Journal of Cell Communication and Signaling最新文献_第4页

High expression of GPR50 promotes the proliferation, migration and autophagy of hepatocellular carcinoma cells in vitro. 高表达 GPR50 可促进体外肝癌细胞的增殖、迁移和自噬。

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub Date: 2023-06-28 DOI: 10.1007/s12079-023-00772-9

Weiming Zhao, Lingling Xi, Guoying Yu, Gaiping Wang, Cuifang Chang

{"title":"High expression of GPR50 promotes the proliferation, migration and autophagy of hepatocellular carcinoma cells in vitro.","authors":"Weiming Zhao, Lingling Xi, Guoying Yu, Gaiping Wang, Cuifang Chang","doi":"10.1007/s12079-023-00772-9","DOIUrl":"10.1007/s12079-023-00772-9","url":null,"abstract":"G protein-coupled receptors (GPCRs) play important roles in tumorigenesis and the development of hepatocellular carcinoma (HCC). GPR50 is an orphan GPCR. Previous studies have indicated that GPR50 could protect against breast cancer development and decrease tumor growth in a xenograft mouse model. However, its role in HCC remains indistinct. To detect the role and the regulation mechanism of GPR50 in HCC, GPR50 expression was analyzed in HCC patients (gene expression omnibus database (GEO) (GSE45436)) and detected in HCC cell line CBRH-7919, and the results showed that GPR50 was significantly up-regulated in HCC patients and CBRH-7919 cell line compared to the corresponding normal control. Gpr50 cDNA was transfected into HCC cell line CBRH-7919, and we found that Gpr50 promoted the proliferation, migration, and autophagy of CBRH-7919. The regulation mechanism of GPR50 in HCC was detected by isobaric tags for relative and absolute quantification (iTRAQ) analysis, and we found that GPR50 promoted HCC was closely related to CCT6A and PGK1. Taken together, GPR50 may promote HCC progression via CCT6A-induced proliferation and PGK1-induced migration and autophagy, and GPR50 could be an important target for HCC.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1435-1447"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9696419","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

Knockdown of Yap attenuates TAA-induced hepatic fibrosis by interaction with hedgehog signals. 通过与刺猬信号相互作用，敲除 Yap 可减轻 TAA 诱导的肝纤维化。

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub Date: 2023-06-20 DOI: 10.1007/s12079-023-00775-6

Ye Zhao, Huiling Wang, Tianhua He, Bo Ma, Guoguang Chen, Chimeng Tzeng

{"title":"Knockdown of Yap attenuates TAA-induced hepatic fibrosis by interaction with hedgehog signals.","authors":"Ye Zhao, Huiling Wang, Tianhua He, Bo Ma, Guoguang Chen, Chimeng Tzeng","doi":"10.1007/s12079-023-00775-6","DOIUrl":"10.1007/s12079-023-00775-6","url":null,"abstract":"Liver fibrosis is an aberrant wound healing response to tissue injury characterized by excessive extracellular matrix deposition and loss of normal liver architecture. Hepatic stellate cells (HSCs) activation is regards to be the major process in liver fibrogenesis which is dynamic and reversible. Both Hippo signaling core factor Yap and Hedgehog (Hh) signaling promote HSCs transdifferentiation thereby regulating the repair process of liver injury. However, the molecular function of YAP and the regulation between Yap and Hh during fibrogenesis remain uncertain. In this study, the essential roles of Yap in liver fibrosis were investigated. Yap was detected to be increased in liver fibrotic tissue by the thioacetamide (TAA)-induced zebrafish embryonic and adult models. Inhibition of Yap by both embryonic morpholino interference and adult's inhibitor treatment was proved to alleviate TAA-induced liver lesions by and histology and gene expression examination. Transcriptomic analysis and gene expression detection showed that Yap and Hh signaling pathway have a cross talking upon TAA-induced liver fibrosis. In addition, TAA induction promoted the nuclear colocalization of YAP and Hh signaling factor GLI2α. This study demonstrates that Yap and Hh play synergistic protective roles in liver fibrotic response and provides new theoretical insight concerning the mechanisms of fibrosis progression.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1335-1354"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9667853","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: 1

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 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub 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":"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 Ca2+ 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 Ca2+; however the presence of extracellular Ca2+ was favorable for enhancing the promoting effects of LETX-VI on dopamine, because LETX-VI facilitated the influx of extracellular Ca2+ through the L-type calcium channels in plasma membrane (PM) to increase cytosolic Ca2+ concentration. LETX-VI was able to penetrate the PM of PC12 cells to act on the Ca2+ channel proteins IP3Rs and RyRs in the endoplasm reticulum (ER) membrane, opening the Ca2+ channels and promoting the release of ER Ca2+ to elevate cytosolic Ca2+ level. With the help of intracellular Ca2+ chelator BAPTA, the elevated cytosolic Ca2+ 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 Ca2+ channels in both PM and ER membrane simultaneously to facilitate extracellular Ca2+ influx and ER Ca2+ release, and thus increases the cytosolic Ca2+ concentration to enhance the promoting effects on the synthesis and release of dopamine.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1309-1321"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","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

Tripartite motif-containing 9 promoted proliferation and migration of bladder cancer cells through CEACAM6-Smad2/3 axis. 含三方基序的 9 通过 CEACAM6-Smad2/3 轴促进膀胱癌细胞的增殖和迁移。

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub Date: 2023-05-30 DOI: 10.1007/s12079-023-00766-7

