Journal of Cell Communication and Signaling最新文献

{"title":"Use and application of organ-on-a-chip platforms in cancer research","authors":"Yifan Yu,&nbsp;TingTing Zhou,&nbsp;Liu Cao","doi":"10.1007/s12079-023-00790-7","DOIUrl":"10.1007/s12079-023-00790-7","url":null,"abstract":"<div>\u0000 \u0000 <p>Tumors are a major cause of death worldwide, and much effort has been made to develop appropriate anti-tumor therapies. Existing in vitro and in vivo tumor models cannot reflect the critical features of cancer. The development of organ-on-a-chip models has enabled the integration of organoids, microfluidics, tissue engineering, biomaterials research, and microfabrication, offering conditions that mimic tumor physiology. Three-dimensional in vitro human tumor models that have been established as organ-on-a-chip models contain multiple cell types and a structure that is similar to the primary tumor. These models can be applied to various foci of oncology research. Moreover, the high-throughput features of microfluidic organ-on-a-chip models offer new opportunities for achieving large-scale drug screening and developing more personalized treatments. In this review of the literature, we explore the development of organ-on-a-chip technology and discuss its use as an innovative tool in basic and clinical applications and summarize its advancement of cancer research.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1163-1179"},"PeriodicalIF":3.6,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138460126","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}

{"title":"miRNAs as short non-coding RNAs in regulating doxorubicin resistance","authors":"Sepideh Mirzaei,&nbsp;Mahshid Deldar Abad Paskeh,&nbsp;Farhad Adhami Moghadam,&nbsp;Maliheh Entezari,&nbsp;Zeinab Khazaei Koohpar,&nbsp;Elahe Sadat Hejazi,&nbsp;Shamin Rezaei,&nbsp;Amirabbas Kakavand,&nbsp;Maryam Aboutalebi,&nbsp;Mohammad Arad Zandieh,&nbsp;Romina Rajabi,&nbsp;Shokooh Salimimoghadam,&nbsp;Afshin Taheriazam,&nbsp;Mehrdad Hashemi,&nbsp;Saeed Samarghandian","doi":"10.1007/s12079-023-00789-0","DOIUrl":"10.1007/s12079-023-00789-0","url":null,"abstract":"<div>\u0000 \u0000 <p>The treatment of cancer patients has been prohibited by chemoresistance. Doxorubicin (DOX) is an anti-tumor compound disrupting proliferation and triggering cell cycle arrest via inhibiting activity of topoisomerase I and II. miRNAs are endogenous RNAs localized in cytoplasm to reduce gene level. Abnormal expression of miRNAs changes DOX cytotoxicity. Overexpression of tumor-promoting miRNAs induces DOX resistance, while tumor-suppressor miRNAs inhibit DOX resistance. The miRNA-mediated regulation of cell death and hallmarks of cancer can affect response to DOX chemotherapy in tumor cells. The transporters such as P-glycoprotein are regulated by miRNAs in DOX chemotherapy. Upstream mediators including lncRNAs and circRNAs target miRNAs in affecting capacity of DOX. The response to DOX chemotherapy can be facilitated after administration of agents that are mostly phytochemicals including curcumol, honokiol and ursolic acid. These agents can regulate miRNA expression increasing DOX's cytotoxicity. Since delivery of DOX alone or in combination with other drugs and genes can cause synergistic impact, the nanoparticles have been introduced for drug sensitivity.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1181-1202"},"PeriodicalIF":3.6,"publicationDate":"2023-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138451496","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}

{"title":"Protease-activated receptor 2 attenuates doxorubicin-induced apoptosis in colon cancer cells","authors":"Himani Shah,&nbsp;Timothy A. Hill,&nbsp;Junxian Lim,&nbsp;David P. Fairlie","doi":"10.1007/s12079-023-00791-6","DOIUrl":"10.1007/s12079-023-00791-6","url":null,"abstract":"<div>\u0000 \u0000 <p>Drug resistance represents a major problem in cancer treatment. Doxorubicin (adriamycin) is an injectable DNA intercalating drug that halts cancer cell growth by inhibiting topoisomerase 2, but its long-term effectiveness is compromised by onset of resistance. This study demonstrates that expression of the PAR2 gene in human colon adenocarcinoma tissue samples was the highest among 32 different cancer types (n = 10,989), and higher in colon adenocarcinoma tissues (n = 331) than normal colon tissues (n = 308), revealing an association between PAR2 expression and human colon cancer. HT29 cells are a human colorectal adenocarcinoma cell line that is sensitive to the chemotherapeutic drug doxorubicin and also expresses PAR2. We find that PAR2 activation in HT29 cells, either by an endogenous protease agonist (trypsin) or an exogenous peptide agonist (2f-LIGRL-NH₂), significantly reduces doxorubicin-induced cell death, reactive oxygen species production, caspase 3/7 activity and cleavage of caspase-8 and caspase-3. Moreover, PAR2-mediated MEK1/2-ERK1/2 pathway induced by 2f-LIGRL-NH₂ leads to upregulated anti-apoptotic MCL-1 and Bcl-xL proteins that promote cellular survival. These findings suggest that activation of PAR2 compromises efficacy of doxorubicin in colon cancer. Further support for this conclusion came from experiments with human colon cancer HT29 cells, either with the PAR2 gene deleted or in the presence of a pharmacological antagonist of PAR2, which showed full restoration of all doxorubicin-mediated effects. Together, these findings reveal a strong link between PAR2 activation and signalling in human colon cancer cells and increased survival against doxorubicin-induced cell death. They support PAR2 antagonism as a possible new strategy for enhancing doxorubicin therapy.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1293-1307"},"PeriodicalIF":3.6,"publicationDate":"2023-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138291007","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}

