Tissue & cell最新文献_第10页

Exploring Caspase-3 overexpression in pheochromocytoma cells: Implications for cancer therapy 探索Caspase-3在嗜铬细胞瘤细胞中的过表达：对癌症治疗的意义。

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-05 DOI: 10.1016/j.tice.2024.102720

Reihaneh Zare , Rita ArabSolghar , Abbas Behzad Behbahni , Farahnaz Zare , Ali Kheirandish , Fatemeh Safari

Malignant pheochromocytomas are infrequent tumors that have a poorer prognosis compared to their benign counterparts. The administration of chemotherapy to patients with pheochromocytoma can result in adverse side effects and a reduced life quality. Alternative and more targeted treatment strategies, such as gene therapy significantly improve the patients’ survival rate and life expectancy. Caspase-3 is a key apoptosis regulator activated by cancer treatments. Recent research shows it also influences tumor relapse and angiogenesis, complicating its role in cancer progression. Further exploration of Caspase-3's diverse functions is needed to clarify its impact on cancer development.

In this study, we established Caspase-3 over expressed pheochromocytoma cell line by the use of lentiviral vector technology. Caspase 3 over expression by up to 3fold led to increase in cell proliferation by up to 12 %. Moreover, increasing in Caspase 3 level of expression resulted in more invasiveness and metastasis. By this way, the wound closure percentage for PC-12 Casp3 + cells reached 76.2 %, which is significantly higher compared to the 52.8 % observed in mock cells. Casp3 + cells were also significantly more sensitive to cisplatin than mock cells with Ic50 of 158.4 μM and 219.5uM respectively according to MTT assay which confirmed by apoptosis assay. Hence, targeting Caspase-3 as a therapeutic approach may enhance the cancer cell sensitivity to chemotherapy, but also increase the cancer cell proliferation, metastases and invasion which may works as a double edge sword.

Conclusion

understanding the effects of Caspase 3 over expression on cancer cells could inspire innovative therapies targeting its non-apoptotic actions, potentially improving cancer treatment outcomes.

恶性嗜铬细胞瘤是少见的肿瘤，与良性肿瘤相比预后较差。嗜铬细胞瘤患者化疗可导致不良副作用和生活质量下降。替代和更有针对性的治疗策略，如基因治疗显着提高患者的存活率和预期寿命。Caspase-3是癌症治疗激活的关键细胞凋亡调节因子。最近的研究表明，它还影响肿瘤复发和血管生成，使其在癌症进展中的作用复杂化。需要进一步探索Caspase-3的多种功能，以阐明其对癌症发展的影响。在本研究中，我们利用慢病毒载体技术建立了Caspase-3过表达的嗜铬细胞瘤细胞系。Caspase 3过表达高达3倍，导致细胞增殖增加高达12% %。此外，Caspase 3表达水平的升高导致其侵袭性和转移性增强。通过这种方法，PC-12 Casp3 + 细胞的伤口愈合率达到76.2 %，明显高于模拟细胞的52.8% %。凋亡实验证实，Casp3 + 细胞对顺铂的敏感性明显高于模拟细胞，其Ic50分别为158.4 μM和219.5 μM。因此，靶向Caspase-3作为一种治疗手段，可能会增强癌细胞对化疗的敏感性，但也会增加癌细胞的增殖、转移和侵袭，这可能是一把双刃剑。结论：了解Caspase 3过表达对癌细胞的影响，可以激发针对其非凋亡作用的创新疗法，可能改善癌症治疗效果。

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引用次数: 0

Disrupted homeostasis in sickle cells: Expanding the comprehension of metabolism adaptation and related therapeutic strategies 镰状细胞的稳态紊乱：拓展对新陈代谢适应性和相关治疗策略的理解。

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-04 DOI: 10.1016/j.tice.2024.102717

Victoria Simões Bernardo , Flaviene Felix Torres , Ana Clara Albertin Zucão , Nayara Alves Chaves , Ilana Luize Rocha Santana , Danilo Grünig Humberto da Silva

