Journal of Cell Communication and Signaling最新文献_第3页

LncRNA HOTTIP promotes LPS-induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP-C LncRNA HOTTIP通过招募DNMT1对SP-C进行表观遗传调控，促进LPS诱导的肺上皮细胞损伤

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-02-27 DOI: 10.1002/ccs3.12020

Shuang Li, Shuangjia Li, Zhanqun Gao, Yang Liu

{"title":"LncRNA HOTTIP promotes LPS-induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP-C","authors":"Shuang Li, Shuangjia Li, Zhanqun Gao, Yang Liu","doi":"10.1002/ccs3.12020","DOIUrl":"https://doi.org/10.1002/ccs3.12020","url":null,"abstract":"The objective of this study was to elucidate the involvement of the long noncoding RNA (lncRNA) HOTTIP in acute lung injury and understand the underlying mechanisms. Relevant expression of mRNAs and proteins were assessed by qRT-PCR and western blot assays. Cell viability was determined by employing the CCK-8 assay, and apoptosis was quantified through TUNEL staining. The concentration of inflammatory factors was measured by ELISA. The degree of DNA methylation was quantified through MSP assay. The interaction between HOTTIP and DNA methyltransferase 1 (DNMT1) was examined by RIP assay. LPS upregulated HOTTIP, whereas downregulated SP-C level in AEC II cells. HOTTIP knockdown inhibited LPS-induced apoptosis and the secretion of inflammatory cytokines (TNF-α, IL-1β and IL-6) in AEC II cells. Mechanistically, HOTTIP recruited DNMT1 to the SP-C promoter, thereby facilitating DNA methylation of SP-C and suppressing its expression. Additionally, inhibitory of SP-C reversed the effects of HOTTIP or DNMT1 knockdown on apoptosis and inflammation in AEC II cells induced by LPS. HOTTIP recruited DNMT1 to epigenetically inhibit SP-C expression, leading to the promotion of lung epithelial cell injury caused by LPS, suggesting that targeting HOTTIP may be an effective strategy for the therapy of lung epithelial cell injury.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140104548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role for CCN1 in lysophosphatidic acid response in PC-3 human prostate cancer cells CCN1 在 PC-3 人类前列腺癌细胞的溶血磷脂酸反应中的作用

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-02-20 DOI: 10.1002/ccs3.12019

Pravita Balijepalli, Brianna K. Knode, Samuel A. Nahulu, Emily L. Abrahamson, Mary P. Nivison, Kathryn E. Meier

{"title":"Role for CCN1 in lysophosphatidic acid response in PC-3 human prostate cancer cells","authors":"Pravita Balijepalli, Brianna K. Knode, Samuel A. Nahulu, Emily L. Abrahamson, Mary P. Nivison, Kathryn E. Meier","doi":"10.1002/ccs3.12019","DOIUrl":"https://doi.org/10.1002/ccs3.12019","url":null,"abstract":"Lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) are bioactive phospholipids that act as mitogens in various cancers. Both LPA and S1P activate G-protein coupled receptors (GPCRs). We examined the role of CCN1/CYR61, an inducible matricellular protein, in LPA-induced signal transduction in PC-3 human prostate cancer cells. We found that both LPA and S1P induced expression of CCN1 and CCN2 within 2–4 h. CCN1 was induced by 18:1-LPA, but not by 18:0-, 18:2-, or 18:3-LPAs. A free fatty acid receptor-4 agonist inhibited LPA-induced CCN1 induction. CCN1 appeared in the ECM within 2 h after LPA addition. LPA caused biphasic activation of Erk MAPK, with an initial peak at 10–20 min followed by a later phase after 6 h. LPA increased adhesion of PC-3 cells to culture substrates (standard culture plates, fibronectin, or extracellular matrix) at 2 h, an intermediate event between early and late LPA signals. Knockdown of CCN1 suppressed LPA-induced adhesion to ECM or fibronectin. ECM from CCN1 knockdown cells was a poor substrate for adhesion, as compared to ECM from control cells. These results suggest that CCN1 contributes to LPA responses in the tumor microenvironment. The LPA-CCN1 axis holds promise for the development of novel therapeutic strategies in cancer.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140104540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lactate drives CD38 signaling to promote Epithelial-Mesenchymal Transition through Snail induction in non-small cell lung cancer cells 乳酸盐通过蜗牛诱导CD38信号传导，促进非小细胞肺癌细胞的上皮-间质转化

