首页 > 最新文献

Growth factors最新文献

英文 中文
L-Glutamine mitigates bile acid-induced inhibition of growth factor activity in rat hepatocyte cultures. L-谷氨酰胺可减轻胆汁酸对大鼠肝细胞生长因子活性的抑制。
IF 1.8 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-08-01 Epub Date: 2024-09-25 DOI: 10.1080/08977194.2024.2407566
Wafa'a Alqabandi, Gursev S Dhaunsi

Bile acid-induced hepatotoxicity is inevitable in Cholestasis pathogenesis and L-Glutamine (L-Gln) has been reported to prevent total parenteral nutrition (TPN)-induced cholestasis in premature neonates. While mechanisms remain unknown, we hypothesize that bile acids impair growth factor (GF) function in hepatocytes which L-glutamine prevents through NAPDH oxidase (NOX) modulation. Glycochenodeoxycholic acid (GCDC, 0-100 µM) when added to primary hepatocyte cultures significantly (p < 0.01) decreased the FBS-induced BrdU incorporation, however inhibition of Fibroblast Growth factor (FGF)- or Hepatocyte growth factor (HGF)-induced DNA synthesis was more pronounced (p < 0.001). L-Gln markedly attenuated GCDC-mediated inhibition of DNA synthesis in both FBS and GF-treated cells. GCDC significantly increased the NADPH oxidase activity and NOX-1 protein expression that were markedly reduced by L-Gln and protein kinase c (PKC) inhibitor, LY-333531. Apocynin (APCN) and diphenyliodonium (DPI) significantly blocked the GCDC-mediated inhibition of GF-induced DNA synthesis. This study demonstrates that bile acid-induced hepatotoxicity involves dysfunction of certain growth factors via protein kinase c (PKC)- mediated NOX modulation which can be corrected, at least partly, by L-glutamine.

胆汁酸诱导的肝毒性在胆汁淤积症的发病机制中不可避免,有报道称左旋谷氨酰胺(L-Gln)可预防早产新生儿全肠外营养(TPN)诱导的胆汁淤积症。虽然其机制尚不清楚,但我们推测胆汁酸会损害肝细胞中生长因子(GF)的功能,而 L-谷氨酰胺可通过 NAPDH 氧化酶(NOX)的调节来防止这种损害。将甘氨胆酸(Glycochenodeoxycholic acid,GCDC,0-100 µM)加入原代肝细胞培养物中可显著(p
{"title":"L-Glutamine mitigates bile acid-induced inhibition of growth factor activity in rat hepatocyte cultures.","authors":"Wafa'a Alqabandi, Gursev S Dhaunsi","doi":"10.1080/08977194.2024.2407566","DOIUrl":"10.1080/08977194.2024.2407566","url":null,"abstract":"<p><p>Bile acid-induced hepatotoxicity is inevitable in Cholestasis pathogenesis and L-Glutamine (L-Gln) has been reported to prevent total parenteral nutrition (TPN)-induced cholestasis in premature neonates. While mechanisms remain unknown, we hypothesize that bile acids impair growth factor (GF) function in hepatocytes which L-glutamine prevents through NAPDH oxidase (NOX) modulation. Glycochenodeoxycholic acid (GCDC, 0-100 µM) when added to primary hepatocyte cultures significantly (p < 0.01) decreased the FBS-induced BrdU incorporation, however inhibition of Fibroblast Growth factor (FGF)- or Hepatocyte growth factor (HGF)-induced DNA synthesis was more pronounced (p < 0.001). L-Gln markedly attenuated GCDC-mediated inhibition of DNA synthesis in both FBS and GF-treated cells. GCDC significantly increased the NADPH oxidase activity and NOX-1 protein expression that were markedly reduced by L-Gln and protein kinase c (PKC) inhibitor, LY-333531. Apocynin (APCN) and diphenyliodonium (DPI) significantly blocked the GCDC-mediated inhibition of GF-induced DNA synthesis. This study demonstrates that bile acid-induced hepatotoxicity involves dysfunction of certain growth factors via protein kinase c (PKC)- mediated NOX modulation which can be corrected, at least partly, by L-glutamine.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"120-127"},"PeriodicalIF":1.8,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345146","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
Tibial transverse transport combined with platelet-rich plasma sustained-release microspheres activates the VEGFA/VEGFR2 pathway to promote microcirculatory reconstruction in diabetic foot ulcer. 胫骨横向运输结合富血小板血浆缓释微球可激活 VEGFA/VEGFR2 通路,促进糖尿病足溃疡的微循环重建。
IF 1.8 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-08-01 Epub Date: 2024-09-27 DOI: 10.1080/08977194.2024.2407318
Weiqiang Wei, Tenglong Jiang, Fan Hu, Hong Liu