Sickle cell disease (SCD) is a hereditary hemolytic anemia associated with the alteration of the membrane composition of the sickle erythrocytes, the loss of glycolysis, dysregulation of the pyruvate phosphatase pathway, and changes in nucleotide metabolism of the sickle red blood cell (RBC). This review provides a comprehensive overview of the impact of the presence of Hb S, which leads to the disruption of the normal RBC metabolism. The intricate interplay between the redox and energetic balance in erythrocytic cells, where the glycolysis, pentose phosphate pathway, and methemoglobin reductase pathways are all altered in sickle RBC, is a key focus. Moreover, this review summarizes the current knowledge about the disease-modifying agents and their action mechanisms based on the sickle RBC alterations previously mentioned (i.e., their association with beneficial effects on the sickle cells' membrane, to their RBCs' energy metabolism, and to their oxidative status). Therefore, providing a comprehensive understanding of how sickle cells cope with the disruption of metabolic homeostasis and the most promising therapeutic agents able to ameliorate the various consequences of abnormal sickle RBC alterations.

镰状细胞病（SCD）是一种遗传性溶血性贫血，与镰状红细胞膜组成改变、糖酵解丧失、丙酮酸磷酸酶途径失调以及镰状红细胞（RBC）核苷酸代谢改变有关。这篇综述提供了Hb S存在的影响的全面概述，它导致正常红细胞代谢的破坏。镰状红细胞中糖酵解、戊糖磷酸途径和高铁血红蛋白还原酶途径都发生改变，红细胞氧化还原和能量平衡之间复杂的相互作用是一个关键的焦点。此外，本文综述了基于上述镰状红细胞改变的疾病修饰剂及其作用机制的最新知识（即它们与镰状细胞膜、红细胞能量代谢和氧化状态的有益作用的关联）。因此，提供镰状细胞如何应对代谢稳态破坏的全面理解，以及能够改善镰状红细胞异常改变的各种后果的最有希望的治疗药物。

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引用次数: 0

Evaluating the anticancer effects of carnosic acid against breast cancer: An In Vitro investigation 鼠尾草酸抗乳腺癌作用的体外研究。

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-03 DOI: 10.1016/j.tice.2024.102718

Aylar Borhan , Ali Bagherlou , Mohammad B. Ghayour

Background

Carnosic acid (CA) has potential anti-cancer properties, but its effectiveness can be improved by combining it with Folic acid (FA). This research aimed to evaluate the impact of CA and CA-FA conjugate on breast cancer cell lines (MCF-7, MDA-MB-231, and MCA10).

Materials and methods

The viability of the cell lines was measured using the MTT assay, and the IC₅₀ was determined to compare the cytotoxicity of CA and CA-FA. The process of programmed cell death was investigated by utilizing Annexin V/PI staining, measuring caspase-3/7 activity, and real-time PCR for apoptotic gene expression. Reactive oxygen species (ROS) were also assessed to determine the extent of oxidative stress.

Results

CA significantly decreased the viability of MCF-7 and MDA-MB-231 cells depending on the dosage, with CA-FA exhibiting enhanced cytotoxicity, particularly in MDA-MB-231 cells. The evaluation of IC₅₀ confirmed that conjugation with FA reduced the IC₅₀ of CA. Apoptosis analysis demonstrated increased apoptosis rates in MCF-7 and MDA-MB-231 cells exposed to treatment with CA and CA-FA, while MCA10 cells showed minimal effects. Caspase-3/7 activity was notably higher in CA-FA-treated cells. Gene expression analysis revealed elevated pro-apoptotic gene activity and reduced anti-apoptotic gene activity, with CA-FA having a more pronounced effect. Cells subjected to CA-FA treatment exhibited a significant increase in ROS levels.

Conclusion

These findings suggest that CA conjugation with FA enhances its cytotoxic effects and promotes apoptosis through increased apoptosis and ROS production. The research emphasizes the promise of CA-FA as a focused treatment approach for aggressive forms of breast cancer, underscoring the need for additional exploration of its practical uses in clinical settings.

