Journal of Receptors and Signal Transduction最新文献_第8页

MicroRNA-320a-containing exosomes from human umbilical cord mesenchymal stem cells curtail proliferation and metastasis in lung cancer by binding to SOX4. 含microrna -320a的人脐带间充质干细胞外泌体通过与SOX4结合抑制肺癌的增殖和转移。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-06-07 DOI: 10.1080/10799893.2021.1918166

Huan Xie, Jie Wang

{"title":"MicroRNA-320a-containing exosomes from human umbilical cord mesenchymal stem cells curtail proliferation and metastasis in lung cancer by binding to SOX4.","authors":"Huan Xie, Jie Wang","doi":"10.1080/10799893.2021.1918166","DOIUrl":"https://doi.org/10.1080/10799893.2021.1918166","url":null,"abstract":"Exosomes from human umbilical cord mesenchymal stem cells (HUCMSCs) containing microRNAs (miRNAs) have been underscored as possible therapeutic options for cancers. Hence, our goal here was to investigate the relevance of miR-320a-containing exosomes from HUCMSCs to lung cancer. First, H1299 and H460 cells were co-cultured with the exosomes overexpressing miR-320a from HUCMSCs. The data displayed that HUCMSCs-secreted exosomes expressing miR-320a exerted anti-tumor effects in vitro and in vivo. Online analysis available at TargetScan database revealed that miR-320a bound to sex-determining region Y-box 4 (SOX4), and the luciferase reporter gene assay clarified this targeting relationship. Next, a β-catenin-specific agonist WAY-262611 was delivered into the H1299 and H460 cells to assess the effects of the Wnt/β-catenin pathway on lung cancer cellular processes. The results demonstrated that WAY-262611 potentiated lung cancer cell viability, invasion, and migration, but inhibited cell apoptosis. Altogether, exosomes carrying miR-320a from HUCMSCs might suppress lung cancer cell growth via the SOX4/Wnt/β-catenin axis, which highpoints the potency of exosomes expressing miR-320a as a possible therapeutic option for lung cancer treatment.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"268-278"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1918166","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39086076","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: 16

Curcumin restrains hepatocellular carcinoma progression depending on the regulation of the circ_0078710/miR-378b/PRIM2 axis. 姜黄素通过调节circ_0078710/miR-378b/PRIM2轴抑制肝细胞癌的进展。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-06-18 DOI: 10.1080/10799893.2021.1936554

Qian Chen, Hai Guo, Yan Zong, Xiaofeng Zhao

{"title":"Curcumin restrains hepatocellular carcinoma progression depending on the regulation of the circ_0078710/miR-378b/PRIM2 axis.","authors":"Qian Chen, Hai Guo, Yan Zong, Xiaofeng Zhao","doi":"10.1080/10799893.2021.1936554","DOIUrl":"https://doi.org/10.1080/10799893.2021.1936554","url":null,"abstract":"Purpose: Curcumin has shown anti-tumor activity in multiple malignancies. The aim of our study was to explore the molecular mechanism behind the anti-tumor activity of curcumin in hepatocellular carcinoma (HCC).Methods: The proliferation, migration, invasion, and apoptosis were analyzed by 5-ethynyl-2'-deoxyuridine (EDU) assay, transwell migration assay, transwell invasion assay, and flow cytometry. Western blot assay and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were conducted to analyze protein and RNA expression. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, and RNA-pull down assay were performed to confirm the interaction between microRNA-378b (miR-378b) and circular RNA_0078710 (circ_0078710) or DNA primase, polypeptide 2 (PRIM2). Tumor xenograft assay was conducted to assess the roles of curcumin and circ_0078710 in vivo.Results: Curcumin stimulation restrained the proliferation, migration, and invasion, and triggered the apoptosis of HCC cells. Curcumin down-regulated the expression of circ_0078710 in HCC cells in a dose-dependent manner. Circ_0078710 knockdown aggravated curcumin-mediated anti-tumor effects in HCC cells. Circ_0078710 acted as a molecular sponge for miR-378b. Circ_0078710 interference-induced effects in curcumin-stimulated HCC cells were partly abolished by the silence of miR-378b. MiR-378b bound to the 3' untranslated region (3'UTR) of PRIM2. PRIM2 overexpression partly reversed circ_0078710 interference-mediated influences in curcumin-treated HCC cells. Circ_0078710 silencing aggravated curcumin-mediated suppressive effect in tumor growth in vivo.Conclusions: Circ_0078710 silencing aggravated curcumin-mediated anti-tumor effects through mediating the miR-378b/PRIM2 signaling in HCC cells.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"313-324"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1936554","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39243224","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: 15

