of TRIM14 was increased in rats with cerebral I/R injury, the protective effect of TRIM14 inhibitor on cerebral I/R injury in rats depends on its anti-apoptotic and anti-inflammatory effect. The underlying mechanism was, at least partially, through regulating NF-κB/NLRP3 pathway.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"197-205"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1887218","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25454060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7