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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 Q3 CELL BIOLOGY 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

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.

细胞通讯网络因子 2(CCN2)分子可促进软骨内骨化和关节软骨再生,而在人类血管内皮细胞和其他类型的细胞中,由 CCN2 合成的环状 RNA(circRNA)可产生于各种基因,并通过吸附 miRNA 来调节基因表达。然而,在软骨细胞中,CCN2衍生的circRNA不仅功能未知,其存在也完全未知。在本研究中,我们调查了CCN2衍生的circRNA在软骨细胞中的表达和功能。通过 RT-PCR 分析,我们观察到了比已知的 CCN2 衍生 circRNA 更小的扩增子,可以特异性地扩增人软骨细胞 HCS-2/8 细胞中的 CCN2 衍生 circRNA。PCR 产物的核苷酸序列表明,HCS-2/8 细胞中的新型 circRNA 与已知的 CCN2 衍生 circRNA 不同。此外,在小鼠软骨母细胞 ATDC5 细胞中,几种 Ccn2 衍生的 circRNA 的表达得到了证实,并观察到它们随着软骨母细胞的分化而变化。接下来,在 HCS-2/8 细胞中敲除了其中一个 circRNA,以研究人 CCN2 衍生 circRNA 的功能。结果发现,CCN2衍生的circRNA被敲除后,凝集素mRNA的表达和蛋白多糖的合成明显减少。我们的数据表明,CCN2衍生的circRNA在软骨细胞中表达,并在软骨分化中发挥作用。CCN2衍生RNA在软骨细胞中的产生和作用。
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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 Q3 CELL BIOLOGY Pub Date : 2023-08-24 DOI: 10.1007/s12079-023-00777-4
Zhichun Gao, Julia M. Houthuijzen, Peter ten Dijke, Derek P. Brazil

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.

GREMLIN1(GREM1)是结构和功能相关的分泌型半胱氨酸结蛋白家族的成员,其作用是封闭和抑制多功能骨形态发生蛋白(BMP)的作用。GREM1 可直接与 BMP 二聚体结合,从而阻止 BMP 介导的 BMP I 型和 II 型受体的激活。多份报告指出,GREM1 的过度表达是导致多种癌症的一个因素。此外,在一种罕见的常染色体显性遗传性结直肠癌中,GREM1 基因被扩增。GREM1对BMP信号的抑制作用与这些肿瘤促进作用有关,包括促进癌细胞干性和激活癌症相关成纤维细胞。此外,GREM1 还能与血管内皮生长因子受体(VEGFR)结合并发出信号,刺激血管生成,还能与表皮生长因子受体和成纤维细胞生长因子受体(EGFR 和 FGFR)结合并发出信号,分别在乳腺癌和前列腺癌中激发肿瘤促进效应。相反,2022 年的一份报告显示,GREM1 能促进胰腺癌的上皮状态,从而抑制胰腺肿瘤的生长和转移。在这篇评论中,我们将回顾这些不同的研究结果,并尝试阐明 GREM1 信号在癌症中的作用。
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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 Q3 CELL BIOLOGY 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

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.

越来越多的研究表明,非典型蛋白激酶C同工酶ι(PKCι)是一种肿瘤蛋白,在胰腺癌发生过程中发挥着多方面的作用,包括维持转化生长、抑制凋亡、增强侵袭性、促进自噬以及促进胰腺肿瘤的免疫抑制性肿瘤微环境。在这项研究中,我们提出了新的证据,证明在胰腺癌细胞中,PKCι 的过表达会增加 STAT3 在 Y705 残基上的磷酸化,同时降低 STAT3 在 S727 残基上的磷酸化。我们进一步证明,STAT3 在 Y705 和 S727 残基上的磷酸化是相互拮抗的,STAT3 Y705 磷酸化与 STAT3 在胰腺癌细胞中的转录活性呈正相关。此外,我们还发现 PKCι 抑制可通过 Y705 去磷酸化来减弱 STAT3 的转录活性,而这似乎是胰腺癌细胞中 S727 磷酸化增强的结果。最后,我们研究并证明,通过调节 STAT3 的活性,PKCι 抑制剂可以协同增强药理 STAT3 抑制剂的抗肿瘤效果,或逆转 MEK 抑制剂引发的抗凋亡副作用,从而成为治疗胰腺癌细胞的前瞻性增敏剂。
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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 Q3 CELL BIOLOGY Pub Date : 2023-07-25 DOI: 10.1007/s12079-023-00771-w
Suchi Chaturvedi, Mainak Biswas, Sushabhan Sadhukhan, Avinash Sonawane

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.

