Journal of Cell Communication and Signaling最新文献_第9页

Potential roles of lncRNA MALAT1-miRNA interactions in ocular diseases lncRNA-MALAT1-miRNA相互作用在眼部疾病中的潜在作用。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-10-23 DOI: 10.1007/s12079-023-00787-2

Ava Nasrolahi, Fatemeh Khojasteh Pour, Abdolah Mousavi Salehi, Bartosz Kempisty, Maryam Hajizadeh, Mostafa Feghhi, Shirin Azizidoost, Maryam Farzaneh

{"title":"Potential roles of lncRNA MALAT1-miRNA interactions in ocular diseases","authors":"Ava Nasrolahi, Fatemeh Khojasteh Pour, Abdolah Mousavi Salehi, Bartosz Kempisty, Maryam Hajizadeh, Mostafa Feghhi, Shirin Azizidoost, Maryam Farzaneh","doi":"10.1007/s12079-023-00787-2","DOIUrl":"10.1007/s12079-023-00787-2","url":null,"abstract":"<div>\u0000 \u0000 <p>Long non-coding RNAs (lncRNAs) are non-protein coding transcripts that are longer than 200 nucleotides in length. LncRNAs are implicated in gene expression at the transcriptional, translational, and epigenetic levels, and thereby impact different cellular processes including cell proliferation, migration, apoptosis, angiogenesis, and immune response. In recent years, numerous studies have demonstrated the significant contribution of lncRNAs to the pathogenesis and progression of various diseases, such as stroke, heart disease, and cancer. Further investigations have shown that lncRNAs have altered expression patterns in ocular tissues and cell lines during pathological conditions. The pathogenesis of various ocular diseases, including glaucoma, cataract, corneal diseases, proliferative vitreoretinopathy, diabetic retinopathy, and retinoblastoma, is influenced by the involvement of specific lncRNAs which play a critical role in the development and progression of these diseases. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a well-researched lncRNA in the context of ocular diseases, which has been shown to exert its biological effects through several signaling pathways and downstream targets. The present review provides a comprehensive summary of the molecular mechanisms underlying the biological functions and roles of MALAT1 in ocular diseases.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1203-1217"},"PeriodicalIF":3.6,"publicationDate":"2023-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49690683","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

Exosomal miR-129 and miR-342 derived from intermittent hypoxia-stimulated vascular smooth muscle cells inhibit the eIF2α/ATF4 axis from preventing calcified aortic valvular disease 来源于间歇性缺氧刺激的血管平滑肌细胞的外泌体miR-129和miR-342抑制eIF2α/ATF4轴预防钙化主动脉瓣疾病。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-10-09 DOI: 10.1007/s12079-023-00785-4

Chen Huang, Xu Han, Linjie Yang, Wei Song, Hualu Zhang, Xiaohua Zhu, Gongcheng Huang, Jing Xu

{"title":"Exosomal miR-129 and miR-342 derived from intermittent hypoxia-stimulated vascular smooth muscle cells inhibit the eIF2α/ATF4 axis from preventing calcified aortic valvular disease","authors":"Chen Huang, Xu Han, Linjie Yang, Wei Song, Hualu Zhang, Xiaohua Zhu, Gongcheng Huang, Jing Xu","doi":"10.1007/s12079-023-00785-4","DOIUrl":"10.1007/s12079-023-00785-4","url":null,"abstract":"<div>\u0000 \u0000 <p>This study aims to elucidate the role of miR-129/miR-342 loaded in exosomes derived from vascular smooth muscle cells (VSMCs) stimulated by intermittent hypoxia in calcified aortic valvular disease (CAVD). Bioinformatics analysis was conducted to identify differentially expressed miRs in VSMCs-derived exosomes and CAVD samples, and their potential target genes were predicted. VSMCs were exposed to intermittent hypoxia to induce stimulation, followed by isolation of exosomes. Valvular interstitial cells (VICs) were cultured in vitro to investigate the impact of miR-129/miR-342 on VICs' osteogenic differentiation and aortic valve calcification with eIF2α. A CAVD mouse model was established using ApoE knockout mice for in vivo validation. In CAVD samples, miR-129 and miR-342 were downregulated, while eIF2α and ATF4 were upregulated. miR-129 and miR-342 exhibited inhibitory effects on eIF2α through targeted regulation. Exosomes released from intermittently hypoxia-stimulated VSMCs contained miR-129 and miR-342. Overexpression of miR-129 and miR-342, or silencing ATF4, suppressed VICs' osteogenic differentiation and aortic valve calcification, which could be rescued by overexpressed eIF2α. Collectively, intermittent hypoxia stimulation of VSMCs leads to the secretion of exosomes that activate the miR-129/miR-342 dual pathway, thereby inhibiting the eIF2α/ATF4 axis and attenuating VICs' osteogenic differentiation and CAVD progression.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1449-1467"},"PeriodicalIF":3.6,"publicationDate":"2023-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41122233","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 3.6 3区生物学

