Biochimica et Biophysica Acta-Gene Regulatory Mechanisms最新文献

A putative PIWIL/piRNA–OTX2 network: An emerging model for epigenetic regulation of cancer stemness in retinoblastoma PIWIL/piRNA-OTX2网络：视网膜母细胞瘤肿瘤干细胞的表观遗传调控新模型

IF 2.6 3区生物学

Biochimica et Biophysica Acta-Gene Regulatory Mechanisms Pub Date : 2025-07-19 DOI: 10.1016/j.bbagrm.2025.195106

Rupa Roy , Subbulakshmi Chidambaram

{"title":"A putative PIWIL/piRNA–OTX2 network: An emerging model for epigenetic regulation of cancer stemness in retinoblastoma","authors":"Rupa Roy , Subbulakshmi Chidambaram","doi":"10.1016/j.bbagrm.2025.195106","DOIUrl":"10.1016/j.bbagrm.2025.195106","url":null,"abstract":"<div><div>Recent findings underscore the critical role of PIWIL/piRNA pathways in cancer, extending their known functions beyond reproductive biology. Retinoblastoma (RB), a rare pediatric retinal tumor, is primarily driven by RB1 gene loss but also involves significant epigenetic alterations. Our previous studies revealed that PIWIL4 is significantly upregulated in RB, and its knockdown disrupts the expression of stemness-associated factors, including OTX2, SOX2, and NANOG. In this review, we have proposed that PIWIL/piRNA complexes might recruit epigenetic modifiers to cis-regulatory modules (CRMs) of the OTX2 gene, modulating chromatin accessibility and transcription factor binding. Aberrant PIWIL4 expression may dysregulate OTX2 expression, impacting stemness-maintaining factors and activating oncogenic pathways, including Wnt/β-catenin signaling, mediated by TSPAN12, EphA2, and ZNF proteins. This conceptual framework positions the PIWIL/piRNA-OTX2 axis as a potential regulator of CSC dynamics, linking it to epigenetic modifications, transcription factor interactions, and neuronal differentiation in RB. Targeting this axis could disrupt stemness-associated pathways and oncogenic signaling, offering new therapeutic strategies to mitigate tumor progression and recurrence in RB and other cancers with similar molecular mechanisms.</div></div>","PeriodicalId":55382,"journal":{"name":"Biochimica et Biophysica Acta-Gene Regulatory Mechanisms","volume":"1868 3","pages":"Article 195106"},"PeriodicalIF":2.6,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144683636","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

Functional characterization of promoter regions in selenoprotein synthesis-relevant genes (sbp2, eefsec and sepsecs) and their selenium-dependent regulation in yellow catfish Pelteobagrus fulvidraco 黄颡鱼硒蛋白合成相关基因（sbp2、eefsec和sepsecs）启动子区功能特征及其硒依赖性调控

IF 2.6 3区生物学

Biochimica et Biophysica Acta-Gene Regulatory Mechanisms Pub Date : 2025-07-04 DOI: 10.1016/j.bbagrm.2025.195105