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-02-14 DOI: 10.1002/ccs3.12018

Yating Lu, Yang Yang, Tao Chang, Qiyun Jiang, Chenfeng Yang, Chunzhe Fu, Huijun Wei, Yuanpeng He, Zhihao Wu

引用次数: 0

IncRNA AC004943.2 regulates miR-135a-5p and PTK2/P13K axis to promote laryngeal squamous cell carcinoma progression IncRNA AC004943.2调控miR-135a-5p和PTK2/P13K轴，促进喉鳞状细胞癌进展

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-02-09 DOI: 10.1002/ccs3.12016

Xiaowen Zhu, Wenming Dong, Meijia Zhang

{"title":"IncRNA AC004943.2 regulates miR-135a-5p and PTK2/P13K axis to promote laryngeal squamous cell carcinoma progression","authors":"Xiaowen Zhu, Wenming Dong, Meijia Zhang","doi":"10.1002/ccs3.12016","DOIUrl":"10.1002/ccs3.12016","url":null,"abstract":"Long noncoding RNAs (lncRNAs) are involved in regulatory processes in laryngeal squamous cell carcinoma (LSCC) at posttranscriptional epigenetic modification level. Yet, the function and underlying mechanism behind lncRNA AC004943.2 in LSCC is still obscure. Therefore, the potential role of AC004943.2 in LSCC progression was investigated. The expression of gene or protein was tested by real-time quantitative polymerase chain reaction and western blot. MTT, colony formation, wound healing, and transwell experiments were applied to detect LSCC cell viability, proliferation, migration and invasion, respectively. The interaction among AC004943.2, miR-135a-5p, and protein tyrosine kinase 2 (PTK2) were analyzed by bioinformatics prediction and luciferase assay. AC004943.2 was highly expressed in LSCC cells compared with normal human bronchial epithelial cells, while miR-135a-5p was lowly expressed. AC004943.2 knockdown or miR-135a-5p overexpression inhibited LSCC cell viability, proliferation, migration and invasion. Mechanistically, AC004943.2 increased PTK2 expression in LSCC cells by sponging miR-135a-5p. Furthermore, miR-135a-5p knockdown inverted the inhibitory effect of AC004943.2 silencing on LSCC cell malignant behaviors. MiR-135a-5p upregulation attenuated the PTK2/PI3K pathway to inhibit progression of LSCC. AC004943.2 facilitated the cancerous phenotypes of LSCC cells by activating the PTK2/PI3K pathway through targeting miR-135a-5p, which furnished a therapeutic candidate for LSCC treatment.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139789559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

JAK3/STAT5 signaling-triggered upregulation of PIK3CD contributes to gastric carcinoma development JAK3/STAT5 信号触发的 PIK3CD 上调有助于胃癌的发展

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-02-07 DOI: 10.1002/ccs3.12017

Qingqing Hu, Ning Dou, Qiong Wu, Yong Gao, Yandong Li, Jingde Chen

{"title":"JAK3/STAT5 signaling-triggered upregulation of PIK3CD contributes to gastric carcinoma development","authors":"Qingqing Hu, Ning Dou, Qiong Wu, Yong Gao, Yandong Li, Jingde Chen","doi":"10.1002/ccs3.12017","DOIUrl":"10.1002/ccs3.12017","url":null,"abstract":"Gastric cancer (GC) is one of the most common solid cancers with high incidence and mortality worldwide. Chronic gastritis and consequent inflammatory microenvironment is known as a major cause leading to gastric carcinogenesis. Here we report that PIK3CD that encodes p110δ, a catalytic subunit of the class IA PI3Ks, is overexpressed and tumorigenic in GC and associated with tumor inflammatory microenvironment. By investigating the data from TCGA database and our immunohistochemical staining and quantitative real-time PCR results from clinical samples, we found PIK3CD exhibits higher expression level in GC tissues compared with adjacent non-tumorous stomach tissues. Genetic silencing of PIK3CD in GC cells retards proliferation and migration in vitro and tumorigenicity and metastasis in vivo. In contrast, enhanced expression of PIK3CD promotes these phenotypes in vitro. Furthermore, pharmacological inhibition of PIK3CD could reduce GC cell viability and colony formation capacities. More importantly, we reveal a relevant mechanism that PIK3CD, but not PIK3CA and PIK3CB, is transcriptionally regulated by the pro-inflammatory IL2/JAK3/STAT5 axis and tumor-infiltrating immune cells such as lymphocytes. These observations may setup a new crosstalk between tumor inflammatory microenvironment, IL2/JAK3/STAT5 signaling and PI3K/AKT signaling. Targeting PIK3CD may be a promising therapy strategy for GC.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139795808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Survivin inhibition ameliorates liver fibrosis by inducing hepatic stellate cell senescence and depleting hepatic macrophage population 抑制 Survivin 可通过诱导肝星状细胞衰老和消耗肝巨噬细胞数量来改善肝纤维化