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

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

{"title":"Dual RNase activity of IRE1 as a target for anticancer therapies","authors":"Sylwia Bartoszewska, Jakub Sławski, James F. Collawn, Rafał Bartoszewski","doi":"10.1007/s12079-023-00784-5","DOIUrl":"10.1007/s12079-023-00784-5","url":null,"abstract":"<div>\u0000 \u0000 <p>The unfolded protein response (UPR) is a cellular mechanism that protects cells during stress conditions in which there is an accumulation of misfolded proteins in the endoplasmic reticulum (ER). UPR activates three signaling pathways that function to alleviate stress conditions and promote cellular homeostasis and cell survival. During unmitigated stress conditions, however, UPR activation signaling changes to promote cell death through apoptosis. Interestingly, cancer cells take advantage of this pathway to facilitate survival and avoid apoptosis even during prolonged cell stress conditions. Here, we discuss different signaling pathways associated with UPR and focus specifically on one of the ER signaling pathways activated during UPR, inositol-requiring enzyme 1α (IRE1). The rationale is that the IRE1 pathway is associated with cell fate decisions and recognized as a promising target for cancer therapeutics. Here we discuss IRE1 inhibitors and how they might prove to be an effective cancer therapeutic.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1145-1161"},"PeriodicalIF":3.6,"publicationDate":"2023-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10280935","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

Insights into the mediation of Ca2+ signaling in the promoting effects of LETX-VI on the synthesis and release of dopamine 洞察 Ca2+ 信号在 LETX-VI 对多巴胺合成和释放的促进作用中的中介作用。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-09-13 DOI: 10.1007/s12079-023-00783-6

Zhixiang Lei, Haiyan Wang, Yiwen Zhai, Minglu Sun, Si Chen, Panfeng Yin, Xianchun Wang

{"title":"Insights into the mediation of Ca2+ signaling in the promoting effects of LETX-VI on the synthesis and release of dopamine","authors":"Zhixiang Lei, Haiyan Wang, Yiwen Zhai, Minglu Sun, Si Chen, Panfeng Yin, Xianchun Wang","doi":"10.1007/s12079-023-00783-6","DOIUrl":"10.1007/s12079-023-00783-6","url":null,"abstract":"<div>\u0000 \u0000 <p>Latroeggtoxin-VI (LETX-VI) is an active protein and was previously demonstrated to have effects on the synthesis and release of dopamine. Hererin, the involvement of Ca<sup>2+</sup> signaling in the effects of LETX-VI on dopamine was systematically investigated, using PC12 cells as a neuron model. LETX-VI was shown to promote dopamine release from PC12 cells both in the presence and absence of extracellular Ca<sup>2+</sup>; however the presence of extracellular Ca<sup>2+</sup> was favorable for enhancing the promoting effects of LETX-VI on dopamine, because LETX-VI facilitated the influx of extracellular Ca<sup>2+</sup> through the L-type calcium channels in plasma membrane (PM) to increase cytosolic Ca<sup>2+</sup> concentration. LETX-VI was able to penetrate the PM of PC12 cells to act on the Ca<sup>2+</sup> channel proteins IP3Rs and RyRs in the endoplasm reticulum (ER) membrane, opening the Ca<sup>2+</sup> channels and promoting the release of ER Ca<sup>2+</sup> to elevate cytosolic Ca<sup>2+</sup> level. With the help of intracellular Ca<sup>2+</sup> chelator BAPTA, the elevated cytosolic Ca<sup>2+</sup> level was proven to play crucial role for the enhanced promoting effects of LETX-VI on dopamine. Taken together, LETX-VI is able to open the Ca<sup>2+</sup> channels in both PM and ER membrane simultaneously to facilitate extracellular Ca<sup>2+</sup> influx and ER Ca<sup>2+</sup> release, and thus increases the cytosolic Ca<sup>2+</sup> concentration to enhance the promoting effects on the synthesis and release of dopamine.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1309-1321"},"PeriodicalIF":3.6,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10215920","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