Kai Zhang , An-Gen Yu , Hua Zheng , Pei-Jia Li , Zhi Luo

{"title":"Functional characterization of promoter regions in selenoprotein synthesis-relevant genes (sbp2, eefsec and sepsecs) and their selenium-dependent regulation in yellow catfish Pelteobagrus fulvidraco","authors":"Kai Zhang , An-Gen Yu , Hua Zheng , Pei-Jia Li , Zhi Luo","doi":"10.1016/j.bbagrm.2025.195105","DOIUrl":"10.1016/j.bbagrm.2025.195105","url":null,"abstract":"<div><div>The study explored the transcriptional regulation of selenoprotein synthesis-relevant genes, such as selenocysteine insertion sequence element binding protein 2 (<em>sbp2</em>), eukaryotic elongation factor (<em>eefsec</em>) and o-phosphoserine selenocysteine tRNA synthase (<em>sepsecs</em>), and their selenium-mediated regulation in yellow catfish <em>Pelteobagrus fulvidraco</em>, an important fish with ecological and economic importance in several Asian countries. We cloned the sequences of <em>sbp2</em>, <em>eefsec</em> and <em>sepsecs</em> promoters, spanning from −2060 bp to +61 bp, −1910 bp to +53 bp and − 1456 bp to +51 bp relative to the TSS, respectively. Through sequential deletion and mutation analysis of their promoters, we identified several functional binding sites: the signal transducer and activator of transcription 1 (STAT1) binding site (−1308 bp to −1322 bp) and the forkhead box protein O1 (FOXO1) binding site (−1778 bp to −1788 bp) in the <em>sbp2</em> promoter; the FOXO1 binding site (−1070 bp to −1080 bp) and the STAT3 binding site (−428 bp to −436 bp) in the <em>eefsec</em> promoter; and the FOXO1 binding site (−721 bp to −731 bp) in the <em>sepsecs</em> promoter. The activity of these binding sites was regulated by selenomethionine (Se-Met) incubation. Furthermore, electrophoretic mobility shift assay and chromatin immunoprecipitation experiments confirmed that these binding sites interact with their corresponding transcription factors above. For the first time, we demonstrated that STAT1 and FOXO1 regulate transcriptional activity of <em>sbp2</em> promoter; STAT3 and FOXO1 regulate transcriptional activity of <em>eefsec</em> promoter; and FOXO1 regulates transcriptional activity of <em>sepsecs</em> promoter. These findings provide novel insights into regulatory mechanisms of selenoprotein synthesis in yellow catfish.</div></div>","PeriodicalId":55382,"journal":{"name":"Biochimica et Biophysica Acta-Gene Regulatory Mechanisms","volume":"1868 3","pages":"Article 195105"},"PeriodicalIF":2.6,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144576996","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

Transposon insertion causes ctnnb2 transcript instability that results in the maternal effect zebrafish ichabod (ich) mutation 转座子插入导致ctnnb2转录不稳定，导致母体效应斑马鱼ichabod （rich）突变。

IF 2.6 3区生物学

Biochimica et Biophysica Acta-Gene Regulatory Mechanisms Pub Date : 2025-06-30 DOI: 10.1016/j.bbagrm.2025.195104

Zsombor Varga , Ferenc Kagan , Shingo Maegawa , Ágnes Nagy , Javan Okendo , Shawn M. Burgess , Eric S. Weinberg , Máté Varga

{"title":"Transposon insertion causes ctnnb2 transcript instability that results in the maternal effect zebrafish ichabod (ich) mutation","authors":"Zsombor Varga , Ferenc Kagan , Shingo Maegawa , Ágnes Nagy , Javan Okendo , Shawn M. Burgess , Eric S. Weinberg , Máté Varga","doi":"10.1016/j.bbagrm.2025.195104","DOIUrl":"10.1016/j.bbagrm.2025.195104","url":null,"abstract":"<div><div>The maternal-effect mutation <em>ichabod</em> (<em>ich</em>) results in ventralized zebrafish embryos due to impaired induction of the dorsal canonical Wnt-signaling pathway. While previous studies linked the phenotype to reduced <em>ctnnb2</em> transcript levels, the causative mutation remained unidentified. Using long-read sequencing, we discovered that the <em>ich</em> phenotype stems from the insertion of a non-autonomous CMC-Enhancer/Suppressor-mutator (CMC-EnSpm) transposon in the 3’UTR of the gene. Through reporter assays, we demonstrate that while wild type <em>ctnnb2</em> mRNAs exhibit remarkably high stability throughout the early stages of development, the insertion of the transposon dramatically reduces transcript stability. Genome-wide mapping of the CMC-EnSpm transposons across multiple zebrafish strains also indicated ongoing transposition activity in the zebrafish genome. Our findings not only resolve the molecular basis of the <em>ich</em> mutation but also highlight the continuing mutagenic potential of endogenous transposons and reveal unexpected aspects of maternal transcript regulation during early zebrafish development.</div></div>","PeriodicalId":55382,"journal":{"name":"Biochimica et Biophysica Acta-Gene Regulatory Mechanisms","volume":"1868 3","pages":"Article 195104"},"PeriodicalIF":2.6,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546267","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

