This study aimed to validate the experimental gene expression level of a common gene in the Aryl Hydrocarbon Receptor (AHR) and RELA in glioblastoma multiforme (GBM) using bioinformatics.
RNAseq data was analyzed to identify differentially expressed genes (DEGs), and LncRNAs related to the regulation of the founded gene were identified by the RNA Interactome Database. Ten healthy controls and 28 GBM patients' tissue samples were gathered, and the change in gene expression levels was measured by real-time PCR.
The results showed that MYBL2 is a common regulator between the AHR and RELA, and the expression of MYBL2, lnc-UCC, and lnc-HOTTIP genes was significantly increased in the GBM group.
Lnc-UCC expression showed significant positive correlations with MYBL2 and lnc-HOTTIP expression levels. Further investigation into these genes and their regulatory mechanisms is need.
{"title":"Introduction of MYBL2 as a common regulator between AHR and RELA: Its relationship with lnc-UCC and lnc-HOTTIP in glioblastoma multiforme","authors":"Ramin Soltani , Alireza Tabibkhooei , Morteza Hadizadeh , Sepideh Parvizpour , Roohallah Mahdi Esferizi , Sorayya Ghasemi","doi":"10.1016/j.genrep.2024.102046","DOIUrl":"10.1016/j.genrep.2024.102046","url":null,"abstract":"<div><div>This study aimed to validate the experimental gene expression level of a common gene in the Aryl Hydrocarbon Receptor (AHR) and RELA in glioblastoma multiforme (GBM) using bioinformatics.</div><div>RNAseq data was analyzed to identify differentially expressed genes (DEGs), and LncRNAs related to the regulation of the founded gene were identified by the RNA Interactome Database. Ten healthy controls and 28 GBM patients' tissue samples were gathered, and the change in gene expression levels was measured by real-time PCR.</div><div>The results showed that MYBL2 is a common regulator between the AHR and RELA, and the expression of MYBL2, lnc-UCC, and lnc-HOTTIP genes was significantly increased in the GBM group.</div><div>Lnc-UCC expression showed significant positive correlations with MYBL2 and lnc-HOTTIP expression levels. Further investigation into these genes and their regulatory mechanisms is need.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":null,"pages":null},"PeriodicalIF":1.0,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142425067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26DOI: 10.1016/j.genrep.2024.102045
Han Yang , Xuerong Sun , Lishan Xu, Shijun Yang, Fan Yan, Guangxiang Zhu, Yanzhi Jiang, Huailiang Xu, Jiayun Wu, Anxiang Wen, Meng Xie, Xue Liu, Qin Wang
Previously, the nr0b1 and nr0b2 genes have been identified in various animals and found to be closely associated with sex determination. In order to investigate the regulatory roles of nr0b1 and nr0b2 genes in the sex determination of Chinese giant salamander (CGS, Andrias davidianus), we obtained the full-length cDNA sequences of nr0b1 and nr0b2 through cloning, determined the characteristics of their tissue expressions and the responses of nr0b1 and nr0b2 to estradiol benzoate (EB) and 17α-methyltestosterone (MT) by using quantitative real-time PCR (qRT-PCR), and evaluated gonad development through histological sections. The full-lengths of cDNA of nr0b1/2 in CGS are separately 1278bp and 789bp. They have complete open reading frames (ORF) of 864bp and 774bp and encode 287 and 257 amino acids respectively. The 3' untranslated regions (UTR) are 276bp and 15bp, and the 5' UTR of nr0b1 is 138bp. In the 3' UTR of nr0b1, a putative polyadenylation signal (AATAAA) is identified. Tissue distribution analysis indicates that nr0b1 is mainly expressed in the pituitary, kidney, and testes, with significant differences between females (ZW-F) and males (ZZ-M) expression in the testes. On the other hand, nr0b2 is mainly expressed in the liver, followed by gonadal tissues. After immersion and feeding with EB and MT, EB's promotion on nr0b1 expression in CGS ovaries and testes is shown, by contrast MT only has a positive effect on nr0b2 in CGS testes. Histological sections show that after EB treatment, both genetic females (ZW-F) and sex-reversed females (ZZ-F) of CGS contain oogonia, indicating that EB can cause sex reversal in CGS; however, after MT treatment, no cellular morphological changes are observed either in genetic females (ZW-F) or in genetic males (ZW-M), indicating that this concentration cannot induce a shift in the sex ratio of CGS. These findings lay the foundation for further investigating the molecular mechanisms by which nr0b1/2 influence the differentiation and maintenance of CGS gonads.