This study proposes to investigate the therapeutic efficacy and mechanism of combining tibial transverse transport (TTT) with platelet-rich plasma (PRP) for diabetic foot ulcer (DFU). The diabetic rabbit model was constructed with Streptozotocin, which was intervened with TTT and PRP. PRP injection combined with TTT significantly promoted vascularisation and enhanced CD31, VEGFA, and VEGFR2 expressions compared to traditional TTT. However, the VEGFR2 inhibitor suppressed these phenomena. In the in vitro injury model, PRP reversed the diminished human umbilical vein endothelial cells (HUVECs) function and vascularisation caused by high-glucose damage. Additionally, PRP reduced inflammation and oxidative stress (approximately 47% ROS level) and enhanced VEGFA and VEGFR2 expression in HUVECs. However, the knockdown of VEGFR2 reversed the effect of PRP. In conclusion, TTT combined with intraosseous flap injection of PRP sustained-release microspheres activated the VEGFA/VEGFR2 pathway to promote microcirculatory reconstruction in DFU. These findings may provide new potential therapeutic strategies for DFU.

本研究旨在探讨胫骨横向运输(TTT)与富血小板血浆(PRP)联合治疗糖尿病足溃疡(DFU)的疗效和机制。用链脲佐菌素构建糖尿病兔模型,并用 TTT 和 PRP 进行干预。与传统的 TTT 相比,PRP 注射结合 TTT 能明显促进血管生成,并增强 CD31、VEGFA 和 VEGFR2 的表达。然而,VEGFR2 抑制剂抑制了这些现象。在体外损伤模型中,PRP 逆转了高葡萄糖损伤导致的人脐静脉内皮细胞(HUVECs)功能减退和血管扩张。此外,PRP 还降低了炎症和氧化应激(ROS 水平约为 47%),并增强了 HUVECs 中 VEGFA 和 VEGFR2 的表达。然而,VEGFR2 的敲除逆转了 PRP 的效果。总之,TTT结合PRP缓释微球的鞘内皮瓣注射激活了VEGFA/VEGFR2通路,促进了DFU的微循环重建。这些发现可能会为 DFU 提供新的潜在治疗策略。
{"title":"Tibial transverse transport combined with platelet-rich plasma sustained-release microspheres activates the VEGFA/VEGFR2 pathway to promote microcirculatory reconstruction in diabetic foot ulcer.","authors":"Weiqiang Wei, Tenglong Jiang, Fan Hu, Hong Liu","doi":"10.1080/08977194.2024.2407318","DOIUrl":"10.1080/08977194.2024.2407318","url":null,"abstract":"<p><p>This study proposes to investigate the therapeutic efficacy and mechanism of combining tibial transverse transport (TTT) with platelet-rich plasma (PRP) for diabetic foot ulcer (DFU). The diabetic rabbit model was constructed with Streptozotocin, which was intervened with TTT and PRP. PRP injection combined with TTT significantly promoted vascularisation and enhanced CD31, VEGFA, and VEGFR2 expressions compared to traditional TTT. However, the VEGFR2 inhibitor suppressed these phenomena. In the <i>in vitro</i> injury model, PRP reversed the diminished human umbilical vein endothelial cells (HUVECs) function and vascularisation caused by high-glucose damage. Additionally, PRP reduced inflammation and oxidative stress (approximately 47% ROS level) and enhanced VEGFA and VEGFR2 expression in HUVECs. However, the knockdown of VEGFR2 reversed the effect of PRP. In conclusion, TTT combined with intraosseous flap injection of PRP sustained-release microspheres activated the VEGFA/VEGFR2 pathway to promote microcirculatory reconstruction in DFU. These findings may provide new potential therapeutic strategies for DFU.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"128-144"},"PeriodicalIF":1.8,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345147","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
VEGF-B is involved in diabetic peripheral neuropathy in patients with type 2 diabetes. VEGF-B 与 2 型糖尿病患者的糖尿病周围神经病变有关。
IF 1.8 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-08-01 Epub Date: 2024-07-12 DOI: 10.1080/08977194.2024.2377553
Ruonan Zhou, Yingying Xue, Ziwei Zhu, Pingyuan Xu, Lixuan Shen, Ziwei Wang, Yingying Xiang, Yue Cao, Xizhong Yu, Wenbin Shang