FAM19A5/S1PR1 signaling pathway regulates the viability and proliferation of mantle cell lymphoma. FAM19A5/S1PR1信号通路调控套细胞淋巴瘤的生存和增殖。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-03-09 DOI: 10.1080/10799893.2021.1895220

Yanfang Wang, Zhenhao Zhang, Wei Wan, Yan Liu, Hongmei Jing, Fei Dong

{"title":"FAM19A5/S1PR1 signaling pathway regulates the viability and proliferation of mantle cell lymphoma.","authors":"Yanfang Wang, Zhenhao Zhang, Wei Wan, Yan Liu, Hongmei Jing, Fei Dong","doi":"10.1080/10799893.2021.1895220","DOIUrl":"https://doi.org/10.1080/10799893.2021.1895220","url":null,"abstract":"Several intracellular pathological processes have been reported to be regulated by the FAM19A5/S1PR1 signaling pathway. However, the role of FAM19A5/S1PR1 signaling pathway in the viability and proliferation of mantle cell lymphoma is not been completely understood. The task of this study is to explore the influence of FAM19A5/S1PR1 signaling pathway in affecting the survival and growth of mantle cell lymphoma. shRNAs against FAM19A5 or S1PR1 were transfected into mantle cell lymphom. Cell viability and proliferation were measured through MTT assay and CCK8 assay, respectively. Our results demonstrated that loss of FAM19A5 significantly reduced the viability of mantle cell lymphom, an effect that was followed by a drop in cell proliferation capacity. Besides, inhibition of S1PR1 also impairs cell survival and interrupt mantle cell lymphom proliferation in vitro. Taken together, our results illustrate that FAM19A5/S1PR1 signaling pathway is associated with the regulation of mantle cell lymphom viability and proliferation. This finding will provide a potential target for the treatment of malignant lymphoma in the clinical practice.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"225-229"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1895220","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25449130","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

SIRT1/NFκB pathway mediates anti-inflammatory and anti-apoptotic effects of rosmarinic acid on in a mouse model of nonalcoholic steatohepatitis (NASH). SIRT1/NFκB 通路介导了迷迭香酸在非酒精性脂肪性肝炎（NASH）小鼠模型中的抗炎和抗凋亡作用。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-03-31 DOI: 10.1080/10799893.2021.1905665

Tahereh Komeili-Movahhed, Mahdi Bassirian, Zahra Changizi, Azam Moslehi

{"title":"SIRT1/NFκB pathway mediates anti-inflammatory and anti-apoptotic effects of rosmarinic acid on in a mouse model of nonalcoholic steatohepatitis (NASH).","authors":"Tahereh Komeili-Movahhed, Mahdi Bassirian, Zahra Changizi, Azam Moslehi","doi":"10.1080/10799893.2021.1905665","DOIUrl":"10.1080/10799893.2021.1905665","url":null,"abstract":"Nonalcoholic steatohepatitis (NASH) is considered as a common liver disease. SIRT1, a pivotal sensor, controls activation of metabolic, inflammatory and apoptotic pathways. Rosmarinic acid (RA) has positive effects on the liver injuries; nevertheless, its mechanisms are not completely studied. The aim of this study was to explore the role of rosmarinic acid on the pathways involved by SIRT1 for amelioration of a mouse model of NASH. To do this, C57/BL6 mice were divided into four equal groups (6 in each group). Animals received saline and rosmarinic acid as the control groups. NASH was induced by methionine-choline-deficient (MCD) diet. In the NASH + RA group, Rosmarinic acid was injected daily in mice fed on an MCD diet. Rosmarinic acid decreased plasma triglyceride, cholesterol, liver Steatosis and oxidative stress. Rosmarinic acid administration also increased SIRT1, Nrf2 and PPARα and decreased SREBP1c, FAS, NFκB and caspase3 expressions. Moreover, TNFα, IL6, P53, Bax/Bcl2 ratio and caspase3 expressions decreased. Our study demonstrated that remarkable effects of rosmarinic acid on the mice with NASH might be due to activation of SIRT1/Nrf2, SIRT1/NFκB and SIRT1/PPARα pathways, which alleviate hepatic steatosis, oxidative stress, inflammation and apoptosis.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"241-250"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1905665","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25533285","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: 19

Uric acid can enhance MAPK pathway-mediated proliferation in rat primary vascular smooth muscle cells via controlling of mitochondria and caspase-dependent cell death. 尿酸可通过控制线粒体和caspase依赖性细胞死亡，增强MAPK途径介导的大鼠血管平滑肌细胞增殖。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-05-30 DOI: 10.1080/10799893.2021.1931320