乳腺癌(BC)是威胁女性生命的疾病之一。尽管全球在癌症检测和治疗方面取得了显著进步,但根据 GLOBACAN 2020 的数据,在大多数国家,乳腺癌仍是第五大主要癌症,估计每 6 人中就有 1 人死于乳腺癌。然而,导致 BC 进展的确切原因仍有待确定。在此,我们回顾了两种新型生物标志物的作用,这两种生物标志物导致了50-70%的BC进展。第一个是表皮生长因子受体(EGFR),它属于ErbB酪氨酸激酶家族,与之相关的信号通路在调节细胞增殖和分裂方面发挥着重要作用。另一种是脂肪酸合成酶(FASN),它是癌细胞发育所需的一种负责新脂质合成的关键酶。这篇综述介绍了表皮生长因子受体介导的途径、它们与 FASN 的相互作用、这两种生物标志物与 BC 的关系,以及克服由它们引起的耐药性的方法。
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引用次数: 0
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 3.6 3区 生物学 Q3 CELL BIOLOGY Pub 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

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.

结肠直肠癌(CRC)是癌症相关死亡的第三大常见原因。据估计,CRC 早期患者的五年相对生存率约为 90%,晚期患者的五年相对生存率约为 14%。因此,需要开发准确的预后标志物。生物信息学能够识别失调的通路和新型生物标志物。我们使用机器学习方法对 TCGA 数据库中的 CRC 患者进行了 RNA 表达谱分析,以确定差异表达基因(DEGs)。利用 Kaplan-Meier 分析评估了生存曲线,以确定预后生物标志物。此外,还评估了分子通路、蛋白-蛋白相互作用、DEGs 的共表达以及 DEGs 与临床数据之间的相关性。然后根据机器学习分析确定了诊断标志物。结果表明,关键的上调基因与 RNA 处理和杂环代谢过程有关,包括 C10orf2、NOP2、DKC1、BYSL、RRP12、PUS7、MTHFD1L 和 PPAT。此外,生存分析还发现 NOP58、OSBPL3、DNAJC2 和 ZMYND19 是预后标志物。联合ROC曲线分析表明,C10orf2 -PPAT- ZMYND19的组合可被视为诊断标志物,其灵敏度、特异性和AUC值分别为0.98、1.00和0.99。最终,ZMYND19 基因在 CRC 患者中得到了验证。总之,新发现的 CRC 生物标记物可能是早期诊断、潜在治疗和改善预后的有效策略。
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引用次数: 0
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 3.6 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2023-06-28 DOI: 10.1007/s12079-023-00772-9
Weiming Zhao, Lingling Xi, Guoying Yu, Gaiping Wang, Cuifang Chang

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.

G 蛋白偶联受体(GPCR)在肿瘤发生和肝细胞癌(HCC)发展过程中发挥着重要作用。GPR50 是一种孤儿 GPCR。以前的研究表明,GPR50 可以防止乳腺癌的发展,并在异种移植小鼠模型中减少肿瘤的生长。然而,它在 HCC 中的作用仍不明确。为了检测GPR50在HCC中的作用和调控机制,研究人员分析了GPR50在HCC患者中的表达(基因表达总括数据库(GEO)(GSE45436)),并检测了HCC细胞株CBRH-7919中的表达,结果表明与相应的正常对照相比,GPR50在HCC患者和CBRH-7919细胞株中显著上调。将Gpr50 cDNA转染到HCC细胞株CBRH-7919中,我们发现Gpr50能促进CBRH-7919的增殖、迁移和自噬。通过同位素标签相对和绝对定量(iTRAQ)分析检测了GPR50在HCC中的调控机制,发现GPR50对HCC的促进作用与CCT6A和PGK1密切相关。综上所述,GPR50可能通过CCT6A诱导的增殖和PGK1诱导的迁移和自噬促进HCC的进展,GPR50可能是HCC的一个重要靶点。
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引用次数: 0
The advance of CCN3 in fibrosis CCN3在纤维化中的进展。
IF 3.6 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2023-06-28 DOI: 10.1007/s12079-023-00778-3
Hui Yin, Na Liu, Xianming Zhou, Jie Chen, Lihua Duan

The extracellular matrix (ECM) is comprised of various extracellular macromolecules, including collagen, enzymes, and glycoproteins, which offer structural and biochemical support to neighboring cells. After tissue injury, extracellular matrix proteins deposit in the damaged tissue to promote tissue healing. However, an imbalance between ECM production and degradation can result in excessive deposition, leading to fibrosis and subsequent organ dysfunction. Acting as a regulatory protein within the extracellular matrix, CCN3 plays a crucial role in numerous biological processes, such as cell proliferation, angiogenesis, tumorigenesis, and wound healing. Many studies have demonstrated that CCN3 can reduce the production of ECM in tissues through diverse mechanisms thereby exerting an inhibitory effect on fibrosis. Consequently, CCN3 emerges as a promising therapeutic target for ameliorating fibrosis.