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-01-25 DOI: 10.1002/ccs3.12015

Sachin Sharma, Shaikh Maryam Ghufran, Mehreen Aftab, Chhagan Bihari, Sampa Ghose, Subhrajit Biswas

{"title":"Survivin inhibition ameliorates liver fibrosis by inducing hepatic stellate cell senescence and depleting hepatic macrophage population","authors":"Sachin Sharma, Shaikh Maryam Ghufran, Mehreen Aftab, Chhagan Bihari, Sampa Ghose, Subhrajit Biswas","doi":"10.1002/ccs3.12015","DOIUrl":"10.1002/ccs3.12015","url":null,"abstract":"Persistent activation of hepatic stellate cells (HSCs) in the injured liver leads to the progression of liver injury from fibrosis to detrimental cirrhosis. In a previous study, we have shown that survivin protein is upregulated during the early activation of HSCs, which triggers the onset of liver fibrosis. However, the therapeutic potential of targeting survivin in a fully established fibrotic liver needs to be investigated. In this study, we chemically induced hepatic fibrosis in mice using carbon tetrachloride (CCl4) for 6 weeks, which was followed by treatment with a survivin suppressant (YM155). We also evaluated survivin expression in fibrotic human liver tissues, primary HSCs, and HSC cell line by histological analysis. αSMA+ HSCs in human and mice fibrotic liver tissues showed enhanced survivin expression, whereas the hepatocytes and quiescent (qHSCs) displayed minimal expression. Alternatively, activated M2 macrophage subtype induced survivin expression in HSCs through the TGF-β-TGF-β receptor-I/II signaling. Inhibition of survivin in HSCs promoted cell cycle arrest and senescence, which eventually suppressed their activation. In vivo, YM155 treatment increased the expression of cell senescence makers in HSCs around fibrotic septa such as p53, p21, and β-galactosidase. YM155 treatment in vivo also reduced the hepatic macrophage population and inflammatory cytokine expression in the liver. In conclusion, downregulation of survivin in the fibrotic liver decreases HSC activation by inducing cellular senescence and modulating macrophage cytokine expression that collectively ameliorates liver fibrosis.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139595992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Proteome-wide assessment of human interactome as a source of capturing domain–motif and domain-domain interactions 作为捕捉结构域-结构域和结构域-结构域相互作用的来源，对人类相互作用组进行全蛋白质组评估

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-01-19 DOI: 10.1002/ccs3.12014

Sobia Idrees, Keshav Raj Paudel

{"title":"Proteome-wide assessment of human interactome as a source of capturing domain–motif and domain-domain interactions","authors":"Sobia Idrees, Keshav Raj Paudel","doi":"10.1002/ccs3.12014","DOIUrl":"10.1002/ccs3.12014","url":null,"abstract":"Protein–protein interactions (PPIs) play a crucial role in various biological processes by establishing domain–motif (DMI) and domain–domain interactions (DDIs). While the existence of real DMIs/DDIs is generally assumed, it is rarely tested; therefore, this study extensively compared high-throughput methods and public PPI repositories as sources for DMI and DDI prediction based on the assumption that the human interactome provides sufficient data for the reliable identification of DMIs and DDIs. Different datasets from leading high-throughput methods (Yeast two-hybrid [Y2H], Affinity Purification coupled Mass Spectrometry [AP-MS], and Co-fractionation-coupled Mass Spectrometry) were assessed for their ability to capture DMIs and DDIs using known DMI/DDI information. High-throughput methods were not notably worse than PPI databases and, in some cases, appeared better. In conclusion, all PPI datasets demonstrated significant enrichment in DMIs and DDIs (p-value <0.001), establishing Y2H and AP-MS as reliable methods for predicting these interactions. This study provides valuable insights for biologists in selecting appropriate methods for predicting DMIs, ultimately aiding in SLiM discovery.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139525496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