Aims: This study aims to explore the potential role of vascular endothelial growth factor-B (VEGF-B) in the pathogenesis of diabetic peripheral neuropathy (DPN). The expression of VEGFRs were reanalysed by using gene arrays of peripheral nerve samples from mouse models of DPN retrieved from the GEO database. 213 T2D patients as well as 31 healthy individuals were recruited. The serum VEGF-B was detected and its relationship with DPN was analysed. The elevated VEGFR1 was the only change of VEGFR gene expression in the peripheral nerve from mouse models of DPN. The level of serum VEGF-B in T2D patients with DPN was higher than that in T2D patients without DPN and healthy people. Analysis of correlation and binary logistic regression confirmed that the increased serum VEGF-B level was an independent risk factor of DPN in T2D patients. VEGF-B-VEGFR1 signaling pathway may be involved in the development of DPN.

目的:本研究旨在探讨血管内皮生长因子-B(VEGF-B)在糖尿病周围神经病变(DPN)发病机制中的潜在作用。研究人员利用从 GEO 数据库中检索到的 DPN 小鼠模型周围神经样本的基因芯片,重新分析了血管内皮生长因子-B 的表达。研究人员招募了 213 名 T2D 患者和 31 名健康人。检测了血清 VEGF-B,并分析了其与 DPN 的关系。VEGFR1 的升高是 DPN 小鼠模型周围神经中 VEGFR 基因表达的唯一变化。患有 DPN 的 T2D 患者血清 VEGF-B 水平高于无 DPN 的 T2D 患者和健康人。相关性和二元逻辑回归分析证实,血清 VEGF-B 水平升高是 T2D 患者发生 DPN 的独立危险因素。VEGF-B-VEGFR1信号通路可能参与了DPN的发病。
{"title":"VEGF-B is involved in diabetic peripheral neuropathy in patients with type 2 diabetes.","authors":"Ruonan Zhou, Yingying Xue, Ziwei Zhu, Pingyuan Xu, Lixuan Shen, Ziwei Wang, Yingying Xiang, Yue Cao, Xizhong Yu, Wenbin Shang","doi":"10.1080/08977194.2024.2377553","DOIUrl":"10.1080/08977194.2024.2377553","url":null,"abstract":"<p><p><b>Aims:</b> This study aims to explore the potential role of vascular endothelial growth factor-B (VEGF-B) in the pathogenesis of diabetic peripheral neuropathy (DPN). The expression of VEGFRs were reanalysed by using gene arrays of peripheral nerve samples from mouse models of DPN retrieved from the GEO database. 213 T2D patients as well as 31 healthy individuals were recruited. The serum VEGF-B was detected and its relationship with DPN was analysed. The elevated VEGFR1 was the only change of VEGFR gene expression in the peripheral nerve from mouse models of DPN. The level of serum VEGF-B in T2D patients with DPN was higher than that in T2D patients without DPN and healthy people. Analysis of correlation and binary logistic regression confirmed that the increased serum VEGF-B level was an independent risk factor of DPN in T2D patients. VEGF-B-VEGFR1 signaling pathway may be involved in the development of DPN.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"101-110"},"PeriodicalIF":1.8,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141599106","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
Statement of Retraction: Elevated Neurotrophin and Neurotrophin Receptor Expression in Spontaneously Hypertensive Rat Lungs. 撤回声明:自发性高血压大鼠肺中神经营养素和神经营养素受体表达的升高。
IF 1.8 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-08-01 Epub Date: 2024-08-16 DOI: 10.1080/08977194.2024.2392373
{"title":"Statement of Retraction: Elevated Neurotrophin and Neurotrophin Receptor Expression in Spontaneously Hypertensive Rat Lungs.","authors":"","doi":"10.1080/08977194.2024.2392373","DOIUrl":"10.1080/08977194.2024.2392373","url":null,"abstract":"","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"146"},"PeriodicalIF":1.8,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987825","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
Expression of Concern. 表达关切。
IF 1.8 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-08-01 Epub Date: 2024-08-28 DOI: 10.1080/08977194.2024.2392344
{"title":"Expression of Concern.","authors":"","doi":"10.1080/08977194.2024.2392344","DOIUrl":"10.1080/08977194.2024.2392344","url":null,"abstract":"","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"145"},"PeriodicalIF":1.8,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080124","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
Comparative effects of 8-week combined resistance exercise training and alternate-day calorie restriction on soluble epidermal growth factor receptor (sEGFR) and adipsin in obese men. 为期 8 周的联合阻力运动训练和隔日热量限制对肥胖男性可溶性表皮生长因子受体(sEGFR)和腺苷的比较效应。
IF 1.8 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-08-01 Epub Date: 2024-07-15 DOI: 10.1080/08977194.2024.2378889
Yousif Hikmat, Alireza Safarzade, Hamid Alizadeh

