IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-23 DOI: 10.1002/iub.2927

Jitendra Singh, Umesh Varshney

引用次数: 0

YTHDF3 rs7464 A > G polymorphism increases Chinese neuroblastoma risk: A multiple-center case-control study. YTHDF3 rs7464 A > G 多态性增加中国人患神经母细胞瘤的风险：一项多中心病例对照研究。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-22 DOI: 10.1002/iub.2923

Huiran Lin, Yongping Chen, Liping Chen, Wenli Zhang, Jinhong Zhu, Xinxin Zhang, Zhonghua Yang, Jiao Zhang, Jiwen Cheng, Li Li, Haixia Zhou, Suhong Li, Zhenjian Zhuo, Jing He

{"title":"YTHDF3 rs7464 A > G polymorphism increases Chinese neuroblastoma risk: A multiple-center case-control study.","authors":"Huiran Lin, Yongping Chen, Liping Chen, Wenli Zhang, Jinhong Zhu, Xinxin Zhang, Zhonghua Yang, Jiao Zhang, Jiwen Cheng, Li Li, Haixia Zhou, Suhong Li, Zhenjian Zhuo, Jing He","doi":"10.1002/iub.2923","DOIUrl":"https://doi.org/10.1002/iub.2923","url":null,"abstract":"Neuroblastoma (NB), a rare childhood cancer originating in nerve tissue. YTHDF3, a member of the YTH domain protein family, is involved in RNA m6A modification and cancer progression. Polymorphisms in YTHDF3 may influence its expression and biological function. Herein, this study estimated the association between YTHDF3 polymorphisms (rs2241753, rs2241754, and rs7464) and NB susceptibility in a multicenter study comprising 898 cases and 1734 controls. We genotyped YTHDF3 candidate polymorphisms by the TaqMan assay. Logistic regression analysis was applied to indicate the possible relationships between these polymorphisms and NB susceptibility, using odds ratios (ORs) and 95% confidence intervals (CIs). Logistic regression analysis revealed that the rs2241753 GA versus GG decreased NB risk (Adjusted OR = 0.84, 95% CI = 0.71-0.997, p = .047), while the rs7464 GG versus AA enhanced NB risk (Adjusted OR = 1.62, 95% CI = 1.20-2.18, p = .002). Additionally, rs7464 GG versus AA/AG showed a higher risk (Adjusted OR = 1.66, 95% CI = 1.24-2.22, p = .0006). Combination analysis showed that having 1-3 risk genotypes versus 0 was associated with increased NB risk (Adjusted OR = 1.28, 95%CI = 1.09-1.51, p = .003). The significance of rs7464 and the risk genotypes combination persisted across multiple subgroups, whereas rs2241754 was significant only in mediastinal NB. False-positive report probability (FPRP) confirmed the reliability of results. Notably, the interaction between rs7464 and rs2241754 may increase NB risk dramatically. Our study demonstrated that YTHDF3 rs7464 A > G significantly affected NB susceptibility, warranting validation in larger sample sizes.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

KRT80 in hepatocellular carcinoma plays oncogenic role via epithelial-mesenchymal transition and PI3K/AKT pathway. 肝细胞癌中的 KRT80 通过上皮-间质转化和 PI3K/AKT 通路发挥致癌作用。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-21 DOI: 10.1002/iub.2925

Ruheng Hua, Xiyue Yan, Jun He, Nuwa Wu, Wangjianfei Yu, Pengfei Yu, Lei Qin

引用次数: 0

Depletion of macrophages and osteoclast precursors mitigates iron overload-mediated bone loss. 消耗巨噬细胞和破骨细胞前体可减轻铁超载介导的骨质流失。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-18 DOI: 10.1002/iub.2928

Vanessa Passin, Maria G Ledesma-Colunga, Sandro Altamura, Martina U Muckenthaler, Ulrike Baschant, Lorenz C Hofbauer, Martina Rauner