细胞外基质(ECM)由各种胞外大分子组成,包括胶原蛋白、酶和糖蛋白,为邻近细胞提供结构和生化支持。组织受伤后,细胞外基质蛋白会沉积在受损组织中,促进组织愈合。然而,细胞外基质蛋白生成和降解之间的失衡会导致过度沉积,从而导致纤维化和随后的器官功能障碍。CCN3 作为细胞外基质中的调节蛋白,在细胞增殖、血管生成、肿瘤发生和伤口愈合等众多生物过程中发挥着至关重要的作用。许多研究表明,CCN3 可通过多种机制减少组织中 ECM 的生成,从而对纤维化产生抑制作用。因此,CCN3 成为改善纤维化的一个有前景的治疗靶点。
{"title":"The advance of CCN3 in fibrosis","authors":"Hui Yin,&nbsp;Na Liu,&nbsp;Xianming Zhou,&nbsp;Jie Chen,&nbsp;Lihua Duan","doi":"10.1007/s12079-023-00778-3","DOIUrl":"10.1007/s12079-023-00778-3","url":null,"abstract":"<div>\u0000 \u0000 <p>The extracellular matrix (ECM) is comprised of various extracellular macromolecules, including collagen, enzymes, and glycoproteins, which offer structural and biochemical support to neighboring cells. After tissue injury, extracellular matrix proteins deposit in the damaged tissue to promote tissue healing. However, an imbalance between ECM production and degradation can result in excessive deposition, leading to fibrosis and subsequent organ dysfunction. Acting as a regulatory protein within the extracellular matrix, CCN3 plays a crucial role in numerous biological processes, such as cell proliferation, angiogenesis, tumorigenesis, and wound healing. Many studies have demonstrated that CCN3 can reduce the production of ECM in tissues through diverse mechanisms thereby exerting an inhibitory effect on fibrosis. Consequently, CCN3 emerges as a promising therapeutic target for ameliorating fibrosis.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1219-1227"},"PeriodicalIF":3.6,"publicationDate":"2023-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9696423","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 TLRs in EGFR-mediated IL-8 secretion by enteroaggregative Escherichia coli-infected cultured human intestinal epithelial cells TLRs在肠道聚集性大肠埃希氏菌感染培养的人肠道上皮细胞分泌表皮生长因子受体介导的IL-8中的作用。
IF 3.6 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2023-06-22 DOI: 10.1007/s12079-023-00776-5
Archana Joon, Shipra Chandel, Sujata Ghosh

Enteroaggregative Escherichia coli (EAEC) is an emerging enteric pathogen associated with persistent diarrhea in travelers, immunocompromised patients and children worldwide. However, the pathogenesis of this organism is yet to be established. In this study, the role of Toll-like receptors (TLRs) was evaluated in epidermal growth factor receptor (EGFR)-mediated IL-8 secretion by EAEC-infected human small intestinal and colonic epithelial cells (INT-407 and HCT-15, respectively). We observed that EAEC-induced upregulation of TLR2, TLR4 and TLR5 transcripts in both types of cells, and the maximum level of these transcripts was seen in cells infected with EAEC-T8 (an invasive clinical isolate). All these TLRs made a significant contribution to the EAEC-T8-mediated EGFR activation in these cells. Furthermore, these TLRs were found to be associated with activation of the downstream effectors (ERK-1/2, PI3 kinase and Akt) and transcription factors (NF-κB, c-Jun, c-Fos and STAT-3) of EGFR-mediated signal transduction pathways. Moreover, the involvement of these TLRs was also noted in IL-8 secretion by both EAEC-T8-infected cell types. Our findings suggest that EAEC-induced upregulation of TLR2, TLR4 and TLR5 is important for the IL-8 response via EGFR-mediated signal transduction pathways in these cells.