背景：鼠尾草酸（CA）具有潜在的抗癌作用，但与叶酸（FA）联合使用可提高其抗癌效果。本研究旨在评估CA和CA- fa偶联物对乳腺癌细胞系（MCF-7、MDA-MB-231和MCA10）的影响。材料和方法：使用MTT法测量细胞系的活力，并确定IC₅0以比较CA和CA- fa的细胞毒性。采用Annexin V/PI染色、检测caspase-3/7活性、实时荧光定量PCR检测凋亡基因表达，研究细胞程序性死亡过程。还评估了活性氧（ROS）以确定氧化应激的程度。结果：CA根据剂量显著降低MCF-7和MDA-MB-231细胞的活力，CA- fa表现出增强的细胞毒性，特别是对MDA-MB-231细胞。对IC₅₀的评估证实，与FA的结合降低了CA的IC₅₀。细胞凋亡分析表明，暴露于CA和CA-FA处理的MCF-7和MDA-MB-231细胞的细胞凋亡率增加，而MCA10细胞的影响最小。Caspase-3/7活性在ca - fa处理的细胞中显著升高。基因表达分析显示促凋亡基因活性升高，抗凋亡基因活性降低，CA-FA的作用更为明显。经CA-FA处理的细胞ROS水平显著升高。结论：CA与FA结合可增强其细胞毒作用，并通过增加细胞凋亡和ROS的产生促进细胞凋亡。该研究强调了CA-FA作为侵袭性乳腺癌的重点治疗方法的前景，强调了在临床环境中进一步探索其实际应用的必要性。

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引用次数: 0

Osteogenic differentiation of mesenchymal stem cell on poly sorbitol sebacate scaffold under shear stress in a bioreactor 生物反应器剪切应力下聚山梨醇癸二酸支架上间充质干细胞的成骨分化。

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2025-01-02 DOI: 10.1016/j.tice.2024.102715

Fatemeh Abbasloo , Bahman Vahidi , Mohammad-Mehdi Khani , Faraz Sigaroodi , Reza Ramezani Sarbandi

Mechanical loading plays a pivotal role in regulating bone anabolic processes. Understanding the optimal mechanical loading parameters for cellular responses is critical for advancing strategies in orthopedic bioreactor-based bone tissue engineering. This study developed a poly (sorbitol sebacate) (PSS) filmscaffold with a sorbitol-to-sebacic acid molar ratio of 1:4. The scaffold underwent extensive characterization, including physical and mechanical property evaluations, biocompatibility assessments, and cell adhesion analysis. The Young's modulus of the PSS polymer was determined to be 6.81 ± 0.44 MPa under dry conditions, 6.37 ± 1.09 MPa in a wet state, and 6.38 ± 0.71 MPa after ethanol washing (70 %). The average contact angle of the PSS film was measured at 88.806 ± 1.644°, indicating moderate hydrophilicity. To investigate the osteogenic potential, a fluid flow inducing a shear stress of 1 Pa at a frequency of 1 Hz was applied to mesenchymal stem cells (MSCs) cultured on the PSS scaffold. Cells were exposed to dynamic fluid flow for one hour daily on days 4, 5, 6, and 7 of culture, followed by a static culture period of 14 days. The expression of osteogenic differentiation markers, including osteopontin (OPN), osteocalcin (OCN), type I collagen, and calcium deposition, was significantly elevated under dynamic conditions compared to static culture. This study highlights the importance of mechanical stimulation in enhancing MSC osteogenesis and underscores the osteoconductive properties of the PSS scaffold. These findings provide valuable insights into scaffold design and mechanical loading strategies for laboratory-based bone tissue engineering applications.