DUSP1 protein's impact on breast cancer: Anticancer response and sensitivity to cisplatin DUSP1蛋白对乳腺癌的影响：抗癌反应和对顺铂的敏感性

IF 2.6 3区生物学

Biochimica et Biophysica Acta-Gene Regulatory Mechanisms Pub Date : 2025-06-25 DOI: 10.1016/j.bbagrm.2025.195103

Sefa Metin , Hilal Altan , Ergün Tercan , Bala Gur Dedeoglu , Hakan Gurdal

{"title":"DUSP1 protein's impact on breast cancer: Anticancer response and sensitivity to cisplatin","authors":"Sefa Metin , Hilal Altan , Ergün Tercan , Bala Gur Dedeoglu , Hakan Gurdal","doi":"10.1016/j.bbagrm.2025.195103","DOIUrl":"10.1016/j.bbagrm.2025.195103","url":null,"abstract":"<div><div>Dual-Specificity Phosphatase 1 (DUSP1) modulates the activity of members of the Mitogen-Activated Protein Kinase (MAPK) family, including p38, JNK, and ERK1/2, which affects various cellular functions in cancer. Moreover, DUSP1 is known to influence the outcomes of cancer chemotherapy. This study aimed to reduce DUSP1 protein expression using CRISPR/Cas9 and siRNA and assess its effects on cell proliferation, migration, and tumor growth potential in triple-negative breast cancer (TNBC) cells. We examined the expression levels of p38, JNK, and ERK1/2, along with their phosphorylated forms, and investigated DUSP1's influence to cisplatin sensitivity<strong><em>.</em></strong> Our findings revealed that the downregulation of DUSP1 expression inhibited the proliferation, migration, and tumor growth potential of TNBC cells. Additionally, BCI, an inhibitor of DUSP1/6, demonstrated anti-proliferative effects on these cells. Decreasing the expression of DUSP1 increased the phosphorylation ratio of p38 and JNK, but not ERK1/2. Moreover, the anticancer response induced by cisplatin was enhanced by reducing DUSP1 expression or by treating the cells with BCI. Notably, cisplatin treatment increased p38 phosphorylation, which was significantly augmented by reduced DUSP1 expression. We also demonstrated that the DUSP1 inhibition-induced anticancer response in these cells predominantly relied on p38 activity. These findings contribute to a better understanding of the role of DUSP1 in breast cancer and offer insights into potential therapeutic strategies targeting DUSP1 to enhance the efficacy of cisplatin treatment. Our study highlights that decreased DUSP1 protein expression and activity mediates an anticancer response and increases the sensitivity of MDA-MB231 cells to cisplatin by regulating p38.</div></div>","PeriodicalId":55382,"journal":{"name":"Biochimica et Biophysica Acta-Gene Regulatory Mechanisms","volume":"1868 3","pages":"Article 195103"},"PeriodicalIF":2.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144482397","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

RhoA functionally collaborates with HSPA1A to promote the migratory phenotype of cancer cells RhoA与HSPA1A在功能上协同促进癌细胞的迁移表型

IF 2.6 3区生物学

Biochimica et Biophysica Acta-Gene Regulatory Mechanisms Pub Date : 2025-06-20 DOI: 10.1016/j.bbagrm.2025.195101

Sumaiya Nabi , Mohammad Amin Hajam , Umar Mushtaq , Aadil Manzoor Baba , Bashir Ahmad Malla , Firdous Ahmad Khanday , Nazir Ahmad Dar