{"title":"The expressions of nr0b1/2 genes in the Chinese giant salamander and their response to estradiol benzoate/17α-methyltestosterone treatment","authors":"Han Yang , Xuerong Sun , Lishan Xu, Shijun Yang, Fan Yan, Guangxiang Zhu, Yanzhi Jiang, Huailiang Xu, Jiayun Wu, Anxiang Wen, Meng Xie, Xue Liu, Qin Wang","doi":"10.1016/j.genrep.2024.102045","DOIUrl":"10.1016/j.genrep.2024.102045","url":null,"abstract":"<div><div>Previously, the <em>nr0b1</em> and <em>nr0b2</em> genes have been identified in various animals and found to be closely associated with sex determination. In order to investigate the regulatory roles of <em>nr0b1</em> and <em>nr0b2</em> genes in the sex determination of Chinese giant salamander (CGS, Andrias davidianus), we obtained the full-length cDNA sequences of <em>nr0b1</em> and <em>nr0b2</em> through cloning, determined the characteristics of their tissue expressions and the responses of <em>nr0b1</em> and <em>nr0b2</em> to estradiol benzoate (EB) and 17α-methyltestosterone (MT) by using quantitative real-time PCR (qRT-PCR), and evaluated gonad development through histological sections. The full-lengths of cDNA of <em>nr0b1/2</em> in CGS are separately 1278bp and 789bp. They have complete open reading frames (ORF) of 864bp and 774bp and encode 287 and 257 amino acids respectively. The 3' untranslated regions (UTR) are 276bp and 15bp, and the 5' UTR of <em>nr0b1</em> is 138bp. In the 3' UTR of <em>nr0b1</em>, a putative polyadenylation signal (AATAAA) is identified. Tissue distribution analysis indicates that <em>nr0b1</em> is mainly expressed in the pituitary, kidney, and testes, with significant differences between females (ZW-F) and males (ZZ-M) expression in the testes. On the other hand, <em>nr0b2</em> is mainly expressed in the liver, followed by gonadal tissues. After immersion and feeding with EB and MT, EB's promotion on <em>nr0b1</em> expression in CGS ovaries and testes is shown, by contrast MT only has a positive effect on <em>nr0b2</em> in CGS testes. Histological sections show that after EB treatment, both genetic females (ZW-F) and sex-reversed females (ZZ-F) of CGS contain oogonia, indicating that EB can cause sex reversal in CGS; however, after MT treatment, no cellular morphological changes are observed either in genetic females (ZW-F) or in genetic males (ZW-M), indicating that this concentration cannot induce a shift in the sex ratio of CGS. These findings lay the foundation for further investigating the molecular mechanisms by which <em>nr0b1/2</em> influence the differentiation and maintenance of CGS gonads.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":null,"pages":null},"PeriodicalIF":1.0,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142425066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26DOI: 10.1016/j.genrep.2024.102047
Amir Sadra Zangouei , Zahra Nasrpour Navaei , Fatemeh Taghavinia , Mohammad Reza Abbaszadegan , Meysam Moghbeli
Introduction
Prostate cancer (PCa) is considered as one of the leading causes of cancer related deaths among males globally. There is a high rate of tumor relapse and metastasis in PCa patients that is associated with chemo-resistance. Beside the elimination of tumor cells, chemotherapy has an adverse effect in normal cells. Therefore, it is required to clarify the molecular tumor biology to introduce novel markers to predict the drug response in PCa patients. Hippo signaling pathway is an important regulator of cell proliferation, migration, and drug response that can be modulated by microRNAs (miRNAs). Since, miR-506 deregulation has been reported in PCs, in the present study we assessed a probable role of miR-506 in regulation of Hippo signaling pathway during prostate tumor cell migration and drug resistance.