Metformin combined with rapamycin ameliorates podocyte injury in idiopathic membranous nephropathy through the AMPK/mTOR signaling pathway 二甲双胍联合雷帕霉素可通过AMPK/mTOR信号通路改善特发性膜性肾病的荚膜损伤。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-09-13 DOI: 10.1007/s12079-023-00781-8

Meichen Ma, Yue Pan, Yue Zhang, Mei Yang, Ying Xi, Baoxu Lin, Wudi Hao, Jianhua Liu, Lina Wu, Yong Liu, Xiaosong Qin

{"title":"Metformin combined with rapamycin ameliorates podocyte injury in idiopathic membranous nephropathy through the AMPK/mTOR signaling pathway","authors":"Meichen Ma, Yue Pan, Yue Zhang, Mei Yang, Ying Xi, Baoxu Lin, Wudi Hao, Jianhua Liu, Lina Wu, Yong Liu, Xiaosong Qin","doi":"10.1007/s12079-023-00781-8","DOIUrl":"10.1007/s12079-023-00781-8","url":null,"abstract":"<div>\u0000 \u0000 <p>Autophagy activation protects against podocyte injury in idiopathic membranous nephropathy (IMN). The AMPK/mTOR signaling pathway is a vital autophagy regulatory pathway. Metformin promotes autophagy, whereas rapamycin is an autophagy agonist. However, the therapeutic mechanisms of metformin and rapamycin in IMN remain unclear. Thus, we examined the mechanisms of action of metformin and rapamycin in IMN by regulating the AMPK/mTOR autophagy signaling pathway. Female Sprague–Dawley (SD) rats were treated with cationic bovine serum albumin (C-BSA) to establish an IMN model and were randomly divided into IMN model, metformin, rapamycin, and metformin + rapamycin groups. A control group was also established. Metformin and rapamycin were used as treatments. Renal histological changes, urinary protein excretion, the protein expression levels of key AMPK/mTOR signaling pathway proteins, renal tissue cell apoptosis, and autophagy-associated proteins (Beclin 1 and LC3) were examined. In addition, a C5b-9 sublysis model using the MPC-5 mouse podocyte cell line was established to verify the effect of metformin combined with rapamycin on podocytes. Metformin combined with rapamycin improved urinary protein excretion in IMN rats. Metformin combined with rapamycin attenuated the inflammatory response, renal fibrosis, and podocyte foot process fusion. In addition, it improved autophagy in podocytes as demonstrated by the enhanced expression of Beclin-1, p-AMPK/AMPK, LC3-II/I, and autophagosomes in podocytes and decreased p-mTOR/mTOR expression. In conclusion, metformin combined with rapamycin decreased proteinuria, improved renal fibrosis and podocyte autophagy via AMPK/mTOR pathway in IMN rats.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1405-1415"},"PeriodicalIF":3.6,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10222369","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

Metformin combined with rapamycin ameliorates podocyte injury in idiopathic membranous nephropathy through the AMPK/mTOR signaling pathway. 二甲双胍联合雷帕霉素通过AMPK/mTOR信号通路改善特发性膜性肾病足细胞损伤。