Segün Doğru, Ekrem Yaşar, Akın Yeşilkaya

{"title":"Uric acid can enhance MAPK pathway-mediated proliferation in rat primary vascular smooth muscle cells via controlling of mitochondria and caspase-dependent cell death.","authors":"Segün Doğru, Ekrem Yaşar, Akın Yeşilkaya","doi":"10.1080/10799893.2021.1931320","DOIUrl":"https://doi.org/10.1080/10799893.2021.1931320","url":null,"abstract":"Hyperuricemia may be a risk factor for cardiovascular diseases such as hypertension and atherosclerosis, but the mechanisms underlying uric acid-induced pathological conditions remain unknown. In this study, we investigated the effect of short time and long-term administration of increasing uric acid concentrations on cell viability, proliferative and apoptotic pathways in vascular smooth muscle cells (VSMCs). Cell viability/proliferation was determined with WST-1 assay. Expression levels of mitogen-activated protein kinases (MAPKs) (phosphorylated (p)-p38 and p-p44/42 MAPK), extrinsic (caspase 3, caspase 8), and intrinsic (B-cell lymphoma-extra-large (Bcl-xL)) apoptotic pathway proteins were measured by Western blotting. In order to assess the proliferative effects of uric acid incubations on VSMCs, we monitored the proliferative/apoptosis signaling pathways for up to 24 h. Our results indicated that uric acid increases cell viability at time and dose-dependently in VSMCs. Immunoblotting results showed that uric acid treatment elevated the expression level of p-p38 MAPK but did markedly reduce the protein levels of p-p44/42, compared with all the uric acid doses-treated VSMCs, especially at 1 h. Uric acid stimulation increased caspase-3 protein levels and decreased Bcl-xL, but did not alter caspase-8 protein expression at the same dose and time. Furthermore, low uric acid incubations (0-7.5 mg/dL) did not affect any signaling pathways for long time points (6-24 h). In conclusion, our study demonstrates for the first time that VSMCs induced with uric acid can affect cell viability, proliferative, and apoptosis pathways at the widest time and dose range. These findings provide a better understanding of the uric acid effects related to vascular impairments.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"293-301"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1931320","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38955208","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

Emodin alleviates high glucose-induced oxidative stress, inflammation and extracellular matrix accumulation of mesangial cells by the circ_0000064/miR-30c-5p/Lmp7 axis. 大黄素通过circ_0000064/miR-30c-5p/Lmp7轴缓解高糖诱导的系膜细胞氧化应激、炎症和细胞外基质积累。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-06-21 DOI: 10.1080/10799893.2021.1933028

Li Sun, Yanquan Han, Chuqiao Shen, Huan Luo, Zhuo Wang

{"title":"Emodin alleviates high glucose-induced oxidative stress, inflammation and extracellular matrix accumulation of mesangial cells by the circ_0000064/miR-30c-5p/Lmp7 axis.","authors":"Li Sun, Yanquan Han, Chuqiao Shen, Huan Luo, Zhuo Wang","doi":"10.1080/10799893.2021.1933028","DOIUrl":"https://doi.org/10.1080/10799893.2021.1933028","url":null,"abstract":"Emodin has been shown to exert a renoprotective effect in diabetic nephropathy (DN). In this paper, we investigated whether circular RNAs (circRNAs) might be involved in the renoprotective mechanism of emodin in DN. The levels of malondialdehyde (MDA), reactive oxygen species (ROS), superoxide dismutase (SOD), interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) were measured using the corresponding assay kits. The expression levels of circ_0000064, microRNA (miR)-30c-5p, large multifunctional protease 7 (Lmp7), fibronectin (FN), and collagen type I (Col.1) were gauged by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Subcellular localization assay was used to assess the cellular localization of circ_0000064. Targeted relationships among circ_0000064, miR-30c-5p and Lmp7 were confirmed by dual-luciferase reporter, RNA pull-down and RNA immunoprecipitation (RIP) assays. Our data showed the alleviative effect of emodin on HG-induced oxidative stress, inflammation and extracellular matrix (ECM) accumulation in SV-MES13 cells. Circ_0000064 was an importantly downstream effector of emodin function in HG-induced SV40-MES13 cells. Moreover, circ_0000064 directly targeted miR-30c-5p, and circ_0000064 modulated Lmp7 expression through miR-30c-5p. Circ_0000064 silencing alleviated HG-induced cell oxidative stress, inflammation and ECM accumulation via up-regulating miR-30c-5p. The enforced expression of miR-30c-5p attenuated HG-induced oxidative stress, inflammation and ECM accumulation in SV40-MES13 cells by targeting Lmp7. Our findings identified that emodin alleviated HG-induced oxidative stress, inflammation and ECM accumulation in SV40-MES13 cells at least partially by the regulation of the circ_0000064/miR-30c-5p/Lmp7 axis.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"302-312"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1933028","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39251005","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