Materials and methods
The mRNA expression levels of Hippo signaling components were assessed in miR-506 ectopic expressed in comparison with control PC3 cells. Apoptosis assay, drug response, and cell migration were also assessed to find the role of miR-506 in prostate tumor cell aggressiveness.
Results
MiR-506 promoted the Hippo signaling pathway via TAZ and CTGF up regulations, while BIRC5, FAT, and C-MYC down regulations in PC3 cells. MiR-506 significantly reduced prostate tumor cell migration (p = 0.019) and Paclitaxel (TXL) resistance (p = 0.0006), while promoted apoptosis (p < 0.0001).
Conclusion
miR-506 exerted a tumor suppressor role during PCa progression by activation of Hippo pathway. MiR-506 targeted the FAT to activate the YAP/TAZ and nuclear translocation where it can bind with TEAD to up regulate the CTGF that resulted in reduced PCa cell migration. The WNT inhibition and C-MYC down regulation by the CTGF resulted in BIRC5 down regulation that induced apoptosis in PCa cells. Therefore, miR-506 can be introduced as a therapeutic marker in PCa following the confirmation by the animal studies and further clinical trials.
{"title":"MicroRNA-506 as a tumor suppressor in prostate cancer by regulation of Hippo signaling pathway","authors":"Amir Sadra Zangouei , Zahra Nasrpour Navaei , Fatemeh Taghavinia , Mohammad Reza Abbaszadegan , Meysam Moghbeli","doi":"10.1016/j.genrep.2024.102047","DOIUrl":"10.1016/j.genrep.2024.102047","url":null,"abstract":"<div><h3>Introduction</h3><div>Prostate cancer (PCa) is considered as one of the leading causes of cancer related deaths among males globally. There is a high rate of tumor relapse and metastasis in PCa patients that is associated with chemo-resistance. Beside the elimination of tumor cells, chemotherapy has an adverse effect in normal cells. Therefore, it is required to clarify the molecular tumor biology to introduce novel markers to predict the drug response in PCa patients. Hippo signaling pathway is an important regulator of cell proliferation, migration, and drug response that can be modulated by microRNAs (miRNAs). Since, miR-506 deregulation has been reported in PCs, in the present study we assessed a probable role of miR-506 in regulation of Hippo signaling pathway during prostate tumor cell migration and drug resistance.</div></div><div><h3>Materials and methods</h3><div>The mRNA expression levels of Hippo signaling components were assessed in miR-506 ectopic expressed in comparison with control PC3 cells. Apoptosis assay, drug response, and cell migration were also assessed to find the role of miR-506 in prostate tumor cell aggressiveness.</div></div><div><h3>Results</h3><div>MiR-506 promoted the Hippo signaling pathway via TAZ and CTGF up regulations, while BIRC5, FAT, and C-MYC down regulations in PC3 cells. MiR-506 significantly reduced prostate tumor cell migration (<em>p</em> = 0.019) and Paclitaxel (TXL) resistance (<em>p</em> = 0.0006), while promoted apoptosis (<em>p</em> < 0.0001).</div></div><div><h3>Conclusion</h3><div>miR-506 exerted a tumor suppressor role during PCa progression by activation of Hippo pathway. MiR-506 targeted the FAT to activate the YAP/TAZ and nuclear translocation where it can bind with TEAD to up regulate the CTGF that resulted in reduced PCa cell migration. The WNT inhibition and C-MYC down regulation by the CTGF resulted in BIRC5 down regulation that induced apoptosis in PCa cells. Therefore, miR-506 can be introduced as a therapeutic marker in PCa following the confirmation by the animal studies and further clinical trials.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":null,"pages":null},"PeriodicalIF":1.0,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142358034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-24DOI: 10.1016/j.genrep.2024.102036
Kazeem A. Alayande, Ivan Schutte, Prudent Mokgokong, Rasheed Adeleke
Comparative genomics was carried out between Bacillus velezensis KV10 and KV15 endophytes isolated from Elytropappus rhinocerotis. The nucleotides from the isolates were sequenced on an Illumina platform and assembled using SPAdes. Taxonomical identification was determined by a measure of evolutionary distance and codon-based phylogenetic trees. Sequence alignment against a representative isolate was assessed with Mauve, and a unique genomic region was determined through genome BLAST against a representative strain using GView. Protein family sorter and comparative pathway tools assigned to RASTtk4 were used to align the shared proteins between the isolates. antiSMASH was used to identify gene clusters for the bioactive secondary metabolites. Identification of mutant variants was determined through SNP calling using BWA-MEM to align the reads and FreeBayes for high-quality variants. B. velezensis KV10 and KV15 have genome sizes of 3,992,370 bp and 3,880,685 bp, and GC contents of 46.37 % and 46.49 %, respectively. There are identified genetic and evolutionary dissimilarities between the two endophytic isolates. Nineteen proteins with well-defined functions were found unique to KV10, while a total of thirty-two proteins were found unique to KV15. Missense or synonymous point mutations were observed at different loci in the KV10 genome; all affected codons are involved in the formation of polyketide synthase and general stress protein (YdbA and YdbB). The affected genes by point mutations in the KV15 are YeeF and FliK. Both strains contain gene clusters putative for biosynthesis of specific antimicrobial metabolites such as difficidin, macrolactin, fengycin, bacillibactin, bacillaene, and bacilysin. While only KV10 has additional gene clusters for mersacidin and surfactin biosynthesis. In addition, biosynthetic metabolites extracted from both strains exhibited notable antimicrobial effectiveness against test Serratia marcescens and Fusarium sp. Both isolates exhibit putative genetic features and are supported by in vitro assessment as promising candidates for biocontrol agents.
{"title":"Comparative genome composition of two closely related biocontrol strains of Bacillus velezensis endophytes","authors":"Kazeem A. Alayande, Ivan Schutte, Prudent Mokgokong, Rasheed Adeleke","doi":"10.1016/j.genrep.2024.102036","DOIUrl":"10.1016/j.genrep.2024.102036","url":null,"abstract":"<div><div>Comparative genomics was carried out between <em>Bacillus velezensis</em> KV10 and KV15 endophytes isolated from <em>Elytropappus rhinocerotis.</em> The nucleotides from the isolates were sequenced on an Illumina platform and assembled using SPAdes. Taxonomical identification was determined by a measure of evolutionary distance and codon-based phylogenetic trees. Sequence alignment against a representative isolate was assessed with Mauve, and a unique genomic region was determined through genome BLAST against a representative strain using GView. Protein family sorter and comparative pathway tools assigned to RASTtk4 were used to align the shared proteins between the isolates. antiSMASH was used to identify gene clusters for the bioactive secondary metabolites. Identification of mutant variants was determined through SNP calling using BWA-MEM to align the reads and FreeBayes for high-quality variants. <em>B. velezensis</em> KV10 and KV15 have genome sizes of 3,992,370 bp and 3,880,685 bp, and GC contents of 46.37 % and 46.49 %, respectively. There are identified genetic and evolutionary dissimilarities between the two endophytic isolates. Nineteen proteins with well-defined functions were found unique to KV10, while a total of thirty-two proteins were found unique to KV15. Missense or synonymous point mutations were observed at different loci in the KV10 genome; all affected codons are involved in the formation of polyketide synthase and general stress protein (<em>YdbA</em> and <em>YdbB</em>). The affected genes by point mutations in the KV15 are <em>YeeF</em> and <em>FliK.</em> Both strains contain gene clusters putative for biosynthesis of specific antimicrobial metabolites such as difficidin, macrolactin, fengycin, bacillibactin, bacillaene, and bacilysin. While only KV10 has additional gene clusters for mersacidin and surfactin biosynthesis. In addition, biosynthetic metabolites extracted from both strains exhibited notable antimicrobial effectiveness against test <em>Serratia marcescens</em> and <em>Fusarium</em> sp. Both isolates exhibit putative genetic features and are supported by in vitro assessment as promising candidates for biocontrol agents.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":null,"pages":null},"PeriodicalIF":1.0,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142326796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-24DOI: 10.1016/j.genrep.2024.102044
Anubhuti Jha, Awanish Kumar
Candida albicans, a dimorphic opportunistic fungal pathogen, poses a significant threat to immunocompromised patients, with infections becoming increasingly severe due to the emergence of multi-drug resistance and the lack of effective treatments. This study investigates the antifungal properties of piperazine, a heterocyclic organic compound, and its mechanism of action against Candida species. In silico molecular docking, analysis was conducted to evaluate the interaction between piperazine and cell wall synthesis proteins, complemented by pharmacokinetic ADMET studies to assess its potential as a drug candidate. The minimum inhibitory concentration for eight Candida species ranged from 256 to 512 μg/mL. Morphological changes in C. albicans treated with piperazine were observed using scanning electron microscopy, revealing significant cell wall damage. Our findings suggest that piperazine could serve as a potential cell wall-targeting antifungal agent, potentially expanding the current arsenal of antifungal therapies.