This study investigated the combined effects of resistance exercise training (RET) and alternate-day calorie restriction (ADCR) on body composition, insulin resistance (IR), insulin resistance-related biomarkers (adipokine adipsin and hepatokine soluble EFGR), and weight loss in obese men. The findings revealed that RET + ADCR induced the greatest reductions in body weight, body fat percentage, and waist-to-hip ratio (WHR) compared to RET and ADCR alone (p < 0.05). Additionally, RET + ADCR resulted in the most significant improvements in IR, as measured by HOMA-IR, and in circulating levels of adipsin and soluble EFGR (p < 0.05). These findings suggest that combining RET and ADCR may be a more effective strategy for improving metabolic health, including body composition, IR, and metabolic tissues' functions, in obese men than either intervention alone.

本研究调查了阻力运动训练(RET)和隔日卡路里限制(ADCR)对肥胖男性的身体组成、胰岛素抵抗(IR)、胰岛素抵抗相关生物标志物(脂肪因子 adipsin 和肝因子可溶性 EFGR)和体重减轻的综合影响。研究结果表明,与单独使用 RET 和 ADCR 相比,RET + ADCR 能最大程度地降低体重、体脂百分比和腰臀比(WHR)(p p p
{"title":"Comparative effects of 8-week combined resistance exercise training and alternate-day calorie restriction on soluble epidermal growth factor receptor (sEGFR) and adipsin in obese men.","authors":"Yousif Hikmat, Alireza Safarzade, Hamid Alizadeh","doi":"10.1080/08977194.2024.2378889","DOIUrl":"10.1080/08977194.2024.2378889","url":null,"abstract":"<p><p>This study investigated the combined effects of resistance exercise training (RET) and alternate-day calorie restriction (ADCR) on body composition, insulin resistance (IR), insulin resistance-related biomarkers (adipokine adipsin and hepatokine soluble EFGR), and weight loss in obese men. The findings revealed that RET + ADCR induced the greatest reductions in body weight, body fat percentage, and waist-to-hip ratio (WHR) compared to RET and ADCR alone (<i>p</i> < 0.05). Additionally, RET + ADCR resulted in the most significant improvements in IR, as measured by HOMA-IR, and in circulating levels of adipsin and soluble EFGR (<i>p</i> < 0.05). These findings suggest that combining RET and ADCR may be a more effective strategy for improving metabolic health, including body composition, IR, and metabolic tissues' functions, in obese men than either intervention alone.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"111-119"},"PeriodicalIF":1.8,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141616278","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
Interleukin-3 production by basal-like breast cancer cells is associated with poor prognosis. 基底样乳腺癌细胞产生的白细胞介素-3与预后不良有关。
IF 1.8 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-05-01 Epub Date: 2024-02-01 DOI: 10.1080/08977194.2023.2297693
Emma J Thompson, Samantha Escarbe, Denis Tvorogov, Gelareh Farshid, Philip A Gregory, Yeesim Khew-Goodall, Stephen Madden, Wendy V Ingman, Geoffrey J Lindeman, Elgene Lim, Angel F Lopez, Claudine S Bonder

