Biochemistry and Cell Biology最新文献_第8页

Exogenous hydrogen sulfide prevents SOD2 degradation to safeguard renal function in diabetic kidney disease. 外源性硫化氢可防止 SOD2 降解，保护糖尿病肾病患者的肾功能

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2024-06-01 Epub Date: 2024-02-28 DOI: 10.1139/bcb-2023-0295

Qian Yang, Mengyi Wang, Huan Wang, Cheng Ren, Yifu Li

{"title":"Exogenous hydrogen sulfide prevents SOD2 degradation to safeguard renal function in diabetic kidney disease.","authors":"Qian Yang, Mengyi Wang, Huan Wang, Cheng Ren, Yifu Li","doi":"10.1139/bcb-2023-0295","DOIUrl":"10.1139/bcb-2023-0295","url":null,"abstract":"Diabetic kidney disease (DKD) is a major contributor to chronic kidney disease. Hydrogen sulfide (H2S) serves as an endogenous gaseous signaling molecule capable of safeguarding renal function within the context of DKD. However, the underlying mechanisms need to be elucidated. This study was undertaken to unveil the mechanisms by which H2S counteracts against DKD. Utilizing mice and human renal tubular epithelial (HK-2) cells, we demonstrated a reduction in cystathionine-γ-lyase/H2S levels within renal tissues of db/db mice and in HK-2 cells subjected to hyperglycemic and hyperlipidemic environments. Notably, we observed that sodium hydrosulfide (NaHS) supplementation could serve as an exogenous source of H2S. Exogenous H2S exhibited the capacity to mitigate the accumulation of reactive oxygen species and attenuate the degradation of superoxide dismutase 2 (SOD2) by Lon protease homolog 1 induced by hyperglycemia and hyperlipidemia, thus affording cellular protection against mitochondrial apoptosis. Consequently, NaHS treatment led to decreased serum levels of blood urea nitrogen and serum creatinine, reflecting alleviated renal damage and thereby preserving renal function in db/db mice. Based on these findings, we propose that exogenous H2S exerts a protective role against DKD by inhibiting SOD2 degradation.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"252-261"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139989190","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

Decreased NMIIA heavy chain phosphorylation at S1943 promotes mitoxantrone resistance by upregulating BCRP and N-cadherin expression in breast cancer cells. 通过上调乳腺癌细胞中 BCRP 和 N-cadherin 的表达，减少 NMIIA 重链在 S1943 处的磷酸化可促进米托蒽醌的耐药性。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2024-06-01 Epub Date: 2024-01-08 DOI: 10.1139/bcb-2023-0232

Kemin Li, Tian Li, Yanan Niu, Yu Gao, Yifan Shi, Yifan He, Xuanping Zhang, Yan Wang, Jing Cao, Xiaoling Hu, Min Chen, Ruizan Shi

{"title":"Decreased NMIIA heavy chain phosphorylation at S1943 promotes mitoxantrone resistance by upregulating BCRP and N-cadherin expression in breast cancer cells.","authors":"Kemin Li, Tian Li, Yanan Niu, Yu Gao, Yifan Shi, Yifan He, Xuanping Zhang, Yan Wang, Jing Cao, Xiaoling Hu, Min Chen, Ruizan Shi","doi":"10.1139/bcb-2023-0232","DOIUrl":"10.1139/bcb-2023-0232","url":null,"abstract":"Mitoxantrone (MX) is an effective treatment for breast cancer; however, high efflux of MX that is accomplished by breast cancer resistance protein (BCRP) leads to acquired multidrug resistance (MDR), reducing MX's therapeutic efficacy in breast cancer. Non-muscle myosin IIA (NMIIA) and its heavy phosphorylation at S1943 have been revealed to play key roles in tumor metastasis and progression, including in breast cancer; however, their molecular function in BCRP-mediated MDR in breast cancer remains unknown. In this study, we revealed that the expression of NMIIA heavy chain phosphorylation at S1943 was downregulated in BCRP-overexpressing breast cancer MCF-7/MX cells, and stable expression of NMIIA-S1943A mutant increased BCRP expression and promoted the resistance of MCF-7/MX cells to MX. Meanwhile, NMIIA S1943 phosphorylation induced by epidermal growth factor (EGF) was accompanied by the downregulation of BCRP in MCF-7/MX cells. Furthermore, stable expression of NMIIA-S1943A in MCF-7/MX cells resulted in upregulation of N-cadherin and the accumulation of β-catenin on the cell surface, which inhibited the nucleus translocation of β-catenin and Wnt/β-catenin-based proliferative signaling. EGF stimulation of MCF-7/MX cells showed the downregulation of N-cadherin and β-catenin. Our results suggest that decreased NMIIA heavy phosphorylation at S1943 increases BCRP expression and promotes MX resistance in breast cancer cells via upregulating N-cadherin expression.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"213-225"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139401629","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