{"title":"RhoA functionally collaborates with HSPA1A to promote the migratory phenotype of cancer cells","authors":"Sumaiya Nabi , Mohammad Amin Hajam , Umar Mushtaq , Aadil Manzoor Baba , Bashir Ahmad Malla , Firdous Ahmad Khanday , Nazir Ahmad Dar","doi":"10.1016/j.bbagrm.2025.195101","DOIUrl":"10.1016/j.bbagrm.2025.195101","url":null,"abstract":"<div><div>RhoA, a member of the GTPase family, plays a pivotal role in attaining a migratory phenotype, mainly by regulating cytoskeleton dynamics, cell adhesion and membrane protrusions. Although many upstream regulators and downstream effectors of RhoA have been identified, the discovery of new interacting partners continues to expand its interactome, providing fresh insights into its regulation and function. Co-immunoprecipitation and fluorescence microscopy were used to study the interaction, localization and morphological effects of HSPA1A and RhoA. The interaction was validated by modulating the protein expression through transfections and silencing approaches. Cell proliferation, migration and viability were assessed using MTT, a Boyden chamber and FACS assays, respectively. Our study identified HSPA1A, as an unexplored interacting partner of RhoA under physiological conditions. Functional analyses showed that the interaction between HSPA1A and RhoA enhances the migratory potential of cancer cells, induces G0/G1 cell cycle arrest and promotes a rounded cell morphology. Under HSPA1A transfection, increased RhoA protein levels were observed, while the silencing of HSPA1A resulted in decreased RhoA levels. This study highlights the critical role of HSPA1A-RhoA interaction in regulating cancer cell migration, morphology and cell cycle progression. These findings lay the groundwork for future research into its potential clinical applications.</div></div>","PeriodicalId":55382,"journal":{"name":"Biochimica et Biophysica Acta-Gene Regulatory Mechanisms","volume":"1868 3","pages":"Article 195101"},"PeriodicalIF":2.6,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144366089","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

ARID1A-driven modulation of EZH2 impedes proliferation and enhances senescence in breast cancer cells arid1a驱动的EZH2调控可抑制乳腺癌细胞的增殖并促进衰老。

IF 2.6 3区生物学

Biochimica et Biophysica Acta-Gene Regulatory Mechanisms Pub Date : 2025-06-19 DOI: 10.1016/j.bbagrm.2025.195102

Neena George , Rayzel Fernandes , Kapaettu Satyamoorthy

{"title":"ARID1A-driven modulation of EZH2 impedes proliferation and enhances senescence in breast cancer cells","authors":"Neena George , Rayzel Fernandes , Kapaettu Satyamoorthy","doi":"10.1016/j.bbagrm.2025.195102","DOIUrl":"10.1016/j.bbagrm.2025.195102","url":null,"abstract":"<div><div>ARID1A mutations, in association with EZH2 overexpression, are linked to various malignancies, particularly those driven by epigenetic dysregulation and associated with therapy resistance. The prevalence of ARID1A mutations is high in ER+ breast cancer, and studies have mainly explored the synthetic lethal effects of these proteins. However, the tumor-suppressive mechanisms of ARID1A are complex and not yet fully understood. In this study, we explored the potential tumor-specific epigenetic antagonism between ARID1A and EZH2 in breast cancer cells, particularly focusing on the modulation of EZH2 by ARID1A through senescence pathway activation. Treatment with DNA-damaging agents induced senescence, which was associated with upregulation of ARID1A expression and a concurrent reduction in EZH2 levels, suggesting a potential role for ARID1A in the induction and maintenance of the senescence phenotype. Overexpression of ARID1A led to reduced EZH2 levels, suppressed cell proliferation in MCF-7 and MDA-MB231 cells, and induced a senescence-like phenotype. These cells exhibited changes in cell-to-cell adhesion, increased filopodium formation, and G0/G1 cell cycle arrest. This antiproliferative effect of ARID1A is mediated through the activation of the p53-p21/p16 axis. Furthermore, ARID1A knockdown-associated downregulation of EZH2 highlights the integral role of ARID1A in destabilizing the expression of EZH2 and contributing to cell cycle arrest. Importantly, we found that dasatinib treatment selectively targeted tumor cells overexpressing ARID1A. These findings provide preliminary insight into the molecular mechanisms by which ARID1A regulates EZH2 and establishes a senescence phenotype, offering valuable directions for developing more effective and personalized treatments.</div></div>","PeriodicalId":55382,"journal":{"name":"Biochimica et Biophysica Acta-Gene Regulatory Mechanisms","volume":"1868 3","pages":"Article 195102"},"PeriodicalIF":2.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340618","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