Breast cancer represents a collection of pathologies with different molecular subtypes, histopathology, risk factors, clinical behavior, and responses to treatment. "Basal-like" breast cancers predominantly lack the receptors for estrogen and progesterone (ER/PR), lack amplification of human epidermal growth factor receptor 2 (HER2) but account for 10-15% of all breast cancers, are largely insensitive to targeted treatment and represent a disproportionate number of metastatic cases and deaths. Analysis of interleukin (IL)-3 and the IL-3 receptor subunits (IL-3RA + CSF2RB) reveals elevated expression in predominantly the basal-like group. Further analysis suggests that IL-3 itself, but not the IL-3 receptor subunits, associates with poor patient outcome. Histology on patient-derived xenografts supports the notion that breast cancer cells are a significant source of IL-3 that may promote disease progression. Taken together, these observations suggest that IL-3 may be a useful marker in solid tumors, particularly triple negative breast cancer, and warrants further investigation into its contribution to disease pathogenesis.

乳腺癌是多种病理类型的集合体,它们具有不同的分子亚型、组织病理学、风险因素、临床表现和对治疗的反应。"基底样 "乳腺癌主要缺乏雌激素和孕激素受体(ER/PR),缺乏人类表皮生长因子受体 2(HER2)的扩增,但占所有乳腺癌的 10-15%,对靶向治疗基本不敏感,在转移病例和死亡病例中的比例过高。对白细胞介素(IL)-3和IL-3受体亚基(IL-3RA + CSF2RB)的分析表明,基底样组主要存在表达升高的现象。进一步分析表明,IL-3本身而非IL-3受体亚基与患者的不良预后有关。患者异种移植物的组织学研究证实,乳腺癌细胞是IL-3的重要来源,可能会促进疾病的进展。综上所述,这些观察结果表明,IL-3 可能是实体瘤,尤其是三阴性乳腺癌的有用标记物,值得进一步研究其对疾病发病机制的作用。
{"title":"Interleukin-3 production by basal-like breast cancer cells is associated with poor prognosis.","authors":"Emma J Thompson, Samantha Escarbe, Denis Tvorogov, Gelareh Farshid, Philip A Gregory, Yeesim Khew-Goodall, Stephen Madden, Wendy V Ingman, Geoffrey J Lindeman, Elgene Lim, Angel F Lopez, Claudine S Bonder","doi":"10.1080/08977194.2023.2297693","DOIUrl":"10.1080/08977194.2023.2297693","url":null,"abstract":"<p><p>Breast cancer represents a collection of pathologies with different molecular subtypes, histopathology, risk factors, clinical behavior, and responses to treatment. \"Basal-like\" breast cancers predominantly lack the receptors for estrogen and progesterone (ER/PR), lack amplification of human epidermal growth factor receptor 2 (HER2) but account for 10-15% of all breast cancers, are largely insensitive to targeted treatment and represent a disproportionate number of metastatic cases and deaths. Analysis of interleukin (IL)-3 and the IL-3 receptor subunits (<i>IL-3RA + CSF2RB</i>) reveals elevated expression in predominantly the basal-like group. Further analysis suggests that IL-3 itself, but not the IL-3 receptor subunits, associates with poor patient outcome. Histology on patient-derived xenografts supports the notion that breast cancer cells are a significant source of IL-3 that may promote disease progression. Taken together, these observations suggest that IL-3 may be a useful marker in solid tumors, particularly triple negative breast cancer, and warrants further investigation into its contribution to disease pathogenesis.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"49-61"},"PeriodicalIF":1.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139650657","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
GALNT6, GALNT14, and Gal-3 in association with GDF-15 promotes drug resistance and stemness of breast cancer via β-catenin axis. GALNT6、GALNT14和Gal-3与GDF-15通过β-catenin轴促进乳腺癌的耐药性和干性。
IF 1.8 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-05-01 Epub Date: 2024-06-18 DOI: 10.1080/08977194.2024.2368907
Ashita Gadwal, Purvi Purohit, Manoj Khokhar, Jeewan Ram Vishnoi, Puneet Pareek, Ramkaran Choudhary, Poonam Elhence, Mithu Banerjee, Praveen Sharma