Histone H4 asymmetrically dimethylated at arginine 3 (H4R3me2a), a mark of super-enhancers. 组蛋白H4在精氨酸3 (H4R3me2a)处不对称二甲基化，这是超级增强子的标志。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2024-04-01 Epub Date: 2023-11-27 DOI: 10.1139/bcb-2023-0211

Sadhana R N Sudhakar, Li Wu, Shrinal Patel, Athanasios Zovoilis, James R Davie

{"title":"Histone H4 asymmetrically dimethylated at arginine 3 (H4R3me2a), a mark of super-enhancers.","authors":"Sadhana R N Sudhakar, Li Wu, Shrinal Patel, Athanasios Zovoilis, James R Davie","doi":"10.1139/bcb-2023-0211","DOIUrl":"10.1139/bcb-2023-0211","url":null,"abstract":"Histone H4 asymmetrically dimethylated at arginine 3 (H4R3me2a) is an active histone mark catalyzed by protein arginine methyltransferase 1 (PRMT1), a major arginine methyltransferase in vertebrates catalyzing asymmetric dimethylation of arginine. H4R3me2a stimulates the activity of lysine acetyltransferases such as CBP/p300, which catalyze the acetylation of H3K27, a mark of active enhancers, super-enhancers, and promoters. There are a few studies on the genomic location of H4R3me2a. In chicken polychromatic erythrocytes, H4R3me2a is found in introns and intergenic regions and binds to the globin locus control region (a super-enhancer) and globin regulatory regions. In this report, we analyzed chromatin immunoprecipitation sequencing data for the genomic location of H4R3me2a in the breast cancer cell line MCF7. As in avian cells, MCF7 H4R3me2a is present in intronic and intergenic regions. Nucleosomes with H4R3me2a and H3K27ac next to nucleosome-free regions are found at super-enhancers, enhancers, and promoter regions of expressed genes. Genes with critical roles in breast cancer cells have broad domains of nucleosomes with H4R3me2a, H3K27ac, and H3K4me3. Our results are consistent with PRMT1-mediated H4R3me2a playing a key role in the chromatin organization of regulatory regions of vertebrate genomes.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"145-158"},"PeriodicalIF":2.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138443628","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

HSPA4 regulated glioma progression via activation of AKT signaling pathway. HSPA4通过激活AKT信号通路调控胶质瘤的进展。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2024-04-01 Epub Date: 2023-06-20 DOI: 10.1139/bcb-2022-0321

Xi Yuan, Xiangdong Sun, Bin Zhou, Shuang Zhao, Yikun Li, Haolang Ming

{"title":"HSPA4 regulated glioma progression via activation of AKT signaling pathway.","authors":"Xi Yuan, Xiangdong Sun, Bin Zhou, Shuang Zhao, Yikun Li, Haolang Ming","doi":"10.1139/bcb-2022-0321","DOIUrl":"10.1139/bcb-2022-0321","url":null,"abstract":"Glioma is still an incurable disease with high invasiveness. Heat shock 70 kDa protein 4 (HSPA4) is a member of the HSP110 family, and is associated with the development and progression of various cancers. In the current study, we assessed the expression of HSPA4 in clinical samples, and found that HSPA4 was up-regulated in glioma tissues and correlated with tumor recurrence and grade. Survival analyses demonstrated that glioma patients with high HSPA4 expression had lower overall survival and disease-free survival times. In vitro knockdown of HSPA4 inhibited glioma cell proliferation, mediated cell cycle arrest at G2 phase and apoptosis, and reduced the migration ability. In vivo, the growth of HSPA4-knockdown xenografts was markedly suppressed compared to the tumors formed by HSPA4-positive control cells. Additionally, Gene set enrichment analyses disclosed that HSPA4 was associated with the PI3K/Akt signaling pathway. The regulatory effect of the AKT activator SC79 on cell proliferation and apoptosis was suppressed by HSPA4 knockdown, indicating that HSPA4 is capable of promoting glioma development. In summary, these data showed that HSPA4 is likely to play a pivotal role in the progression of glioma, and consequently may be a promising therapeutic target for glioma therapy.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"159-168"},"PeriodicalIF":2.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9667241","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