{"title":"Depletion of macrophages and osteoclast precursors mitigates iron overload-mediated bone loss.","authors":"Vanessa Passin, Maria G Ledesma-Colunga, Sandro Altamura, Martina U Muckenthaler, Ulrike Baschant, Lorenz C Hofbauer, Martina Rauner","doi":"10.1002/iub.2928","DOIUrl":"https://doi.org/10.1002/iub.2928","url":null,"abstract":"Iron is an essential element for physiological cellular processes, but is toxic in excess. Iron overload diseases are commonly associated with low bone mass. Increased bone resorption by osteoclasts as well as decreased bone formation by osteoblasts have been implicated in bone loss under iron overload conditions. However, the exact contribution of individual cell types has not yet been formally tested. In this study, we aimed to investigate the role of osteoclast precursors in iron overload-induced bone loss. To that end, we used clodronate liposomes to deplete phagocytic cells (including macrophages and osteoclast precursors) in male C57BL/6J mice that were exposed to ferric derisomaltose. Bone microarchitecture and bone turnover were assessed after 4 weeks. The application of clodronate resulted in the efficient depletion of circulating myeloid-lineage cells by about 70%. Depletion of osteoclast precursors mitigated iron overload-induced trabecular bone loss at the lumbar vertebrae and distal femur. While clodronate treatment led to a profound inhibition of bone turnover in control mice, it significantly reduced osteoclast numbers in iron-treated mice without further impacting the bone formation rate or serum PINP levels. Our observations suggest that even though bone formation is markedly suppressed by iron overload, osteoclasts also play a key role in iron overload-induced bone loss and highlight them as potential therapeutic targets.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

KGF secreted from HSCs activates PAK4/BMI1, promotes HCC stemness through PI3K/AKT pathway. 造血干细胞分泌的KGF可激活PAK4/BMI1，并通过PI3K/AKT途径促进HCC干细胞的形成。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-15 DOI: 10.1002/iub.2929

Qinghua Li, Qiuyang Chen, Wenchao Wang, Rongrong Xie, Zhen Li, Dawei Chen

{"title":"KGF secreted from HSCs activates PAK4/BMI1, promotes HCC stemness through PI3K/AKT pathway.","authors":"Qinghua Li, Qiuyang Chen, Wenchao Wang, Rongrong Xie, Zhen Li, Dawei Chen","doi":"10.1002/iub.2929","DOIUrl":"10.1002/iub.2929","url":null,"abstract":"In our present study, we investigated the interaction between HSCs and HCC, also explored the molecular mechanism. Clinical samples were collected from HCC and adjacent tissue with different degree of liver fibrosis. HCC cells were co-cultured with LX-2 cell by Transwell system or cultured with conditioned medium (CM), which was collected from LX-2. The tumor spheroid growth and colony formation analyses were performed to evaluate the cell stemness. Flow cytometry analysis was conducted on cell apoptosis after 5-Fu treatment. Co-immunoprecipitation assay confirmed the interaction between BMI1 and PAK4. Our results showed that BMI1 was highly expressed in HCC and was correlated with HCC liver fibrosis. Both co-cultured with LX-2 and cultured with CM promoted HCC stemness, also increased KGF level and BMI1 expression. KGF treatment had a similar effect with co-culture with LX-2 on HCC. BMI1 overexpression promoted HCC stemness and activated PI3K/AKT pathway, which was reversed by PI3K inhibition. PAK4 was activated by KGF, then phosphorylated S315 site and promoted protein stability of BMI1, therefore enhanced HCC stemness. BMI1 also had a promote effect on liver fibrosis. In summary, we found that KGF secreted by HSCs activated PAK4, which phosphorylated S315 and promoted protein stability of BMI1, and further promoted liver fibrosis and HCC stemness through the PI3K/AKT signaling pathway. Our present study deeply studied the interaction and mechanism between HSCs and HCC, which might provide a new insight for HCC therapy.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

RETRACTION: Nutritional Flavonoids Modulate Estrogen Receptor α Signaling. 回归：营养类黄酮调节雌激素受体 α 信号传导

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-07 DOI: 10.1002/iub.2926

引用次数: 0

Aminoacyl-tRNA synthetase defects in neurological diseases. 神经系统疾病中的氨基酰-tRNA 合成酶缺陷。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-02 DOI: 10.1002/iub.2924

Hong Zhang, Jiqiang Ling

引用次数: 0

Correction to “Astrakurkurone, a Sesquiterpenoid From Wild Edible Mushroom, Targets Liver Cancer Cells by Modulating Bcl-2 Family Proteins” 对 "野生食用菌中的一种倍半萜类化合物 Astrakurkurone 通过调节 Bcl-2 家族蛋白靶向肝癌细胞 "的更正。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-10-29 DOI: 10.1002/iub.2921

引用次数: 0

Coexisting bacterial aminoacyl-tRNA synthetase paralogs exhibit distinct phylogenetic backgrounds and functional compatibility with Escherichia coli 与大肠杆菌共存的细菌氨基酰-tRNA 合成酶同系物表现出不同的系统发育背景和功能兼容性。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-10-17 DOI: 10.1002/iub.2920

Alexander A. Radecki, Ariana Fantasia-Davis, Juan S. Maldonado, Joshua W. Mann, Stephanie Sepulveda-Camacho, Pearl Morosky, Jordan Douglas, Oscar Vargas-Rodriguez