{"title":"Piperazine reveals as a cell wall targeting antifungal agent against Candida albicans","authors":"Anubhuti Jha, Awanish Kumar","doi":"10.1016/j.genrep.2024.102044","DOIUrl":"10.1016/j.genrep.2024.102044","url":null,"abstract":"<div><div><em>Candida albicans</em>, a dimorphic opportunistic fungal pathogen, poses a significant threat to immunocompromised patients, with infections becoming increasingly severe due to the emergence of multi-drug resistance and the lack of effective treatments. This study investigates the antifungal properties of piperazine, a heterocyclic organic compound, and its mechanism of action against <em>Candida</em> species. In silico molecular docking, analysis was conducted to evaluate the interaction between piperazine and cell wall synthesis proteins, complemented by pharmacokinetic ADMET studies to assess its potential as a drug candidate. The minimum inhibitory concentration for eight <em>Candida</em> species ranged from 256 to 512 μg/mL. Morphological changes in <em>C. albicans</em> treated with piperazine were observed using scanning electron microscopy, revealing significant cell wall damage. Our findings suggest that piperazine could serve as a potential cell wall-targeting antifungal agent, potentially expanding the current arsenal of antifungal therapies.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":null,"pages":null},"PeriodicalIF":1.0,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142358035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Low temperature stress negatively impacts plant growth and development, reducing crop yields by disrupting metabolite production and accumulation. Cassia obtusifolia L., a widely cultivated medicinal plant in subtropical regions, is particularly vulnerable to such stress. Methyl jasmonate (MeJA) regulates plant growth, defense mechanisms, and secondary metabolite production. This study investigated how C. obtusifolia responds to low temperature stress under MeJA treatment using transcriptomic and metabolomic approaches. MeJA treatment upregulated several transcription factor families, including APE/ERF-ERF, WRKY, NAC, and MYB-related, which modulated the plant's response to cold stress. These transcription factors influenced the expression of genes involved in glycolysis, sugar metabolism, and amino acid pathways, contributing to the plant's adaptive responses. Differentially expressed genes were associated with key metabolic processes such as flavonoid biosynthesis, ribosome function, glycolysis/gluconeogenesis, and sugar metabolism. Using H-NMR and LC-MS techniques, we observed that MeJA induced the accumulation of sugars and amino acids in the leaves of C. obtusifolia seedlings under cold stress, while levels of three flavonoid compounds Isoliquiritigenin, Kaempferol-7-O-glucoside, and Phloretin significantly decreased. Enrichment analysis indicated that MeJA modulates the biosynthetic pathways of these compounds in a dose-dependent manner. Integrating metabolomic and transcriptomic data further elucidated alterations in the flavonoid biosynthetic network and other metabolic pathways under low temperature stress. These findings offer insights into the molecular mechanisms underlying flavonoid synthesis and other metabolic adjustments in C. obtusifolia under MeJA treatment.