机械负荷在调节骨合成代谢过程中起着关键作用。了解细胞反应的最佳机械载荷参数对于推进骨科生物反应器骨组织工程的策略至关重要。本研究制备了一种山梨醇与癸二酸摩尔比为1:4的聚山梨醇癸二酸酯（PSS）薄膜支架。支架进行了广泛的表征，包括物理和机械性能评估、生物相容性评估和细胞粘附分析。PSS聚合物的杨氏模量确定为6.81 ±0.44  MPa在干燥条件下, 6.37±1.09  MPa处于潮湿的状态,和6.38 ±0.71  MPa乙醇洗涤后(70 %)。PSS膜的平均接触角为88.806 ± 1.644°，为中等亲水性。为了研究成骨潜能，在PSS支架上培养的间充质干细胞（MSCs）上施加频率为1 Hz、剪切应力为1 Pa的流体。在培养的第4、5、6、7天，细胞每天在动态流体中暴露1小时，然后静培养14天。与静态培养相比，动态条件下骨桥蛋白（OPN）、骨钙素（OCN）、I型胶原蛋白和钙沉积等成骨分化标志物的表达显著升高。本研究强调了机械刺激在促进间充质干细胞成骨中的重要性，并强调了PSS支架的骨传导特性。这些发现为基于实验室的骨组织工程应用的支架设计和机械加载策略提供了有价值的见解。

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引用次数: 0

LPCAT1 reduces inflammatory response, apoptosis and barrier damage of nasal mucosal epithelial cells caused by allergic rhinitis through endoplasmic reticulum stress LPCAT1通过内质网应激减少变应性鼻炎引起的鼻黏膜上皮细胞的炎症反应、凋亡和屏障损伤。

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-12-31 DOI: 10.1016/j.tice.2024.102712

Liang Wu , Juan Wang

Allergic rhinitis (AR), common in children and adolescents, involves Lysophosphatidylcholine acyltransferase 1 (LPCAT1) catalyzing surfactant lipid biosynthesis and suppressing endoplasmic reticulum expression. However, the precise mechanism underlying the impact of LPCAT1 on epithelial cell damage in AR remains elusive. Hence, the present investigation elucidated the potential effect of LPCAT1 on epithelial cell damage in AR by inhibiting endoplasmic reticulum stress. To assess cell viability, CCK8 assay was employed. Additionally, western blotting was utilized to evaluate the expression of endoplasmic reticulum stress-associated proteins ATF6, CHOP, p-eIF2α, p-IRE1, and LPCAT1. Subsequently, an interference plasmid targeting LPCAT1 was constructed, and western blot analysis was conducted to determine interference level of LPCAT1. An ELISA assay was employed to quantify the concentrations of TNFα, IL-1β, IL-6, GM-CSF, and eotaxin. Additionally, flow cytometry and western blotting techniques were utilized to evaluate cellular apoptosis, whereas immunofluorescence staining was applied to detect the expression levels of ZO-1. Our findings indicated that IL-13 stimulation resulted in an elevated expression of ER stress proteins and LPCAT1 in nasal mucosal epithelial cells. Furthermore, LPCAT1 interference diminished the expression of inflammatory mediators, apoptosis markers, barrier disruption indicators, and ER stress proteins in IL-13-stimulated nasal mucosal epithelial cells. Further, by inhibiting ER stress, LPCAT1 interference diminished the expression of inflammatory factors, apoptosis, and barrier damage in nasal mucosal epithelial cells stimulated by IL-13. Concisely, LPCAT1 ameliorates AR-induced inflammation, apoptosis, and barrier impairment in nasal mucosal epithelial cells by modulating ER stress, implying its potential as a novel therapeutic target for AR.