Yeast profilin mutants inhibit classical nuclear import and alter the balance between actin and tubulin levels. 酵母谱蛋白突变体抑制经典核输入，改变肌动蛋白和微管蛋白水平之间的平衡。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2024-04-01 Epub Date: 2023-12-04 DOI: 10.1139/bcb-2023-0223

Ursula Stochaj

引用次数: 0

The role of BCL2L13 in glioblastoma: turning a need into a target. BCL2L13在胶质母细胞瘤中的作用:将需求转化为靶标。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2024-04-01 Epub Date: 2023-11-21 DOI: 10.1139/bcb-2023-0221

Joadi Jacobs, Rosa Iranpour, Amir Barzegar Behrooz, Simone C da Silva Rosa, Saeid Ghavami

{"title":"The role of BCL2L13 in glioblastoma: turning a need into a target.","authors":"Joadi Jacobs, Rosa Iranpour, Amir Barzegar Behrooz, Simone C da Silva Rosa, Saeid Ghavami","doi":"10.1139/bcb-2023-0221","DOIUrl":"10.1139/bcb-2023-0221","url":null,"abstract":"Glioblastoma (GBM) is the most common aggressive central nervous system cancer. GBM has a high mortality rate, with a median survival time of 12-15 months after diagnosis. A poor prognosis and a shorter life expectancy may result from resistance to standard treatments such as radiation and chemotherapy. Temozolomide has been the mainstay treatment for GBM, but unfortunately, there are high rates of resistance with GBM bypassing apoptosis. A proposed mechanism for bypassing apoptosis is decreased ceramide levels, and previous research has shown that within GBM cells, B cell lymphoma 2-like 13 (BCL2L13) can inhibit ceramide synthase. This review aims to discuss the causes of resistance in GBM cells, followed by a brief description of BCL2L13 and an explanation of its mechanism of action. Further, lipids, specifically ceramide, will be discussed concerning cancer and GBM cells, focusing on ceramide synthase and its role in developing GBM. By gathering all current information on BCL2L13 and ceramide synthase, this review seeks to enable an understanding of these pieces of GBM in the hope of finding an effective treatment for this disease.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"127-134"},"PeriodicalIF":2.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138290180","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

Evolution of techniques and tools for replication fork proteome and protein interaction studies. 复制叉蛋白质组和蛋白质相互作用研究技术和工具的演变。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2024-04-01 Epub Date: 2023-12-19 DOI: 10.1139/bcb-2023-0215

Carla-Marie Jurkovic, François-Michel Boisvert

引用次数: 0

The m6A reader IGF2BP2 promotes the progression of esophageal squamous cell carcinoma cells by increasing the stability of OCT4 mRNA. m6A阅读器IGF2BP2通过增加OCT4 mRNA的稳定性来促进食管鳞状细胞癌细胞的进展。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2024-04-01 Epub Date: 2023-11-02 DOI: 10.1139/bcb-2023-0067

Rong Zhao, Ting Li, Xinran Zhao, Ziyi Yang, Liying Ma, Xiaoxia Wang

{"title":"The m6A reader IGF2BP2 promotes the progression of esophageal squamous cell carcinoma cells by increasing the stability of OCT4 mRNA.","authors":"Rong Zhao, Ting Li, Xinran Zhao, Ziyi Yang, Liying Ma, Xiaoxia Wang","doi":"10.1139/bcb-2023-0067","DOIUrl":"10.1139/bcb-2023-0067","url":null,"abstract":"Esophageal squamous cell carcinoma (ESCC) is a common malignancy with high morbidity and mortality. Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) serves as a reader of RNA m6A (N6 methyladenosine) modification to regulate gene expression at the post-transcriptional level. Emerging evidence suggests that IGF2BP2 plays critical roles in tumorigenesis and malignant development. However, the biological function and molecular mechanism of IGF2BP2 in ESCC are not well understood. Here, we found that IGF2BP2 expression was upregulated in esophageal cancer tissues and ESCC cells, and IGF2BP2 overexpression enhanced proliferation, migration, invasion, and stem cell-like properties of ESCC cells. Conversely, the knockdown of IGF2BP2 expression inhibited malignant phenotype of ESCC cells. Mechanistically, IGF2BP2 upregulated octomer-binding transcription factor 4 (OCT4) mRNA expression, and RNA immunoprecipitation (RIP) assay proved that IGF2BP2 could interact with OCT4 mRNA. Moreover, OCT4 was modified at m6A confirmed by methylated m6A RNA immunoprecipitation (Me-RIP)-qPCR assay, and IGF2BP2 knockdown reduced OCT4 mRNA stability. These results suggested that IGF2BP2 served as a reader for m6A-modified OCT4, thus increased OCT4 mRNA expression by regulating its stability. Furthermore, the knockdown of OCT4 could reverse the effects of IGF2BP2 on ESCC cells. In conclusion, these data indicate that IGF2BP2, as a reader for m6A, plays an oncogenic role by regulating OCT4 expression in ESCC, which provides new insights into targeting IGF2BP2/OCT4 axis for the therapy of ESCC.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"169-178"},"PeriodicalIF":2.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71420300","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