{"title":"Coexisting bacterial aminoacyl-tRNA synthetase paralogs exhibit distinct phylogenetic backgrounds and functional compatibility with Escherichia coli","authors":"Alexander A. Radecki, Ariana Fantasia-Davis, Juan S. Maldonado, Joshua W. Mann, Stephanie Sepulveda-Camacho, Pearl Morosky, Jordan Douglas, Oscar Vargas-Rodriguez","doi":"10.1002/iub.2920","DOIUrl":"10.1002/iub.2920","url":null,"abstract":"Aminoacyl-tRNA synthetases (aaRSs) are universally essential enzymes that synthesize aminoacyl-tRNA substrates for protein synthesis. Although most organisms require a single aaRS gene for each proteinogenic amino acid to translate their genetic information, numerous species encode multiple gene copies of an aaRS. Growing evidence indicates that organisms acquire extra aaRS genes to sustain or adapt to their unique lifestyle. However, predicting and defining the function of repeated aaRS genes remains challenging due to their potentially unique physiological role in the host organism and the inconsistent annotation of repeated aaRS genes in the literature. Here, we carried out comparative, phylogenetic, and functional studies to determine the activity of coexisting paralogs of tryptophanyl-, tyrosyl-, seryl-, and prolyl-tRNA synthetases encoded in several human pathogenic bacteria. Our analyses revealed that, with a few exceptions, repeated aaRSs involve paralogous genes with distinct phylogenetic backgrounds. Using a collection of Escherichia coli strains that enabled the facile characterization of aaRS activity in vivo, we found that, in almost all cases, one aaRS displayed transfer RNA (tRNA) aminoacylation activity, whereas the other was not compatible with E. coli. Together, this work illustrates the challenges of identifying, classifying, and predicting the function of aaRS paralogs and highlights the complexity of aaRS evolution. Moreover, these results provide new insights into the potential role of aaRS paralogs in the biology of several human pathogens and foundational knowledge for the investigation of the physiological role of repeated aaRS paralogs across bacteria.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"76 12","pages":"1139-1153"},"PeriodicalIF":3.7,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142465891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Genetic variations in NER pathway gene polymorphisms and Wilms tumor risk: A six-center case–control study in East China NER通路基因多态性的遗传变异与Wilms肿瘤风险：华东地区六中心病例对照研究。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-10-16 DOI: 10.1002/iub.2919

Xueli Zhan, Haixia Zhou, Changmi Deng, Rui-Xi Hua, Lingling Pan, Shouhua Zhang, Hongting Lu, Shaohua He, Yizhen Wang, Jichen Ruan, Chunlei Zhou, Jing He

{"title":"Genetic variations in NER pathway gene polymorphisms and Wilms tumor risk: A six-center case–control study in East China","authors":"Xueli Zhan, Haixia Zhou, Changmi Deng, Rui-Xi Hua, Lingling Pan, Shouhua Zhang, Hongting Lu, Shaohua He, Yizhen Wang, Jichen Ruan, Chunlei Zhou, Jing He","doi":"10.1002/iub.2919","DOIUrl":"10.1002/iub.2919","url":null,"abstract":"The nucleotide excision repair (NER) system is one of the main ways to protect organisms from DNA damage caused by endogenous and exogenous carcinogens. NER deficiency increases genome mutations, chromosomal aberrations, and cancer viability. However, the genetic association between Wilms tumor and NER pathway gene polymorphisms needs to be further validated. We assessed the associations between 19 NER gene polymorphisms and Wilms tumor susceptibility in 416 cases and 936 controls from East China via the TaqMan method. We found that xeroderma pigmentosum group D (XPD) rs238406 and rs13181 significantly decreased the risk of Wilms tumor [adjusted odds ratio (OR) = 0.59, 95% confidence interval (CI) = 0.46–0.75, p <.0001; adjusted OR = 0.63, 95% CI = 0.44–0.89, p = .009, respectively]. Furthermore, the rs751402 and rs2296147 polymorphisms in the xeroderma pigmentosum group G (XPG) gene were significantly correlated with an increased risk for Wilms tumor (adjusted OR = 1.47, 95% CI = 1.03–2.09, p = .034; adjusted OR = 2.14, 95% CI = 1.29–3.56, p = .003, respectively). Expression quantitative trait loci (eQTL) analysis revealed that these four polymorphisms may affect the expression of genes that are adjacent to XPD and XPG. Our study provides evidence that XPD and XPG gene polymorphisms are associated with Wilms tumor risk. Nonetheless, these findings should be confirmed in a larger sample size.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"76 12","pages":"1392-1402"},"PeriodicalIF":3.7,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142465892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

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