过敏性鼻炎（AR）常见于儿童和青少年，涉及溶血磷脂酰胆碱酰基转移酶1 （LPCAT1）催化表面活性剂脂质生物合成并抑制内质网表达。然而，LPCAT1对AR中上皮细胞损伤影响的确切机制尚不清楚。因此，本研究阐明了LPCAT1通过抑制内质网应激对AR上皮细胞损伤的潜在作用。采用CCK8法测定细胞活力。此外，western blotting检测内质网应激相关蛋白ATF6、CHOP、p-eIF2α、p-IRE1和LPCAT1的表达。随后构建靶向LPCAT1的干扰质粒，通过western blot分析LPCAT1的干扰水平。采用ELISA法定量TNFα、IL-1β、IL-6、GM-CSF和eotaxin的浓度。此外，流式细胞术和western blotting技术检测细胞凋亡，免疫荧光染色检测ZO-1表达水平。我们的研究结果表明，IL-13刺激导致鼻黏膜上皮细胞内质网应激蛋白和LPCAT1的表达升高。此外，LPCAT1干扰降低了il -13刺激的鼻黏膜上皮细胞中炎症介质、凋亡标志物、屏障破坏指标和内质网应激蛋白的表达。此外，通过抑制内质网应激，LPCAT1干扰降低IL-13刺激的鼻黏膜上皮细胞中炎症因子的表达、细胞凋亡和屏障损伤。简而言之，LPCAT1通过调节内质网应激改善AR诱导的鼻黏膜上皮细胞炎症、凋亡和屏障损伤，这意味着它有可能成为AR的新治疗靶点。

{"title":"LPCAT1 reduces inflammatory response, apoptosis and barrier damage of nasal mucosal epithelial cells caused by allergic rhinitis through endoplasmic reticulum stress","authors":"Liang Wu , Juan Wang","doi":"10.1016/j.tice.2024.102712","DOIUrl":"10.1016/j.tice.2024.102712","url":null,"abstract":"<div><div>Allergic rhinitis (AR), common in children and adolescents, involves Lysophosphatidylcholine acyltransferase 1 (LPCAT1) catalyzing surfactant lipid biosynthesis and suppressing endoplasmic reticulum expression. However, the precise mechanism underlying the impact of LPCAT1 on epithelial cell damage in AR remains elusive. Hence, the present investigation elucidated the potential effect of LPCAT1 on epithelial cell damage in AR by inhibiting endoplasmic reticulum stress. To assess cell viability, CCK8 assay was employed. Additionally, western blotting was utilized to evaluate the expression of endoplasmic reticulum stress-associated proteins ATF6, CHOP, p-eIF2α, p-IRE1, and LPCAT1. Subsequently, an interference plasmid targeting LPCAT1 was constructed, and western blot analysis was conducted to determine interference level of LPCAT1. An ELISA assay was employed to quantify the concentrations of TNFα, IL-1β, IL-6, GM-CSF, and eotaxin. Additionally, flow cytometry and western blotting techniques were utilized to evaluate cellular apoptosis, whereas immunofluorescence staining was applied to detect the expression levels of ZO-1. Our findings indicated that IL-13 stimulation resulted in an elevated expression of ER stress proteins and LPCAT1 in nasal mucosal epithelial cells. Furthermore, LPCAT1 interference diminished the expression of inflammatory mediators, apoptosis markers, barrier disruption indicators, and ER stress proteins in IL-13-stimulated nasal mucosal epithelial cells. Further, by inhibiting ER stress, LPCAT1 interference diminished the expression of inflammatory factors, apoptosis, and barrier damage in nasal mucosal epithelial cells stimulated by IL-13. Concisely, LPCAT1 ameliorates AR-induced inflammation, apoptosis, and barrier impairment in nasal mucosal epithelial cells by modulating ER stress, implying its potential as a novel therapeutic target for AR.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102712"},"PeriodicalIF":2.7,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Cell origin and microenvironment: The players of differentiation capacity in human mesenchymal stem cells

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-12-31 DOI: 10.1016/j.tice.2024.102709

Seyed Mehdi Hoseini , Fateme Montazeri

Mesenchymal stem cells (MSCs) have several important properties that make them desirable for regenerative medicine. These properties include immunomodulatory ability, growth factor production, and differentiation into various cell types. Despite extensive research and promising results in clinical trials, our understanding of MSC biology, their mechanism of action, and their targeted and routine use in clinics is limited. Differentiation of human MSCs (hMSCs) is a complex process influenced by various elements such as growth factors, pharmaceutical compounds, microRNAs, 3D scaffolds, and mechanical and electrical stimulation. Research has shown that different culture conditions can affect the differentiation potential of hMSCs obtained from multiple fetal and adult sources. Additionally, it seems that what affects the differentiation capacities of these cells is their secretory characteristics, which are influenced by the origin of the cells and the local microenvironment where the cells are located. The review can provide insights into the microenvironment-based mechanisms involved in MSC differentiation, which can be valuable for future therapeutic applications.

