Biochemistry and Cell Biology最新文献

筛选
英文 中文
Cell-in-cell-mediated intercellular communication exacerbates the pro-inflammatory progression in asthma. 细胞间介导的细胞间通讯加剧了哮喘的炎症进展。
IF 2.9 3区 生物学
Biochemistry and Cell Biology Pub Date : 2024-06-01 Epub Date: 2024-04-03 DOI: 10.1139/bcb-2023-0228
Shan Wang, Bowen Liu, Huiru He, Jiahao Huang, Fangping He, Ying He, Ailin Tao
{"title":"Cell-in-cell-mediated intercellular communication exacerbates the pro-inflammatory progression in asthma.","authors":"Shan Wang, Bowen Liu, Huiru He, Jiahao Huang, Fangping He, Ying He, Ailin Tao","doi":"10.1139/bcb-2023-0228","DOIUrl":"10.1139/bcb-2023-0228","url":null,"abstract":"<p><p>Cell-in-cell (CIC) structures have been suggested to mediate intracellular substance transport between cells and have been found widely in inflammatory lung tissue of asthma. The aim of this study was to investigate the significance of CIC structures in inflammatory progress of asthma. CIC structures and related inflammatory pathways were analyzed in asthmatic lung tissue and normal lung tissue of mouse model. In vitro, the activation of inflammatory pathways by CIC-mediated intercellular communication was analyzed by RNA-Seq and verified by Western blotting and immunofluorescence. Results showed that CIC structures of lymphocytes and alveolar epithelial cells in asthmatic lung tissue mediated intercellular substance (such as mitochondria) transfer and promoted pro-inflammation in two phases. At early phase, internal lymphocytes triggered inflammasome-dependent pro-inflammation and cell death of itself. Then, degraded lymphocytes released cellular contents such as mitochondria inside alveolar epithelial cells, further activated multi-pattern-recognition receptors and NF-kappa B signaling pathways of alveolar epithelial cells, and thereby amplified pro-inflammatory response in asthma. Our work supplements the mechanism of asthma pro-inflammation progression from the perspective of CIC structure of lymphocytes and alveolar epithelial cells, and provides a new idea for anti-inflammatory therapy of asthma.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140849340","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
Granulocyte pro-myeloperoxidase is redundantly processed by proprotein convertase furin and PC7 in HL-60 cells. 粒细胞前髓过氧化物酶在 HL-60 细胞中被前蛋白转化酶呋喃和 PC7 重复处理。
IF 2.9 3区 生物学
Biochemistry and Cell Biology Pub Date : 2024-06-01 Epub Date: 2024-03-14 DOI: 10.1139/bcb-2023-0339
Vanessa Lapointe, Frédéric Couture
{"title":"Granulocyte pro-myeloperoxidase is redundantly processed by proprotein convertase furin and PC7 in HL-60 cells.","authors":"Vanessa Lapointe, Frédéric Couture","doi":"10.1139/bcb-2023-0339","DOIUrl":"10.1139/bcb-2023-0339","url":null,"abstract":"<p><p>Neutrophil myeloperoxidase/H<sub>2</sub>O<sub>2</sub>/chloride system is a key mechanism to control pathogen infection. This enzyme, myeloperoxidase, plays a pivotal role in the arsenal of azurophilic granules that are released through degranulation upon neutrophil activation, which trigger local hypochlorous acid production. Myeloperoxidase gene encodes a protein precursor named promyeloperoxidase that arbors a propeptide that gets cleaved later during secretory routing in post-endoplasmic reticulum compartments. Although evidence suggested that this processing event was performed by one or different enzymes from the proprotein convertases family, the identity of this enzyme was never investigated. In this work, the naturally producing myeloperoxidase promyelocytic cell line HL-60 was used to investigate promyeloperoxidase cleavage during granulocytic differentiation in response to proprotein convertase inhibitors decanoyl-RVKR-chloromethylketone and hexa-d-arginine. Stable PC knockdown of endogenously expressed proprotein convertases, furin and PC7, was achieved using lentiviral delivery of shRNAs. None of the knockdown cell line could reproduce the effect of the pan-proprotein convertases inhibitor decanoyl-RVKR-chloromethylketone that accumulated intracellular promyeloperoxidase stores in HL-60 cells, therefore illustrating that both furin and PC7 redundantly process this proprotein.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140130651","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
Protamines and the sperm nuclear basic proteins Pandora's Box of insects. 原胺和精子核基本蛋白 昆虫的潘多拉魔盒
IF 2.9 3区 生物学
Biochemistry and Cell Biology Pub Date : 2024-06-01 Epub Date: 2024-02-26 DOI: 10.1139/bcb-2023-0363
Melissa R Leyden, Brent Gowen, Rodrigo Gonzalez-Romero, Jose Maria Eirin-Lopez, Bo-Hyun Kim, Fumio Hayashi, Jay McCartney, Patrick C Zhang, Miyoko Kubo-Irie, Jeffrey Shabanowitz, Donald F Hunt, Patrick Ferree, Harold Kasinsky, Juan Ausió