{"title":"Mutant p53 gain-of-function stimulates canonical Wnt signaling via PI3K/AKT pathway in colon cancer","authors":"Eduardo Alvarado-Ortiz,&nbsp;Elizabeth Ortiz-Sánchez,&nbsp;Miguel Angel Sarabia-Sánchez,&nbsp;Karen Griselda de la Cruz-López,&nbsp;Alejandro García-Carrancá,&nbsp;Martha Robles-Flores","doi":"10.1007/s12079-023-00793-4","DOIUrl":"10.1007/s12079-023-00793-4","url":null,"abstract":"<div>\u0000 \u0000 <p>Aberrant canonical Wnt signaling is a hallmark of colon cancer. The <i>TP53</i> tumor suppressor gene is altered in many solid tumors, including colorectal cancer, resulting in mutant versions of p53 (mut-p53) that lose their tumor suppressor capacities and acquire new-oncogenic functions (GOFs) critical for disease progression. Although the mechanisms related to mut-p53 GOF have been explored extensively, the relevance of mut-p53 in the canonical Wnt pathway is not well defined. This work investigated the influence of mut-p53 compared to wt-p53 in β-catenin-dependent Wnt signaling. Using the TCGA public data from Pan-Cancer and the GEPIA2 platform, an in silico analysis of wt-p53 versus mut-p53 genotyped colorectal cancer patients showed that <i>TP53</i> (p53) and <i>CTNNB1</i> (β-catenin) are significantly overexpressed in colorectal cancer, compared with normal tissue. Using p53 overexpression or p53 knockdown assays of wt-p53 or mut-p53, we found that while wt-p53 antagonizes canonical Wnt signaling, mut-p53 induces the opposite effect, improving the β-catenin-dependent transcriptional activity and colony formation ability of colon cancer cells, which were both decreased by mut-p53 knockdown expression. The mechanism involved in mut-p53-induced activation of canonical Wnt appears to be via AKT-mediated phosphorylation of Ser 552 of β-catenin, which is known to stabilize and enhance its transcriptional activity. We also found that while wt-p53 expression contributes to 5-FU sensitivity in colon cancer cells, the RITA p53 reactivating molecule counteracted the resistance against 5-FU in cells expressing mut-p53. Our results indicate that mut-p53 GOF acts as a positive regulator of canonical Wnt signaling and participates in the induction of resistance to 5-FU in colon cancer cells.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1389-1403"},"PeriodicalIF":3.6,"publicationDate":"2023-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138047032","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}

{"title":"GPR56 signaling pathway network and its dynamics in the mesenchymal transition of glioblastoma","authors":"Raksha A. Ganesh,&nbsp;Krishnan Venkataraman,&nbsp;Ravi Sirdeshmukh","doi":"10.1007/s12079-023-00792-5","DOIUrl":"10.1007/s12079-023-00792-5","url":null,"abstract":"<div>\u0000 \u0000 <p>G protein-coupled receptor 56 (GPR56/ADGRG1) is a multifunctional adhesion GPCR involved in diverse biological processes ranging from development to cancer. In our earlier study, we reported that GPR56 is expressed heterogeneously in glioblastoma (GBM) and is involved in the mesenchymal transition, making it a promising therapeutic target (Ganesh et al<i>.</i>, 2022). Despite its important role in cancer, its mechanism of action or signaling is not completely understood. Thus, based on transcriptomic, proteomic, and phosphoproteomic differential expression data of GPR56 knockdown U373-GBM cells included in our above study along with detailed literature mining of the molecular events plausibly associated with GPR56 activity, we have constructed a signaling pathway map of GPR56 as may be applicable in mesenchymal transition in GBM. The map incorporates more than 100 molecular entities including kinases, receptors, ion channels, and others associated with Wnt, integrin, calcium signaling, growth factors, and inflammation signaling pathways. We also considered intracellular and extracellular factors that may influence the activity of the pathway entities. Here we present a curated signaling map of GPR56 in the context of GBM and discuss the relevance and plausible cross-connectivity across different axes attributable to GPR56 function.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1527-1535"},"PeriodicalIF":3.6,"publicationDate":"2023-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138047031","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}