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引用次数: 0

KPNA2/KPNB1 promotes the malignant progression of gastric cancer induced by M2 macrophage polarization

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-12-31 DOI: 10.1016/j.tice.2024.102714

Juan Bai , Ping Chen , Qingxia Zhou , Xiaojun Tie , Xiao Xia , Yan Wang , Ling Jin

Macrophages in the tumor microenvironment (TME) regulated gastric cancer progression, but the mechanism of macrophage polarization in gastric cancer progression remained unclear. This study mainly explored the molecular mechanism of macrophage polarization in the tumor microenvironment and its impact on the progression of gastric cancer. KPNA2 and KPNB1 expressions in cancer tissues and adjacent non-cancerous tissues were quantified via RT-qPCR and western blot. A correlation analysis was conducted between KPNA2 and KPNB1 expressions, utilizing the GEPIA2 database to link them with macrophage polarization. KPNA2-KPNB1 interaction was investigated on STRING, verified by Co-IP and IF assays. Raw246.7 cells were transfected with KPNA2 overexpression with or without si-KPNB1 plasmids. Then, M1/M2 macrophage markers and the proportion of M2 macrophages were measured by RT-qPCR, western blot, and IF. Co-culturing transfected Raw246.7 with MFC cells showed gastric cancer cell proliferation, apoptosis, migration, and invasion via CCK-8, flow cytometry, and transwell assays. KPNA2 and KPNB1 in gastric cancer tissues were elevated, exhibiting a positive correlation between them. KPNA2 overexpression facilitated the differentiation of macrophages into M2 type. KPNA2 overexpression in macrophages co-cultured with MFC cells stimulated MFC cells proliferation, repressed apoptosis, and enhanced migration/invasion. The interaction between KPNA2 and KPNB1 was confirmed through Co-IP and IF assays. Si-KPNB1 reversed the effects of KPNA2 overexpression on macrophages and gastric cancer cells. KPNA2 promoted the M2 polarization of macrophages by upregulating KPNB1, thereby inducing the proliferation and metastasis of gastric cancer.

{"title":"KPNA2/KPNB1 promotes the malignant progression of gastric cancer induced by M2 macrophage polarization","authors":"Juan Bai , Ping Chen , Qingxia Zhou , Xiaojun Tie , Xiao Xia , Yan Wang , Ling Jin","doi":"10.1016/j.tice.2024.102714","DOIUrl":"10.1016/j.tice.2024.102714","url":null,"abstract":"<div><div>Macrophages in the tumor microenvironment (TME) regulated gastric cancer progression, but the mechanism of macrophage polarization in gastric cancer progression remained unclear. This study mainly explored the molecular mechanism of macrophage polarization in the tumor microenvironment and its impact on the progression of gastric cancer. KPNA2 and KPNB1 expressions in cancer tissues and adjacent non-cancerous tissues were quantified via RT-qPCR and western blot. A correlation analysis was conducted between KPNA2 and KPNB1 expressions, utilizing the GEPIA2 database to link them with macrophage polarization. KPNA2-KPNB1 interaction was investigated on STRING, verified by Co-IP and IF assays. Raw246.7 cells were transfected with KPNA2 overexpression with or without si-KPNB1 plasmids. Then, M1/M2 macrophage markers and the proportion of M2 macrophages were measured by RT-qPCR, western blot, and IF. Co-culturing transfected Raw246.7 with MFC cells showed gastric cancer cell proliferation, apoptosis, migration, and invasion via CCK-8, flow cytometry, and transwell assays. KPNA2 and KPNB1 in gastric cancer tissues were elevated, exhibiting a positive correlation between them. KPNA2 overexpression facilitated the differentiation of macrophages into M2 type. KPNA2 overexpression in macrophages co-cultured with MFC cells stimulated MFC cells proliferation, repressed apoptosis, and enhanced migration/invasion. The interaction between KPNA2 and KPNB1 was confirmed through Co-IP and IF assays. Si-KPNB1 reversed the effects of KPNA2 overexpression on macrophages and gastric cancer cells. KPNA2 promoted the M2 polarization of macrophages by upregulating KPNB1, thereby inducing the proliferation and metastasis of gastric cancer.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102714"},"PeriodicalIF":2.7,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143137339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