Growth rate is related to elongation of RNA polymerase II transcription in Saccharomyces cerevisiae 酿酒酵母菌的生长速率与RNA聚合酶II转录的伸长有关。

IF 2.6 3区生物学

Biochimica et Biophysica Acta-Gene Regulatory Mechanisms Pub Date : 2025-06-08 DOI: 10.1016/j.bbagrm.2025.195100

A.I. Garrido-Godino , R. González , M. Martín-Expósito , S. Chávez , J.E. Pérez-Ortín , F. Navarro

{"title":"Growth rate is related to elongation of RNA polymerase II transcription in Saccharomyces cerevisiae","authors":"A.I. Garrido-Godino , R. González , M. Martín-Expósito , S. Chávez , J.E. Pérez-Ortín , F. Navarro","doi":"10.1016/j.bbagrm.2025.195100","DOIUrl":"10.1016/j.bbagrm.2025.195100","url":null,"abstract":"<div><div>Cells must adapt to changing environmental conditions to maintain their fitness and to compete with other genotypes during the natural selection process. The growth rate (GR) is a determining factor in this competition, and it influences gene expression. Some genes increase mRNA levels, while others decrease with the GR. mRNA levels depend on the dynamic balance between their synthesis by RNA polymerase II and their degradation rates. RNA polymerase I and III are also influenced by the GR because they transcribe protein synthesis machinery required to make proteins that increase cell mass during growth. Although RNA levels have been extensively studied in relation to the GR in many organisms, synthesis and degradation rates have, however, been much less investigated. In a previous work, we found a positive correlation between RNA polymerase (RNA pol) II transcription and mRNA degradation with GRs in yeast in batch cultures. Here we extend our study under constant growth conditions in a chemostat and find that overall chromatin-associated RNA pol II levels increase in parallel with the GR. This increase appears to involve the accumulation of partially dephosphorylated RNA pol II with a greater tendency to backtracking, which suggests that the GR modifies the phosphorylation state of RNA pol II at the elongation level. RNA pol I also increases its association with chromatin with the GR, which confirms the general dependence of at least RNA pol I and II transcription on the GR.</div></div>","PeriodicalId":55382,"journal":{"name":"Biochimica et Biophysica Acta-Gene Regulatory Mechanisms","volume":"1868 3","pages":"Article 195100"},"PeriodicalIF":2.6,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144267947","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

Insights into the target-directed miRNA degradation mechanism in Drosophila ovarian cell culture 果蝇卵巢细胞培养中靶向miRNA降解机制的研究

IF 2.6 3区生物学

Biochimica et Biophysica Acta-Gene Regulatory Mechanisms Pub Date : 2025-05-04 DOI: 10.1016/j.bbagrm.2025.195092

Natalia Akulenko , Elena Mikhaleva , Sofya Marfina , Ivan Kutelev , Dmitry Kornyakov , Vlad Bobrov , Andrei Artamonov , Georgij Arapidi , Victoria Shender , Sergei Ryazansky