{"title":"Protamines and the sperm nuclear basic proteins Pandora's Box of insects.","authors":"Melissa R Leyden, Brent Gowen, Rodrigo Gonzalez-Romero, Jose Maria Eirin-Lopez, Bo-Hyun Kim, Fumio Hayashi, Jay McCartney, Patrick C Zhang, Miyoko Kubo-Irie, Jeffrey Shabanowitz, Donald F Hunt, Patrick Ferree, Harold Kasinsky, Juan Ausió","doi":"10.1139/bcb-2023-0363","DOIUrl":"10.1139/bcb-2023-0363","url":null,"abstract":"<p><p>Insects are the largest group of animals when it comes to the number and diversity of species. Yet, with the exception of <i>Drosophila</i>, no information is currently available on the primary structure of their sperm nuclear basic proteins (SNBPs). This paper represents the first attempt in this regard and provides information about six species of Neoptera: <i>Poecillimon thessalicus, Graptosaltria nigrofuscata, Apis mellifera, Nasonia vitripennis, Parachauliodes continentalis</i>, and <i>Tribolium castaneum</i>. The SNBPs of these species were characterized by acetic acid urea gel electrophoresis (AU-PAGE) and high-performance liquid chromatography fractionated. Protein sequencing was obtained using a combination of mass spectrometry sequencing, Edman N-terminal degradation sequencing and genome mining. While the SNBPs of several of these species exhibit a canonical arginine-rich protamine nature, a few of them exhibit a protamine-like composition. They appear to be the products of extensive cleavage processing from a precursor protein which are sometimes further processed by other post-translational modifications that are likely involved in the chromatin transitions observed during spermiogenesis in these organisms.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139970779","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 2.9 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":"<p><p>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.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.9,"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
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 2.9 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":"<p><p>Diabetic kidney disease (DKD) is a major contributor to chronic kidney disease. Hydrogen sulfide (H<sub>2</sub>S) 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 H<sub>2</sub>S counteracts against DKD. Utilizing mice and human renal tubular epithelial (HK-2) cells, we demonstrated a reduction in cystathionine-γ-lyase/H<sub>2</sub>S 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 H<sub>2</sub>S. Exogenous H<sub>2</sub>S 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 H<sub>2</sub>S exerts a protective role against DKD by inhibiting SOD2 degradation.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.9,"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
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 2.9 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":"<p><p>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.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.9,"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 2.9 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":"<p><p>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.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.9,"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 2.9 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
{"title":"Yeast profilin mutants inhibit classical nuclear import and alter the balance between actin and tubulin levels.","authors":"Ursula Stochaj","doi":"10.1139/bcb-2023-0223","DOIUrl":"10.1139/bcb-2023-0223","url":null,"abstract":"<p><p>Profilin is a small protein that controls actin polymerization in yeast and higher eukaryotes. In addition, profilin has emerged as a multifunctional protein that contributes to other processes in multicellular organisms. This study focuses on profilin (Pfy1) in the budding yeast <i>Saccharomyces cerevisiae.</i> The primary sequences of yeast Pfy1 and its metazoan orthologs diverge vastly. However, structural elements of profilin are conserved among different species. To date, the full spectrum of Pfy1 functions has yet to be defined. The current work explores the possible involvement of yeast profilin in nuclear protein import. To this end, a panel of well-characterized yeast profilin mutants was evaluated. The experiments demonstrate that yeast profilin (<i>i</i>) regulates nuclear protein import, (<i>ii</i>) determines the subcellular localization of essential nuclear transport factors, and (<i>iii</i>) controls the relative abundance of actin and tubulin. Together, these results define yeast profilin as a moonlighting protein that engages in multiple essential cellular activities.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138481788","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
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 2.9 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":"<p><p>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.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.9,"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
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 2.9 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":"<p><p>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.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.9,"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
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
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
确定
请完成安全验证×
相关产品
×
本文献相关产品
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信