N-acetylgalactosaminyltransferases (GALNTs) are a polypeptide responsible for aberrant glycosylation in breast cancer (BC), but the mechanism is unclear. In this study, expression levels of GALNT6, GALNT14, and Gal-3 were assessed in BC, and their association with GDF-15, β-catenin, stemness (SOX2 and OCT4), and drug resistance marker (ABCC5) was evaluated. Gene expression of GALNT6, GALNT14, Gal-3, GDF-15, OCT4, SOX2, ABCC5, and β-catenin in tumor and adjacent non-tumor tissues (n = 30) was determined. The same was compared with GEO-microarray datasets. A significant increase in the expression of candidate genes was observed in BC tumor compared to adjacent non-tumor tissue; and in pre-therapeutic patients compared to post-therapeutic. GALNT6, GALNT14, Gal-3, and GDF-15 showed positive association with β-catenin, SOX2, OCT4, and ABCC5 and were significantly associated with poor Overall Survival. Our findings were also validated via in silico analysis. Our study suggests that GALNT6, GALNT14, and Gal-3 in association with GDF-15 promote stemness and intrinsic drug resistance in BC, possibly by β-catenin signaling pathway.

N-乙酰半乳糖氨酰转移酶(GALNTs)是导致乳腺癌(BC)糖基化异常的多肽,但其机制尚不清楚。本研究评估了GALNT6、GALNT14和Gal-3在乳腺癌中的表达水平,并评估了它们与GDF-15、β-catenin、干性(SOX2和OCT4)和耐药性标志物(ABCC5)的关联。测定了肿瘤和邻近非肿瘤组织(n = 30)中 GALNT6、GALNT14、Gal-3、GDF-15、OCT4、SOX2、ABCC5 和 β-catenin 的基因表达。结果与 GEO 微阵列数据集进行了比较。与邻近的非肿瘤组织相比,在 BC 肿瘤中观察到候选基因的表达明显增加;与治疗后相比,在治疗前患者中观察到候选基因的表达明显增加。GALNT6、GALNT14、Gal-3和GDF-15与β-catenin、SOX2、OCT4和ABCC5呈正相关,并与总生存期差显著相关。我们的研究结果还通过硅学分析得到了验证。我们的研究表明,GALNT6、GALNT14和Gal-3与GDF-15可能通过β-catenin信号通路促进了BC的干性和内在耐药性。
{"title":"GALNT6, GALNT14, and Gal-3 in association with GDF-15 promotes drug resistance and stemness of breast cancer <i>via</i> β-catenin axis.","authors":"Ashita Gadwal, Purvi Purohit, Manoj Khokhar, Jeewan Ram Vishnoi, Puneet Pareek, Ramkaran Choudhary, Poonam Elhence, Mithu Banerjee, Praveen Sharma","doi":"10.1080/08977194.2024.2368907","DOIUrl":"10.1080/08977194.2024.2368907","url":null,"abstract":"<p><p>N-acetylgalactosaminyltransferases (GALNTs) are a polypeptide responsible for aberrant glycosylation in breast cancer (BC), but the mechanism is unclear. In this study, expression levels of GALNT6, GALNT14, and Gal-3 were assessed in BC, and their association with GDF-15, β-catenin, stemness (SOX2 and OCT4), and drug resistance marker (ABCC5) was evaluated. Gene expression of GALNT6, GALNT14, Gal-3, GDF-15, OCT4, SOX2, ABCC5, and β-catenin in tumor and adjacent non-tumor tissues (<i>n</i> = 30) was determined. The same was compared with GEO-microarray datasets. A significant increase in the expression of candidate genes was observed in BC tumor compared to adjacent non-tumor tissue; and in pre-therapeutic patients compared to post-therapeutic. GALNT6, GALNT14, Gal-3, and GDF-15 showed positive association with β-catenin, SOX2, OCT4, and ABCC5 and were significantly associated with poor Overall Survival. Our findings were also validated <i>via in silico</i> analysis. Our study suggests that GALNT6, GALNT14, and Gal-3 in association with GDF-15 promote stemness and intrinsic drug resistance in BC, possibly by β-catenin signaling pathway.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"84-100"},"PeriodicalIF":1.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141418549","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
PLA2G2D fosters angiogenesis in non-small cell lung cancer through aerobic glycolysis. PLA2G2D通过有氧糖酵解促进非小细胞肺癌的血管生成
IF 1.8 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-05-01 Epub Date: 2024-01-01 DOI: 10.1080/08977194.2023.2297702
Huaizhong Zhang, Keng Chen, Yongqing Zhou, Zhuo Cao, Cunlai Xu, Lin Zhou, Gongzhi Wu, Congxiong Peng, Songqing Lai, Xuhui Wu