IGF2BPs-regulated TIN2 confers the malignant biological behaviors of gastric cancer cells

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-12-31 DOI: 10.1016/j.tice.2024.102716

Fang Li, Yadong Zhou, Zhiming Liao, Da Huang, Ziqing Zhang, Guoqun Chen

Background

Telomere maintenance is an important feature of tumor cells. Telomeric-repeat binding factor 1 interaction nuclear protein 2 (TIN2), a key member of the shelterin proteins, functions in regulating telomere structure, length and function. Our work sought to investigate the role of TIN2 in controlling gastric cancer (GC) malignant biological behaviors.

Methods

The mRNA and protein expressions were examined by qRT-PCR, western blot and immunofluorescence assays. The relative telomerase activity and telomere length were detected using the corresponding kit and qRT-PCR, respectively. The proliferation, migration and invasion abilities were detected by CCK8 and transwell assays, respectively. Cellular oxidative stress level and Fe^2 + content were assessed by DCFH-DA staining and ELISA assays, respectively. The interaction between IGF2BP1/2/3 and TIN2 was analyzed by RIP and RNA pull down assays.

Results

TIN2 expression was significantly increased in GC cells compared with it in gastric mucosal epithelial cells. TIN2 knockdown could impair telomerase function and induce DNA injury in GC cells. Moreover, silencing of TIN2 greatly repressed cell proliferation, metastasis, and autophagy in GC cells. Likewise, the antioxidant capacity and Fe²⁺ content were enhanced after TIN2 depletion, leading to the activation of cellular ferroptosis. In terms of mechanism, TIN2 mRNA could be recognized by IGF2BP1/2/3, and its mRNA expression and stability were decreased upon IGF2BP1/2/3 was knocked down.

Conclusion

Knockdown of TIN2 could restrained telomerase function and the malignant abilities of proliferation, metastasis and autophagy but induced ferroptosis of GC cells, which suggested that targeting TIN2 might be a therapeutic strategy for GC

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引用次数: 0

Immunohistochemical identification of ACE-2 (SARS-COV II entry mechanism) in the gastrointestinal tract, kidney and lung of rhesus monkeys (Macaca mulatta) and squirrel monkeys (Saimiri sciureus) 恒河猴（Macaca mulatta）和松鼠猴（Saimiri sciureus）胃肠道、肾脏和肺中ACE-2 （SARS-COV II进入机制）的免疫组化鉴定

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-12-31 DOI: 10.1016/j.tice.2024.102711

Larissa dos Santos Sebould Marinho , Márcia Cristina Ribeiro Andrade , Cláudia Andréa de Araújo Lopes , Kassia Valéria Gomes Coelho da Silva , Kauet de Matos Gama e Souza , Clarice Machado-Santos

SARS-Cov-2 is a corona virus that causes COVID-19 disease, a viral infection responsible for the pandemic decreed by the World Health Organization in March 2020. Angiotensin-converting enzyme 2 (ACE-2) functions as the main receptor for SARS-Cov-2. The study aimed to detect the expression of ACE-2 in the gastrointestinal tract, kidney, and lung in the rhesus monkeys and squirrel monkeys. The sections from 18 rhesus monkey and 17 squirrel monkeys were incubated with rabbit polyclonal antibody to ACE2 (ab65863). In the lung of the rhesus monkeys, the presence of ACE-2 was noted in the bronchial mucosa of the respiratory epithelium. In the kidney, there was irregular in the proximal convoluted tubules. In the pyloric stomach, duodenum and in the large intestine it was observed on the surface of the lining epithelium. In the lung of the squirrel monkeys, this marking was present in both the ciliated cylindrical and goblet cell sof the bronchi. In the kidney light marking was observed along the surfasse of the cubic epithelium of the proximal convoluted tubules and in the renal glomerulus. No markings were observed throughout the stomach and intense staining was observed along the surfasse of the intestinal epithelium of the duodenum, jejunum and ileum, as well as in the intestinal glands. In our study, we can observe not able differences in the distribution of ACE2 between the two species of primates analysed. These differences must be considered in experimental studies on this disease, which continues to be a topic of notable importance for Public Health.