Optimized total RNA isolation from bovine sperm with enhanced sperm head lysis. 优化从牛精子中分离总RNA，增强精子头裂解。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2024-04-01 Epub Date: 2023-11-10 DOI: 10.1139/bcb-2023-0231

Saurabh Tiwari, Abdallah Shahat, John Kastelic, Nehal Thakor, Jacob Thundathil

{"title":"Optimized total RNA isolation from bovine sperm with enhanced sperm head lysis.","authors":"Saurabh Tiwari, Abdallah Shahat, John Kastelic, Nehal Thakor, Jacob Thundathil","doi":"10.1139/bcb-2023-0231","DOIUrl":"10.1139/bcb-2023-0231","url":null,"abstract":"Increasing evidence of sperm RNA's role in fertilization and embryonic development has provided impetus for its isolation and thorough characterization. Sperm are considered tough-to-lyse cells due to the compact condensed DNA in sperm heads. Lack of consensus among bovine sperm RNA isolation protocols introduces experimental variability in transcriptome studies. Here, we describe an optimized method for total RNA isolation from bovine sperm using the TRIzol reagent. This study critically investigated the effects of various lysis conditions on sperm RNA isolation. Sperm suspended in TRIzol were subjected to a combination of mechanical treatments (sonication and passage through a 30G needle and syringe) and chemical treatments (supplementation with reducing agents 1,4-dithiothreitol and tris(2-carboxyethyl) phosphine hydrochloride (TCEP)). Microscopic evaluation of sperm lysis confirmed preferential sperm tail versus sperm head lysis. Interestingly, only TCEP-supplemented TRIzol (both mechanical treatments) had progressive sperm head lysis and consistently yielded total sperm RNA. Furthermore, RNA integrity was confirmed based on the electrophoresis profile and an absence of genomic DNA and somatic cells (e.g., epithelial cells, spermatids, etc.) with RT-qPCR. Our findings highlighted the importance of sperm lysis, specifically of the sperm head using TCEP with mechanical treatment, in total RNA isolation and presented a bovine-specific sperm RNA isolation method to reduce experimental variabilities.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"194-205"},"PeriodicalIF":2.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72208212","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

Identification of critical mitochondrial hub gene for facial nerve regeneration. 鉴定面部神经再生的关键线粒体枢纽基因

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2024-04-01 Epub Date: 2023-12-12 DOI: 10.1139/bcb-2023-0224

Xiaofang Cao, Yan Zhang, Yu Shi, Ying Li, Li Gao, Xiumei Wang, Liang Sun

{"title":"Identification of critical mitochondrial hub gene for facial nerve regeneration.","authors":"Xiaofang Cao, Yan Zhang, Yu Shi, Ying Li, Li Gao, Xiumei Wang, Liang Sun","doi":"10.1139/bcb-2023-0224","DOIUrl":"10.1139/bcb-2023-0224","url":null,"abstract":"Mitochondria play a critical role in nerve regeneration, yet the impact of gene expression changes related to mitochondria in facial nerve regeneration remains unknown. To address this knowledge gap, we analyzed the expression profile of the facial motor nucleus (FMN) using data obtained from the Gene Expression Omnibus (GEO) database (GSE162977). By comparing different time points in the data, we identified differentially expressed genes (DEGs). Additionally, we collected mitochondria-related genes from the Gene Ontology (GO) database and intersected them with the DEGs, resulting in the identification of mitochondria-related DEGs (MIT-DEGs). To gain further insights, we performed functional enrichment and pathway analysis of the MIT-DEGs. To explore the interactions among these MIT-DEGs, we constructed a protein-protein interaction (PPI) network using the STRING database and identified hub genes using the Degree algorithm of Cytoscape software. To validate the relevance of these genes to nerve regeneration, we established a rat facial nerve injury (FNI) model and conducted a series of experiments. Through these experiments, we confirmed three MIT-DEGs (Myc, Lyn, and Cdk1) associated with facial nerve regeneration. Our findings provide valuable insights into the transcriptional changes of mitochondria-related genes in the FMN following FNI, which can contribute to the development of new treatment strategies for FNI.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"179-193"},"PeriodicalIF":2.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138796361","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