Non-small cell lung cancer (NSCLC) stands prominent among the prevailing and formidable oncological entities. The immune and metabolic-related molecule Phospholipase A2, group IID (PLA2G2D) exerts promotional effects on tumor progression. However, its involvement in cancer angiogenesis remains elusive. Therefore, this investigation delved into the functional significance of PLA2G2D concerning angiogenesis in NSCLC. This study analyzed the expression and enriched pathways of PLA2G2D in NSCLC tissues through bioinformatics analysis, and measured the expression of PLA2G2D in NSCLC cells using qRT-PCR and western blot (WB). Subsequently, the viability and angiogenic potential of NSCLC cells were assessed employing CCK-8 and angiogenesis assays, respectively. The expression profile of angiogenic factors was analyzed through WB. Finally, the expression of glycolysis pathway-related genes, extracellular acidification rate and oxygen consumption rate, and the levels of pyruvate, lactate, citrate, and malate were analyzed in NSCLC cells using qRT-PCR, Seahorse XF 96, and related kits. Bioinformatics analysis revealed the upregulation of PLA2G2D in NSCLC tissues and its association with VEGF and glycolysis signaling pathways. Molecular and cellular experiments demonstrated that upregulated PLA2G2D promoted the viability, angiogenic ability, and glycolysis pathway of NSCLC cells. Rescue assays revealed that the effects of high expression of PLA2G2D on the viability, angiogenic ability, and glycolysis of NSCLC cells were weakened after the addition of the glycolysis inhibitor 2-DG. In summary, PLA2G2D plays a key role in NSCLC angiogenesis through aerobic glycolysis, displaying great potential as a target for anti-angiogenesis therapy.