{"title":"Insights into the target-directed miRNA degradation mechanism in Drosophila ovarian cell culture","authors":"Natalia Akulenko , Elena Mikhaleva , Sofya Marfina , Ivan Kutelev , Dmitry Kornyakov , Vlad Bobrov , Andrei Artamonov , Georgij Arapidi , Victoria Shender , Sergei Ryazansky","doi":"10.1016/j.bbagrm.2025.195092","DOIUrl":"10.1016/j.bbagrm.2025.195092","url":null,"abstract":"<div><div>Target-directed miRNA degradation (TDMD) is a process of post-transcriptional regulation of miRNA stability in animals induced by an extended pairing of Ago-bound miRNAs with specialized complementary RNA targets. As suggested by studies on human cell culture, Ago engaged with the extended duplex is recognized by the ZSWIM8 receptor of the Cullin-RING-ligase complex (CRL3), which also contains Cul3, EloB, and EloC proteins. The CRL activity is accelerated by the neddylation of Cul3 with the involvement of the E2 conjugating protein UbcE2M. The CRL ubiquitinates Ago, resulting in proteolysis of Ago and degradation of the released miRNAs. To date, the molecular mechanism of TDMD has not been studied in other species. To further characterize TDMD in animals, we investigated the protein Dora, the <em>Drosophila</em> ortholog of ZSWIM8, in the culture of <em>Drosophila</em> ovarian somatic cells (OSC). We showed that Dora in OSCs localizes in protein granules unrelated to P- and GW-bodies. The <em>dora</em> knockout resulted in the accumulation of multiple miRNAs, including miR-7-5p, and transcriptome-wide affected the mRNA targets of differentially expressed miRNAs. We also showed that Dora associates with proteins of the CRL3 complex, and the depletion of CRL3 components or inhibition of Cul3 neddylation upregulates miR-7-5p. We concluded that the molecular mechanism of TDMD is conserved in humans and <em>Drosophila</em>. Finally, we found that cells without Dora have an impaired Notch signaling pathway, indicating that TDMD in OSCs may contribute to the modulation of the Notch pathway.</div></div>","PeriodicalId":55382,"journal":{"name":"Biochimica et Biophysica Acta-Gene Regulatory Mechanisms","volume":"1868 2","pages":"Article 195092"},"PeriodicalIF":2.6,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143912978","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

Navigating the tumor landscape: VEGF, MicroRNAs, and the future of cancer treatment 导航肿瘤景观：VEGF， microrna和癌症治疗的未来

IF 2.6 3区生物学

Biochimica et Biophysica Acta-Gene Regulatory Mechanisms Pub Date : 2025-05-03 DOI: 10.1016/j.bbagrm.2025.195091

K.P. Ameya, P.P. Ashikha Shirin Usman, Durairaj Sekar

{"title":"Navigating the tumor landscape: VEGF, MicroRNAs, and the future of cancer treatment","authors":"K.P. Ameya, P.P. Ashikha Shirin Usman, Durairaj Sekar","doi":"10.1016/j.bbagrm.2025.195091","DOIUrl":"10.1016/j.bbagrm.2025.195091","url":null,"abstract":"<div><div>Cancer progression is a multifaceted process influenced by complex interactions within the tumor microenvironment (TME). Central to these dynamics are Vascular Endothelial Growth Factor (VEGF) signalling and microRNA (miRNA) modulation, both of which play critical roles in tumor growth and angiogenesis. VEGF is essential for promoting blood vessel formation; however, its splice variant, VEGF165b, acts as an anti-angiogenic factor, presenting a paradox challenging conventional cancer therapies. Meanwhile, miRNAs regulate gene expression that significantly impacts tumor behaviour by targeting various mRNAs involved in signalling pathways. The interplay between VEGF and miRNAs opens new avenues for targeted therapies designed to disrupt the networks supporting tumor growth. Additionally, the concept of exploiting the unique properties of VEGF splice variants is being explored to develop novel treatments that enhance anti-angiogenic effects while minimizing side effects. Understanding this is crucial for advancing personalized therapies that can effectively address the challenges posed by tumor adaptability and resistance mechanisms.</div></div>","PeriodicalId":55382,"journal":{"name":"Biochimica et Biophysica Acta-Gene Regulatory Mechanisms","volume":"1868 2","pages":"Article 195091"},"PeriodicalIF":2.6,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906728","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 crucial role of small heat shock proteins in prostate cancer: mechanisms and new therapeutic perspectives 小热休克蛋白在前列腺癌中的关键作用：机制和新的治疗前景

IF 2.6 3区生物学

Biochimica et Biophysica Acta-Gene Regulatory Mechanisms Pub Date : 2025-04-11 DOI: 10.1016/j.bbagrm.2025.195090

Yuankang Feng , Jialu Ma , Zhihao Bo , Dan Yue , Yong Wang

引用次数: 0