Zhao-Cun Zhang, Hai-Feng Zhao, Zhuang Sun, Yi Li, Ming-Lei Zhong, Bao-Hai Wang, Xian-Zhou Jiang

{"title":"Tripartite motif-containing 9 promoted proliferation and migration of bladder cancer cells through CEACAM6-Smad2/3 axis.","authors":"Zhao-Cun Zhang, Hai-Feng Zhao, Zhuang Sun, Yi Li, Ming-Lei Zhong, Bao-Hai Wang, Xian-Zhou Jiang","doi":"10.1007/s12079-023-00766-7","DOIUrl":"10.1007/s12079-023-00766-7","url":null,"abstract":"Studies have shown that tripartite motif-containing (TRIM) family proteins function as E3 ubiquitin ligases and play essential roles in cancer biology. In the present study, we validated a contribution of TRIM9 to bladder cancer progression. 296 patients derived from The Cancer Genome Atlas (TCGA) database and 22 clinical specimens were included, in which accumulated TRIM9 correlated with the poor prognosis and higher relapse in bladder patients. In vitro, TRIM9 promoted bladder cancer cells Biu-87 and T24 cell proliferation and migration. Meanwhile, overexpression of TRIM9 reduced the chemosensitivity in Biu-87 and T24 to mitomycin C (MMC) and gemcitabine (GEM). As an underlying mechanism, we found that TRIM9 stimulated carcinoembryonic antigen 6 (CEACAM6) upregulation, which further facilitated Smad2/3-matrix metalloproteinase 2 (MMP2) signaling activation both in vitro and in vivo. Those results indicated that TRIM9 facilitated bladder cancer development and chemoresistance by CEACAM6-Smad2/3 axis. TRIM9 and its associated molecules could be a potential diagnostic indicator and therapeutic target in bladder cancer.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1323-1333"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9540310","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: 1

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 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub 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":"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":" ","pages":"1405-1415"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","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

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 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub 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":"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.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1203-1217"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","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

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 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub Date: 2023-07-25 DOI: 10.1007/s12079-023-00771-w

Suchi Chaturvedi, Mainak Biswas, Sushabhan Sadhukhan, Avinash Sonawane

引用次数: 1

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 : 2023-12-01 Epub 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":"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.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1417-1433"},"PeriodicalIF":3.6,"publicationDate":"2023-12-01","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

The advance of CCN3 in fibrosis. CCN3在纤维化中的进展。

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub Date: 2023-06-28 DOI: 10.1007/s12079-023-00778-3

Hui Yin, Na Liu, Xianming Zhou, Jie Chen, Lihua Duan

引用次数: 1

Identification of ZMYND19 as a novel biomarker of colorectal cancer: RNA-sequencing and machine learning analysis. 将 ZMYND19 鉴定为结直肠癌的新型生物标记物：RNA测序和机器学习分析

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 Epub Date: 2023-07-10 DOI: 10.1007/s12079-023-00779-2

Ghazaleh Khalili-Tanha, Reza Mohit, Alireza Asadnia, Majid Khazaei, Mohammad Dashtiahangar, Mina Maftooh, Mohammadreza Nassiri, Seyed Mahdi Hassanian, Majid Ghayour-Mobarhan, Mohammad Ali Kiani, Gordon A Ferns, Jyotsna Batra, Elham Nazari, Amir Avan

{"title":"Identification of ZMYND19 as a novel biomarker of colorectal cancer: RNA-sequencing and machine learning analysis.","authors":"Ghazaleh Khalili-Tanha, Reza Mohit, Alireza Asadnia, Majid Khazaei, Mohammad Dashtiahangar, Mina Maftooh, Mohammadreza Nassiri, Seyed Mahdi Hassanian, Majid Ghayour-Mobarhan, Mohammad Ali Kiani, Gordon A Ferns, Jyotsna Batra, Elham Nazari, Amir Avan","doi":"10.1007/s12079-023-00779-2","DOIUrl":"10.1007/s12079-023-00779-2","url":null,"abstract":"Colorectal cancer (CRC) is the third most common cause of cancer-related deaths. The five-year relative survival rate for CRC is estimated to be approximately 90% for patients diagnosed with early stages and 14% for those diagnosed at an advanced stages of disease, respectively. Hence, the development of accurate prognostic markers is required. Bioinformatics enables the identification of dysregulated pathways and novel biomarkers. RNA expression profiling was performed in CRC patients from the TCGA database using a Machine Learning approach to identify differential expression genes (DEGs). Survival curves were assessed using Kaplan-Meier analysis to identify prognostic biomarkers. Furthermore, the molecular pathways, protein-protein interaction, the co-expression of DEGs, and the correlation between DEGs and clinical data have been evaluated. The diagnostic markers were then determined based on machine learning analysis. The results indicated that key upregulated genes are associated with the RNA processing and heterocycle metabolic process, including C10orf2, NOP2, DKC1, BYSL, RRP12, PUS7, MTHFD1L, and PPAT. Furthermore, the survival analysis identified NOP58, OSBPL3, DNAJC2, and ZMYND19 as prognostic markers. The combineROC curve analysis indicated that the combination of C10orf2 -PPAT- ZMYND19 can be considered as diagnostic markers with sensitivity, specificity, and AUC values of 0.98, 1.00, and 0.99, respectively. Eventually, ZMYND19 gene was validated in CRC patients. In conclusion, novel biomarkers of CRC have been identified that may be a promising strategy for early diagnosis, potential treatment, and better prognosis.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":" ","pages":"1469-1485"},"PeriodicalIF":4.1,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713961/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9764247","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: 3