非小细胞肺癌(NSCLC)是最常见、最可怕的肿瘤之一。与免疫和代谢相关的分子磷脂酶 A2 组 IID(PLA2G2D)对肿瘤的进展具有促进作用。然而,它在癌症血管生成中的参与仍然难以捉摸。因此,本研究探讨了 PLA2G2D 在 NSCLC 血管生成中的功能意义。本研究通过生物信息学分析了PLA2G2D在NSCLC组织中的表达和富集途径,并利用qRT-PCR和Western blot(WB)检测了PLA2G2D在NSCLC细胞中的表达。随后,分别采用 CCK-8 和血管生成试验评估了 NSCLC 细胞的活力和血管生成潜能。通过 WB 分析了血管生成因子的表达谱。最后,利用 qRT-PCR、Seahorse XF 96 和相关试剂盒分析了 NSCLC 细胞中糖酵解途径相关基因、细胞外酸化率和耗氧率的表达,以及丙酮酸、乳酸、柠檬酸和苹果酸的水平。生物信息学分析表明,PLA2G2D 在 NSCLC 组织中上调,并与血管内皮生长因子和糖酵解信号通路相关。分子和细胞实验表明,上调的 PLA2G2D 促进了 NSCLC 细胞的活力、血管生成能力和糖酵解途径。挽救实验显示,在加入糖酵解抑制剂 2-DG 后,高表达 PLA2G2D 对 NSCLC 细胞的活力、血管生成能力和糖酵解的影响减弱。综上所述,PLA2G2D通过有氧糖酵解在NSCLC血管生成中发挥着关键作用,有望成为抗血管生成治疗的靶点。
{"title":"PLA2G2D fosters angiogenesis in non-small cell lung cancer through aerobic glycolysis.","authors":"Huaizhong Zhang, Keng Chen, Yongqing Zhou, Zhuo Cao, Cunlai Xu, Lin Zhou, Gongzhi Wu, Congxiong Peng, Songqing Lai, Xuhui Wu","doi":"10.1080/08977194.2023.2297702","DOIUrl":"10.1080/08977194.2023.2297702","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) stands prominent among the prevailing and formidable oncological entities. The immune and metabolic-related molecule Phospholipase A2, group IID (PLA2G2D) exerts promotional effects on tumor progression. However, its involvement in cancer angiogenesis remains elusive. Therefore, this investigation delved into the functional significance of PLA2G2D concerning angiogenesis in NSCLC. This study analyzed the expression and enriched pathways of PLA2G2D in NSCLC tissues through bioinformatics analysis, and measured the expression of PLA2G2D in NSCLC cells using qRT-PCR and western blot (WB). Subsequently, the viability and angiogenic potential of NSCLC cells were assessed employing CCK-8 and angiogenesis assays, respectively. The expression profile of angiogenic factors was analyzed through WB. Finally, the expression of glycolysis pathway-related genes, extracellular acidification rate and oxygen consumption rate, and the levels of pyruvate, lactate, citrate, and malate were analyzed in NSCLC cells using qRT-PCR, Seahorse XF 96, and related kits. Bioinformatics analysis revealed the upregulation of PLA2G2D in NSCLC tissues and its association with VEGF and glycolysis signaling pathways. Molecular and cellular experiments demonstrated that upregulated PLA2G2D promoted the viability, angiogenic ability, and glycolysis pathway of NSCLC cells. Rescue assays revealed that the effects of high expression of PLA2G2D on the viability, angiogenic ability, and glycolysis of NSCLC cells were weakened after the addition of the glycolysis inhibitor 2-DG. In summary, PLA2G2D plays a key role in NSCLC angiogenesis through aerobic glycolysis, displaying great potential as a target for anti-angiogenesis therapy.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"74-83"},"PeriodicalIF":1.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139073795","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
FOXN2, identified as a novel biomarker in serum, modulates the transforming growth factor-beta signaling pathway through its interaction with partitioning defective 6 homolog alpha, contributing to the pathogenesis of gastric cancer 被确定为血清中新型生物标记物的 FOXN2 通过与分割缺陷 6 同源物 alpha 的相互作用调节转化生长因子-β 信号通路,从而促进胃癌的发病机制
IF 1.8 4区 生物学 Q4 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-04 DOI: 10.1080/08977194.2023.2297700
Liang Li, XueFeng Sun, Mei Zhang, BangShuo Zhang, Yi Yang, Sheng Wang
Dysregulated expression of Forkhead Box N2 (FOXN2) has been detected in various cancer types. However, the underlying mechanisms by which FOXN2 contributes to the onset and progression of gastric c...
在多种癌症类型中都发现了叉头盒N2(FOXN2)的表达失调。然而,FOXN2导致胃癌发病和进展的潜在机制是什么?
{"title":"FOXN2, identified as a novel biomarker in serum, modulates the transforming growth factor-beta signaling pathway through its interaction with partitioning defective 6 homolog alpha, contributing to the pathogenesis of gastric cancer","authors":"Liang Li, XueFeng Sun, Mei Zhang, BangShuo Zhang, Yi Yang, Sheng Wang","doi":"10.1080/08977194.2023.2297700","DOIUrl":"https://doi.org/10.1080/08977194.2023.2297700","url":null,"abstract":"Dysregulated expression of Forkhead Box N2 (FOXN2) has been detected in various cancer types. However, the underlying mechanisms by which FOXN2 contributes to the onset and progression of gastric c...","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":"39 1","pages":""},"PeriodicalIF":1.8,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140073436","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
期刊
Growth factors
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1