GREM1 signaling in cancer: tumor promotor and suppressor? 癌症中的 GREM1 信号传导：肿瘤促进因子还是抑制因子？

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub Date: 2023-08-24 DOI: 10.1007/s12079-023-00777-4

Zhichun Gao, Julia M Houthuijzen, Peter Ten Dijke, Derek P Brazil

{"title":"GREM1 signaling in cancer: tumor promotor and suppressor?","authors":"Zhichun Gao, Julia M Houthuijzen, Peter Ten Dijke, Derek P Brazil","doi":"10.1007/s12079-023-00777-4","DOIUrl":"10.1007/s12079-023-00777-4","url":null,"abstract":"GREMLIN1 (GREM1) is member of a family of structurally and functionally related secreted cysteine knot proteins, which act to sequester and inhibit the action of multifunctional bone morphogenetic proteins (BMPs). GREM1 binds directly to BMP dimers, thereby preventing BMP-mediated activation of BMP type I and type II receptors. Multiple reports identify the overexpression of GREM1 as a contributing factor in a broad range of cancers. Additionally, the GREM1 gene is amplified in a rare autosomal dominant inherited form of colorectal cancer. The inhibitory effects of GREM1 on BMP signaling have been linked to these tumor-promoting effects, including facilitating cancer cell stemness and the activation of cancer-associated fibroblasts. Moreover, GREM1 has been described to bind and signal to vascular endothelial growth factor receptor (VEGFR) and stimulate angiogenesis, as well as epidermal and fibroblast growth factor receptor (EGFR and FGFR) to elicit tumor-promoting effects in breast and prostate cancer, respectively. In contrast, a 2022 report revealed that GREM1 can promote an epithelial state in pancreatic cancers, thereby inhibiting pancreatic tumor growth and metastasis. In this commentary, we will review these disparate findings and attempt to provide clarity around the role of GREM1 signaling in cancer.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1517-1526"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10116936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expression and function of CCN2-derived circRNAs in chondrocytes. 源自 CCN2 的 circRNA 在软骨细胞中的表达和功能

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub Date: 2023-09-11 DOI: 10.1007/s12079-023-00782-7

Soma Kato, Kazumi Kawata, Takashi Nishida, Tomomi Mizukawa, Masaharu Takigawa, Seiji Iida, Satoshi Kubota

{"title":"Expression and function of CCN2-derived circRNAs in chondrocytes.","authors":"Soma Kato, Kazumi Kawata, Takashi Nishida, Tomomi Mizukawa, Masaharu Takigawa, Seiji Iida, Satoshi Kubota","doi":"10.1007/s12079-023-00782-7","DOIUrl":"10.1007/s12079-023-00782-7","url":null,"abstract":"Cellular communication network factor 2 (CCN2) molecules promote endochondral ossification and articular cartilage regeneration, and circular RNAs (circRNAs), which arise from various genes and regulate gene expression by adsorbing miRNAs, are known to be synthesized from CCN2 in human vascular endothelial cells and other types of cells. However, in chondrocytes, not only the function but also the presence of CCN2-derived circRNA remains completely unknown. In the present study, we investigated the expression and function of CCN2-derived circRNAs in chondrocytes. Amplicons smaller than those from known CCN2-derived circRNAs were observed using RT-PCR analysis that could specifically amplify CCN2-derived circRNAs in human chondrocytic HCS-2/8 cells. The nucleotide sequences of the PCR products indicated novel circRNAs in the HCS-2/8 cells that were different from known CCN2-derived circRNAs. Moreover, the expression of several Ccn2-derived circRNAs in murine chondroblastic ATDC5 cells was confirmed and observed to change alongside chondrocytic differentiation. Next, one of these circRNAs was knocked down in HCS-2/8 cells to investigate the function of the human CCN2-derived circRNA. As a result, CCN2-derived circRNA knockdown significantly reduced the expression of aggrecan mRNA and proteoglycan synthesis. Our data suggest that CCN2-derived circRNAs are expressed in chondrocytes and play a role in chondrogenic differentiation. Production and role of CCN2-derived RNAs in chondrocytes.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1501-1515"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10202882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dual RNase activity of IRE1 as a target for anticancer therapies. 作为抗癌疗法靶点的 IRE1 的双重 RNase 活性。

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub Date: 2023-09-18 DOI: 10.1007/s12079-023-00784-5

Sylwia Bartoszewska, Jakub Sławski, James F Collawn, Rafał Bartoszewski

引用次数: 1