Baicalin attenuates XRCC1-mediated DNA repair to enhance the sensitivity of lung cancer cells to cisplatin. 黄芩苷可减弱xrcc1介导的DNA修复，增强肺癌细胞对顺铂的敏感性。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-03-15 DOI: 10.1080/10799893.2021.1892132

Zhangyong Yin, Enguo Chen, Xiaoping Cai, Enhui Gong, Yuling Li, Cunlai Xu, Zaiting Ye, Zhuo Cao, Jiongwei Pan

{"title":"Baicalin attenuates XRCC1-mediated DNA repair to enhance the sensitivity of lung cancer cells to cisplatin.","authors":"Zhangyong Yin, Enguo Chen, Xiaoping Cai, Enhui Gong, Yuling Li, Cunlai Xu, Zaiting Ye, Zhuo Cao, Jiongwei Pan","doi":"10.1080/10799893.2021.1892132","DOIUrl":"https://doi.org/10.1080/10799893.2021.1892132","url":null,"abstract":"Baicalin plays important roles in different types of cancer. A previous report showed that baicalin attenuates cisplatin resistance in lung cancer. However, its mechanism remains unclear. In this study, we investigated the effect and mechanism of baicalin on DNA repair and sensitivity of lung cancer cells to cisplatin. A549 and A549/DPP cells were treated with baicalin and cisplatin. A549/DPP cells were transfected with XRCC1 and siXRCC1. Cell viability and DNA damage were detected by MTT and comet assay. Apoptosis rate and cell cycle were detected by flow cytometry assay. The expressions of Bax, Bcl-2, and Cyclin D1 were detected by western blot. XRCC1 expression was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot. Baicalin and cisplatin decreased cell viability in A549 and A549/DPP cells in dose-dependent manner. Baicalin enhanced the effect of cisplatin on promoting apoptosis, arresting cell on S stage and triggering DNA damage accompanied with the upregulation of Bcl-2-associated X protein (Bax) and downregulation of B-cell lymphoma 2 (Bcl-2) and Cyclin D1 in A549/DPP cells. Moreover, baicalin promoted the inhibitory effect of cisplatin on XRCC1 expression in A549 and A549/DPP cells. However, the synthetic effects of baicalin and cisplatin on A549/DPP cells were partially inhibited by XRCC1 overexpression and promoted by XRCC1 knockdown. This study demonstrates that baicalin interferes with XRCC1-mediated cellar DNA repair to sensitize lung cancer cells to cisplatin.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"215-224"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1892132","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25478666","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

Selective thyroid hormone receptor beta agonist, GC-1, is capable to reduce growth of colorectal tumor in syngeneic mouse models 选择性甲状腺激素受体激动剂GC-1在同基因小鼠模型中能够抑制结直肠肿瘤的生长

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-27 DOI: 10.1080/10799893.2022.2032748

K. Pourvali, Ghazaleh Shimi, Arman Ghorbani, Azam Shakery, F. Shirazi, H. Zand

{"title":"Selective thyroid hormone receptor beta agonist, GC-1, is capable to reduce growth of colorectal tumor in syngeneic mouse models","authors":"K. Pourvali, Ghazaleh Shimi, Arman Ghorbani, Azam Shakery, F. Shirazi, H. Zand","doi":"10.1080/10799893.2022.2032748","DOIUrl":"https://doi.org/10.1080/10799893.2022.2032748","url":null,"abstract":"Abstract Objective The effect of thyroid hormone (TH) on cancers was proposed more than 100 years ago; however, conclusions are conflicting. THs are precisely regulated at tissue and cellular levels. It seems that this regulation is altered in cancers. Thyroid hormone receptor beta (TRβ) has anti-proliferative and tumor-suppressive effects in many cancer cells. Therefore, we decided to investigate thyroid hormone receptor beta (THRB) expression and activation by the selective agonist, GC-1, on tumor growth in a syngeneic mouse model of colorectal cancer (CRC) and colon cell lines. Methods In vitro cell viability assay using MTT analysis, cell cycle analysis by PI staining, and FACS analysis were performed. In vivo tumor growth measurements were carried out by caliper and [18F] Fluoro-2-deoxy-2-D-glucose (FDG) – PET imaging. Gene expressions were determined using quantitative-PCR. Results Some concentrations of GC-1 had a marked negative effect on the cell viability of colorectal cell lines. Cell cycle analysis showed that the anti-proliferative effect of GC-1 may not result from cell cycle arrest or apoptosis. Tumor growth analysis in mice harboring colorectal tumor showed that GC-1 treatment for 8 d profoundly inhibited tumor growth and 18FDG uptake. THRB expression was decreased in mice tumor; however, it was upregulated following GC-1 administration. Conclusions Our results showed that specific activation of TRβ by GC-1 had negative effect on tumor growth and restored its gene expression in tumors of CRC mice model.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"4 1","pages":"495 - 502"},"PeriodicalIF":2.8,"publicationDate":"2022-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82822624","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