SARS-Cov-2是一种冠状病毒，会导致COVID-19疾病，这是世界卫生组织于2020年3月颁布的导致大流行的病毒感染。血管紧张素转换酶2 （ACE-2）是SARS-Cov-2的主要受体。本研究旨在检测ACE-2在恒河猴和松鼠猴胃肠道、肾脏和肺中的表达。用兔抗ACE2多克隆抗体（ab65863）孵育18只恒河猴和17只松鼠猴。在恒河猴肺中，呼吸上皮支气管黏膜中可见ACE-2的存在。肾脏近曲小管呈不规则。在幽门胃、十二指肠和大肠的粘膜表面可见。在松鼠猴的肺中，这种标记存在于支气管的纤毛圆柱形细胞和杯状细胞中。肾近曲小管立方上皮表面及肾小球可见光斑。整个胃未见标记，十二指肠、空肠、回肠肠上皮表面及肠腺呈强烈染色。在我们的研究中，我们可以观察到ACE2在分析的两种灵长类动物之间的分布没有显著差异。在对这种疾病的实验研究中必须考虑到这些差异，这仍然是对公共卫生具有显著重要性的主题。

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引用次数: 0

Targeting Siglec-15 mediates mitochondrial retrograde regulation of cervical cancer development 靶向siglece -15介导子宫颈癌发展的线粒体逆行调控。

IF 2.7 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2024-12-31 DOI: 10.1016/j.tice.2024.102713

Jing Wang , Zenghui Li , Yifan He , Yongli Chu

Cervical cancer (CCA) is the predominant cause of fatalities from gynecologic malignancies, with metastasis responsible for 80 % of cancer-related mortalities. This study preliminarily examined the involvement of Sialic Acid Binding Ig Like Lectin 15 (Siglec-15) in the development of CCA and its probable mechanisms. We assessed the capacity of Siglec-15 to modulate CCA progression by establishing knockdown and overexpression Siglec-15 cell lines, supplemented with animal models, using both in vivo and in vitro dual investigations. Our findings indicate that Siglec-15 is significantly expressed in CCA cell lines and is intimately associated with the proliferation, migration, and invasion capabilities of CCA cells, as well as mitochondrial ROS homeostasis. The suppression of Siglec-15 expression markedly reduced tumor growth in mice, potentially due to Siglec-15’s role in regulating the Mitogen-Activated Protein Kinase (MAPK) signaling pathway, which mediates the retrograde regulation of mitochondrial ROS homeostasis. Siglec-15 may emerge as a novel therapeutic target and prognostic marker for patients with CCA.

宫颈癌（CCA）是妇科恶性肿瘤死亡的主要原因，其转移占癌症相关死亡率的80% %。本研究初步探讨了唾液酸结合Ig样凝集素15 （Siglec-15）在CCA发生中的作用及其可能的机制。我们通过建立低敲和过表达的siglece -15细胞系，并辅以动物模型，利用体内和体外双重研究，评估了siglece -15调节CCA进展的能力。我们的研究结果表明，siglece -15在CCA细胞系中显著表达，并与CCA细胞的增殖、迁移和侵袭能力以及线粒体ROS稳态密切相关。抑制siglece -15的表达可显著降低小鼠肿瘤生长，可能是由于siglece -15调节丝裂原活化蛋白激酶（MAPK）信号通路，该通路介导线粒体ROS稳态的逆行调节。siglece -15可能成为CCA患者新的治疗靶点和预后标志物。

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引用次数: 0