肠道聚集性大肠杆菌(EAEC)是一种新出现的肠道病原体,与全球旅行者、免疫力低下患者和儿童的持续腹泻有关。然而,这种病菌的致病机理尚未确定。本研究评估了 Toll 样受体(TLRs)在表皮生长因子受体(EGFR)介导的 EAEC 感染人小肠和结肠上皮细胞(分别为 INT-407 和 HCT-15)分泌 IL-8 中的作用。我们观察到,EAEC 在两种细胞中都诱导了 TLR2、TLR4 和 TLR5 转录本的上调,而在感染了 EAEC-T8(一种侵袭性临床分离物)的细胞中,这些转录本的水平最高。所有这些 TLR 都对 EAEC-T8 介导的表皮生长因子受体在这些细胞中的激活起了重要作用。此外,还发现这些 TLR 与表皮生长因子受体介导的信号转导途径的下游效应因子(ERK-1/2、PI3 激酶和 Akt)和转录因子(NF-κB、c-Jun、c-Fos 和 STAT-3)的激活有关。此外,这些 TLRs 也参与了 EAEC-T8 感染细胞的 IL-8 分泌。我们的研究结果表明,EAEC 诱导的 TLR2、TLR4 和 TLR5 上调对这些细胞通过表皮生长因子受体介导的信号转导途径产生 IL-8 反应非常重要。
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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 3.6 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2023-06-20 DOI: 10.1007/s12079-023-00775-6
Ye Zhao, Huiling Wang, Tianhua He, Bo Ma, Guoguang Chen, Chimeng Tzeng

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.

肝纤维化是对组织损伤的一种异常伤口愈合反应,其特点是细胞外基质过度沉积和正常肝脏结构丧失。肝星状细胞(HSCs)活化被认为是肝纤维化的主要过程,而肝纤维化是动态和可逆的。Hippo信号转导核心因子Yap和Hedgehog(Hh)信号转导都能促进造血干细胞的转分化,从而调节肝损伤的修复过程。然而,YAP的分子功能以及Yap和Hh在纤维化过程中的调控作用仍不确定。本研究探讨了Yap在肝纤维化中的重要作用。硫代乙酰胺(TAA)诱导的斑马鱼胚胎和成鱼模型检测到肝纤维化组织中的Yap增加。通过组织学和基因表达检测,证明通过胚胎吗啉干扰和成鱼抑制剂处理抑制Yap可减轻TAA诱导的肝脏病变。转录组分析和基因表达检测表明,Yap和Hh信号通路在TAA诱导的肝纤维化过程中存在交叉对话。此外,TAA诱导促进了YAP和Hh信号因子GLI2α的核共定位。该研究表明,Yap和Hh在肝纤维化反应中发挥协同保护作用,并为肝纤维化进展机制提供了新的理论依据。
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引用次数: 0
Emerging roles of the long non-coding RNA NEAT1 in gynecologic cancers 长链非编码RNA NEAT1在妇科癌症中的新作用
IF 4.1 3区 生物学 Q3 CELL BIOLOGY Pub Date : 2023-06-13 DOI: 10.1007/s12079-023-00746-x
Maryam Farzaneh, Mahrokh Abouali Gale Dari, Amir Anbiyaiee, Sajad Najafi, Dian Dayer, Abdolah Mousavi Salehi, Mona Keivan, Mehri Ghafourian, Shahab Uddin, Shirin Azizidoost

Gynecologic cancers are a worldwide problem among women. Recently, molecular targeted therapy opened up an avenue for cancer diagnosis and treatment. Long non-coding RNAs (lncRNAs) are RNA molecules (> 200 nt) that are not translated into protein, and interact with DNA, RNA, and proteins. LncRNAs were found to play pivotal roles in cancer tumorigenesis and progression. Nuclear paraspeckle assembly transcript 1 (NEAT1) is a lncRNA that mediates cell proliferation, migration, and EMT in gynecologic cancers by targeting several miRNAs/mRNA axes. Therefore, NEAT1 may function as a potent biomarker for the prediction and treatment of breast, ovarian, cervical, and endometrial cancers. In this narrative review, we summarized various NEAT1-related signaling pathways that are critical in gynecologic cancers.

妇科癌症是一个世界性的妇女问题。近年来,分子靶向治疗为癌症的诊断和治疗开辟了新的途径。长链非编码RNA (Long non-coding RNA, lncRNAs)是不被翻译成蛋白质的RNA分子(> 200nt),它们与DNA、RNA和蛋白质相互作用。LncRNAs被发现在癌症的发生和发展中起着关键作用。核旁散粒组装转录本1 (NEAT1)是一种lncRNA,通过靶向几种mirna /mRNA轴介导妇科肿瘤细胞增殖、迁移和EMT。因此,NEAT1可能作为预测和治疗乳腺癌、卵巢癌、宫颈癌和子宫内膜癌的有效生物标志物。在这篇叙述性综述中,我们总结了各种neat1相关的信号通路,这些信号通路在妇科癌症中至关重要。
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引用次数: 1
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