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-09-13 DOI: 10.2139/ssrn.4257549

Meichen Ma, Yue Pan, Yue Zhang, Mei Yang, Ying Xi, Baoxu Lin, Wudi Hao, Jianhua Liu, Lina Wu, Yong Liu, Xiaosong Qin

{"title":"Metformin combined with rapamycin ameliorates podocyte injury in idiopathic membranous nephropathy through the AMPK/mTOR signaling pathway.","authors":"Meichen Ma, Yue Pan, Yue Zhang, Mei Yang, Ying Xi, Baoxu Lin, Wudi Hao, Jianhua Liu, Lina Wu, Yong Liu, Xiaosong Qin","doi":"10.2139/ssrn.4257549","DOIUrl":"https://doi.org/10.2139/ssrn.4257549","url":null,"abstract":"Autophagy activation protects against podocyte injury in idiopathic membranous nephropathy (IMN). The AMPK/mTOR signaling pathway is a vital autophagy regulatory pathway. Metformin promotes autophagy, whereas rapamycin is an autophagy agonist. However, the therapeutic mechanisms of metformin and rapamycin in IMN remain unclear. Thus, we examined the mechanisms of action of metformin and rapamycin in IMN by regulating the AMPK/mTOR autophagy signaling pathway. Female Sprague-Dawley (SD) rats were treated with cationic bovine serum albumin (C-BSA) to establish an IMN model and were randomly divided into IMN model, metformin, rapamycin, and metformin + rapamycin groups. A control group was also established. Metformin and rapamycin were used as treatments. Renal histological changes, urinary protein excretion, the protein expression levels of key AMPK/mTOR signaling pathway proteins, renal tissue cell apoptosis, and autophagy-associated proteins (Beclin 1 and LC3) were examined. In addition, a C5b-9 sublysis model using the MPC-5 mouse podocyte cell line was established to verify the effect of metformin combined with rapamycin on podocytes. Metformin combined with rapamycin improved urinary protein excretion in IMN rats. Metformin combined with rapamycin attenuated the inflammatory response, renal fibrosis, and podocyte foot process fusion. In addition, it improved autophagy in podocytes as demonstrated by the enhanced expression of Beclin-1, p-AMPK/AMPK, LC3-II/I, and autophagosomes in podocytes and decreased p-mTOR/mTOR expression. In conclusion, metformin combined with rapamycin decreased proteinuria, improved renal fibrosis and podocyte autophagy via AMPK/mTOR pathway in IMN rats. The metformin and rapamycin decreased proteinuria and inproved renal fibrosis in IMN model rats.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"1 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47747792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: 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 3.6 3区生物学

Journal of Cell Communication and Signaling Pub 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":"<div>\u0000 \u0000 <p>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 <i>CCN2</i> in human vascular endothelial cells and other types of cells. However, in chondrocytes, not only the function but also the presence of <i>CCN2</i>-derived circRNA remains completely unknown. In the present study, we investigated the expression and function of <i>CCN2</i>-derived circRNAs in chondrocytes. Amplicons smaller than those from known <i>CCN2</i>-derived circRNAs were observed using RT-PCR analysis that could specifically amplify <i>CCN2</i>-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 <i>CCN2</i>-derived circRNAs. Moreover, the expression of several <i>Ccn2</i>-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 <i>CCN2</i>-derived circRNA. As a result, <i>CCN2</i>-derived circRNA knockdown significantly reduced the expression of aggrecan mRNA and proteoglycan synthesis. Our data suggest that <i>CCN2</i>-derived circRNAs are expressed in chondrocytes and play a role in chondrogenic differentiation.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1501-1515"},"PeriodicalIF":3.6,"publicationDate":"2023-09-11","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

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 3.6 3区生物学

Journal of Cell Communication and Signaling Pub 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":"<div>\u0000 \u0000 <p>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 <i>GREM1</i> 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.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1517-1526"},"PeriodicalIF":3.6,"publicationDate":"2023-08-24","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