{"title":"Dual impacts of mesenchymal stem cell-derived exosomes on cancer cells: unravelling complex interactions","authors":"Babak Jahangiri,&nbsp;Mohammad Khalaj-Kondori,&nbsp;Elahe Asadollahi,&nbsp;Ali Kian Saei,&nbsp;Majid Sadeghizadeh","doi":"10.1007/s12079-023-00794-3","DOIUrl":"10.1007/s12079-023-00794-3","url":null,"abstract":"<div>\u0000 \u0000 <p>Mesenchymal stem cells (MSCs) are multipotent, self-renewing stromal cells found in a variety of adult tissues. MSCs possess a remarkable ability to migrate towards tumor sites, known as homing. This homing process is mediated by various factors, including chemokines, growth factors, and extracellular matrix components present in the tumor microenvironment. MSCs release extracellular vesicles known as exosomes (MSC-Exos), which have been suggested to serve a key role in mediating a wide variety of MSC activities. Through cell–cell communication, MSC-Exos have been shown to alter recipient cell phenotype or function and play as a novel cell-free alternative for MSC-based cell therapy. However, MSC recruitment to tumors allows for their interaction with cancer cells and subsequent regulation of tumor behavior. MSC-Exos act as tumor niche modulators via transferring exosomal contents, such as specific proteins or genetic materials, to the nearby cancer cells, leading to either promotion or suppression of tumorigenesis, angiogenesis, and metastasis, depending on the specific microenvironmental cues and recipient cell characteristics. Consequently, there is still a debate about the precise relationship between tumor cells and MSC-Exos, and it is unclear how MSC-Exos impacts tumor cells. Although the dysregulation of miRNAs is caused by the progression of cancer, they also play a direct role in either promoting or inhibiting tumor growth as they act as either oncogenes or tumor suppressors. The utilization of MSC-Exos may prove to be an effective method for restoring miRNA as a means of treating cancer. This review aimed to present the existing understanding of the impact that MSC-Exos could have on cancer. To begin with, we presented a brief explanation of exosomes, MSCs, and MSC-Exos. Following this, we delved into the impact of MSC-Exos on cancer growth, EMT, metastasis, angiogenesis, resistance to chemotherapy and radiotherapy, and modulation of the immune system.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1229-1247"},"PeriodicalIF":3.6,"publicationDate":"2023-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136397572","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}

{"title":"Unpacking the complexity of nuclear IL-33 (nIL-33): a crucial regulator of transcription and signal transduction","authors":"Zengbin Wang,&nbsp;Nanhong Tang","doi":"10.1007/s12079-023-00788-1","DOIUrl":"10.1007/s12079-023-00788-1","url":null,"abstract":"<div>\u0000 \u0000 <p>Interleukin-33 (IL-33) (NF-HEV), a chromatin-associated nuclear cytokine, is a member of the IL-1 family. IL-33 possesses a nuclear localization signal and a homeodomain (a structure resembling a helix-turn-helix) that can bind to nuclear chromatin. Research has revealed that IL-33 can function as a nuclear factor to regulate various biological processes. This review discusses the cellular localization, functional effects, and immune regulation of full length IL-33 (FLIL-33), cytokine IL-33 (sIL-33) and nuclear IL-33 (nIL-33). In addition, the post-translational modifications of nIL-33 and the hypothesis of using nIL-33 as a treatment method were also summarized. A multidisciplinary approach is required which integrates methods and techniques from genomics, proteomics, cell biology and immunology to provide comprehensive insights into the function and therapeutic potential of nIL-33.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1131-1143"},"PeriodicalIF":3.6,"publicationDate":"2023-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50158041","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}

{"title":"Potential roles of lncRNA MALAT1-miRNA interactions in ocular diseases","authors":"Ava Nasrolahi,&nbsp;Fatemeh Khojasteh Pour,&nbsp;Abdolah Mousavi Salehi,&nbsp;Bartosz Kempisty,&nbsp;Maryam Hajizadeh,&nbsp;Mostafa Feghhi,&nbsp;Shirin Azizidoost,&nbsp;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}

{"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,&nbsp;Xu Han,&nbsp;Linjie Yang,&nbsp;Wei Song,&nbsp;Hualu Zhang,&nbsp;Xiaohua Zhu,&nbsp;Gongcheng Huang,&nbsp;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}

{"title":"Dual RNase activity of IRE1 as a target for anticancer therapies","authors":"Sylwia Bartoszewska,&nbsp;Jakub Sławski,&nbsp;James F. Collawn,&nbsp;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}