Upregulation of SDHA inhibited proliferation, migration, and invasion of clear cell renal cell carcinoma cells via inactivation of the Wnt/β-catenin pathway. SDHA的上调通过抑制Wnt/β-catenin通路的失活，抑制透明细胞肾细胞癌细胞的增殖、迁移和侵袭。

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: 10.1080/10799893.2021.1883060

Xiaolong Xu, Naiwei Zhang, Ruxu Gao, Jianfeng Wang, Zhihong Dai, Jianbin Bi

{"title":"Upregulation of SDHA inhibited proliferation, migration, and invasion of clear cell renal cell carcinoma cells via inactivation of the Wnt/β-catenin pathway.","authors":"Xiaolong Xu, Naiwei Zhang, Ruxu Gao, Jianfeng Wang, Zhihong Dai, Jianbin Bi","doi":"10.1080/10799893.2021.1883060","DOIUrl":"https://doi.org/10.1080/10799893.2021.1883060","url":null,"abstract":"Clear cell renal cell carcinoma (ccRCC) is a common genitourinary malignancy with high mortality. Recent findings suggest that the succinate dehydrogenase complex subunit A (SDHA) is lowly expressed in many types of cancers and involved in tumorigenesis. However, the potential regulatory roles and molecular mechanisms by which SDHA affects the development and progression of ccRCC remain largely unknown. In this study, our results showed that there was significant downregulation of SDHA in ccRCC tissue relative to corresponding non-cancerous tissue, and low expression of SDHA was associated with Fuhrman pathological grade, tumor size, TNM stage, metastasis, and poor prognosis in ccRCC patients. Moreover, overexpression of SDHA inhibited the proliferation, invasion, and migration capacities of ccRCC cells. Mechanistically, SDHA impeded the proliferation and metastasis of ccRCC cells by inactivation of the Wnt/β-catenin pathway. In vivo experiments, SDHA suppressed ccRCC growth in a nude mouse model. In conclusion, our study results indicated that SDHA may act as a new molecular marker for judging the occurrence and development of ccRCC and serve as a therapeutic target for the treatment of human ccRCC.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"180-188"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1883060","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25380914","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

Catestatin enhances ATP-induced activation of glial cells mediated by purinergic receptor P2X₄. Catestatin增强嘌呤能受体P2X4介导的atp诱导的胶质细胞活化。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-01-27 DOI: 10.1080/10799893.2021.1878536

Errong Du, Anhui Wang, Rongping Fan, Lilou Rong, Runan Yang, Juping Xing, Xiangchao Shi, Bao Qiao, Ruoyang Yu, Changshui Xu

{"title":"Catestatin enhances ATP-induced activation of glial cells mediated by purinergic receptor P2X4.","authors":"Errong Du, Anhui Wang, Rongping Fan, Lilou Rong, Runan Yang, Juping Xing, Xiangchao Shi, Bao Qiao, Ruoyang Yu, Changshui Xu","doi":"10.1080/10799893.2021.1878536","DOIUrl":"https://doi.org/10.1080/10799893.2021.1878536","url":null,"abstract":"The activation of glial cells and its possible mechanism play an extremely important role in understanding the pathophysiological process of some clinical diseases, and catestatin (CST) is involved in regulating this activation. In this project, we found that CST could enhance the activation of satellite glial cells (SGCs) and microglial cells and that the expression of P2X4 was increased; the co-expression of the P2X4 receptor with glial fibrillary acidic protein (GFAP) and the P2X4 receptor with CD11b was also increased significantly in glial cells of the ATP + CST group, and TNF-α and IL-1β also showed a rising trend; the expression of phosphorylated ERK1/2 was also increased in the ATP + CST group. In summary, we conclude that CST could enhance ATP-induced activation of SGCs and microglial cells mediated by the P2X4 receptor and that the ERK1/2 signaling pathway may be involved in this activation process.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"160-168"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1878536","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38867276","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