PKCι induces differential phosphorylation of STAT3 to modify STAT3-related signaling pathways in pancreatic cancer cells PKCι 可诱导 STAT3 发生不同程度的磷酸化，从而改变胰腺癌细胞中与 STAT3 相关的信号通路。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-08-07 DOI: 10.1007/s12079-023-00780-9

Junli Wang, Sijia Weng, Yue Zhu, Hongmei Chen, Jueyu Pan, Shuoyu Qiu, Yufeng Liu, Dapeng Wei, Tongbo Zhu

{"title":"PKCι induces differential phosphorylation of STAT3 to modify STAT3-related signaling pathways in pancreatic cancer cells","authors":"Junli Wang, Sijia Weng, Yue Zhu, Hongmei Chen, Jueyu Pan, Shuoyu Qiu, Yufeng Liu, Dapeng Wei, Tongbo Zhu","doi":"10.1007/s12079-023-00780-9","DOIUrl":"10.1007/s12079-023-00780-9","url":null,"abstract":"<div>\u0000 \u0000 <p>An increasing number of studies have documented atypical protein kinase C isoform ι (PKCι) as an oncoprotein playing multifaceted roles in pancreatic carcinogenesis, including sustaining the transformed growth, prohibiting apoptosis, strengthening invasiveness, facilitating autophagy, as well as promoting the immunosuppressive tumor microenvironment of pancreatic tumors. In this study, we present novel evidence that PKCι overexpression increases STAT3 phosphorylation at the Y705 residue while decreasing STAT3 phosphorylation at the S727 residue in pancreatic cancer cells. We further demonstrate that STAT3 phosphorylation at Y705 and S727 residues is mutually antagonistic, and that STAT3 Y705 phosphorylation is positively related to the transcriptional activity of STAT3 in pancreatic cancer cells. Furthermore, we discover that PKCι inhibition attenuates STAT3 transcriptional activity via Y705 dephosphorylation, which appears to be resulted from enhanced phosphorylation of S727 in pancreatic cancer cells. Finally, we investigate and prove that by modulating the STAT3 activity, the PKCι inhibitor can synergistically enhance the antitumor effects of pharmacological STAT3 inhibitors or reverse the anti-apoptotic side effects incited by the MEK inhibitor, thereby posing as a prospective sensitizer in the treatment of pancreatic cancer cells.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1417-1433"},"PeriodicalIF":3.6,"publicationDate":"2023-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10001137","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 of EGFR and FASN in breast cancer progression 表皮生长因子受体和 FASN 在乳腺癌进展中的作用。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-07-25 DOI: 10.1007/s12079-023-00771-w

Suchi Chaturvedi, Mainak Biswas, Sushabhan Sadhukhan, Avinash Sonawane

{"title":"Role of EGFR and FASN in breast cancer progression","authors":"Suchi Chaturvedi, Mainak Biswas, Sushabhan Sadhukhan, Avinash Sonawane","doi":"10.1007/s12079-023-00771-w","DOIUrl":"10.1007/s12079-023-00771-w","url":null,"abstract":"<div>\u0000 \u0000 <p>Breast cancer (BC) emerged as one of the life-threatening diseases among females. Despite notable improvements made in cancer detection and treatment worldwide, according to GLOBACAN 2020, BC is the fifth leading cancer, with an estimated 1 in 6 cancer deaths, in a majority of countries. However, the exact cause that leads to BC progression still needs to be determined. Here, we reviewed the role of two novel biomarkers responsible for 50–70% of BC progression. The first one is epidermal growth factor receptor (EGFR) which belongs to the ErbB tyrosine kinases family, signalling pathways associated with it play a significant role in regulating cell proliferation and division. Another one is fatty acid synthase (FASN), a key enzyme responsible for the de novo lipid synthesis required for cancer cell development. This review presents a rationale for the EGFR-mediated pathways, their interaction with FASN, communion of these two biomarkers with BC, and improvements to overcome drug resistance caused by them.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1249-1282"},"PeriodicalIF":3.6,"publicationDate":"2023-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9866677","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