低温胁迫会对植物的生长和发育产生负面影响，通过破坏代谢产物的产生和积累而降低作物产量。决明子是亚热带地区广泛种植的药用植物，特别容易受到这种胁迫的影响。茉莉酸甲酯（MeJA）能调节植物的生长、防御机制和次生代谢物的产生。本研究采用转录组学和代谢组学方法，研究了在 MeJA 处理下 C. obtusifolia 如何应对低温胁迫。MeJA 处理可上调多个转录因子家族，包括 APE/ERF-ERF、WRKY、NAC 和 MYB 相关因子，从而调节植物对低温胁迫的响应。这些转录因子影响了参与糖酵解、糖代谢和氨基酸途径的基因的表达，促进了植物的适应性反应。差异表达的基因与黄酮类化合物生物合成、核糖体功能、糖酵解/糖醛酸生成和糖代谢等关键代谢过程有关。利用 H-NMR 和 LC-MS 技术，我们观察到 MeJA 诱导了冷胁迫下 C. obtusifolia 幼苗叶片中糖和氨基酸的积累，而三种黄酮类化合物 Isoliquiritigenin、Kaempferol-7-O-glucoside 和 Phloretin 的水平显著下降。富集分析表明，MeJA 以剂量依赖的方式调节了这些化合物的生物合成途径。整合代谢组和转录组数据进一步阐明了低温胁迫下类黄酮生物合成网络和其他代谢途径的变化。这些研究结果有助于深入了解在 MeJA 处理下 C. obtusifolia 中黄酮类化合物合成和其他代谢调整的分子机制。
{"title":"Transcriptomic and metabolomic investigations of methyl jasmonate-mediated enhancement of low temperature stress resistance in Cassia obtusifolia L.","authors":"Yue Zhang , Weiling Jiang , Abdullah, Biru Shi, Yuan Gao, Xia Yang, Zhimei Xing, Tingting Zhang, Lifeng Han, Xiaoxuan Tian","doi":"10.1016/j.genrep.2024.102040","DOIUrl":"10.1016/j.genrep.2024.102040","url":null,"abstract":"<div><div>Low temperature stress negatively impacts plant growth and development, reducing crop yields by disrupting metabolite production and accumulation. <em>Cassia obtusifolia</em> L., a widely cultivated medicinal plant in subtropical regions, is particularly vulnerable to such stress. Methyl jasmonate (MeJA) regulates plant growth, defense mechanisms, and secondary metabolite production. This study investigated how <em>C. obtusifolia</em> responds to low temperature stress under MeJA treatment using transcriptomic and metabolomic approaches. MeJA treatment upregulated several transcription factor families, including APE/ERF-ERF, WRKY, NAC, and MYB-related, which modulated the plant's response to cold stress. These transcription factors influenced the expression of genes involved in glycolysis, sugar metabolism, and amino acid pathways, contributing to the plant's adaptive responses. Differentially expressed genes were associated with key metabolic processes such as flavonoid biosynthesis, ribosome function, glycolysis/gluconeogenesis, and sugar metabolism. Using H-NMR and LC-MS techniques, we observed that MeJA induced the accumulation of sugars and amino acids in the leaves of <em>C. obtusifolia</em> seedlings under cold stress, while levels of three flavonoid compounds Isoliquiritigenin, Kaempferol-7-O-glucoside, and Phloretin significantly decreased. Enrichment analysis indicated that MeJA modulates the biosynthetic pathways of these compounds in a dose-dependent manner. Integrating metabolomic and transcriptomic data further elucidated alterations in the flavonoid biosynthetic network and other metabolic pathways under low temperature stress. These findings offer insights into the molecular mechanisms underlying flavonoid synthesis and other metabolic adjustments in <em>C. obtusifolia</em> under MeJA treatment.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":null,"pages":null},"PeriodicalIF":1.0,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142425065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-21DOI: 10.1016/j.genrep.2024.102042
Hengrui Liu , Zheng Guo , Panpan Wang
Cancer research is profoundly influenced by the complex interplay of gene expression, yet conventional studies often emphasize genes with high expression levels, potentially overlooking those that contribute subtly to tumorigenesis. This review challenges the standard paradigms by questioning the direct causality often attributed to high gene expression in cancer progression and underscores the importance of distinguishing correlation from causation. It highlights how traditional bulk data analysis might mask crucial cell-specific gene activities, a limitation increasingly addressed by emerging single-cell and spatial transcriptomics, albeit with their own inherent challenges. Additionally, the review delves into the critical roles of both oncogenes and tumor driver genes, advocating for a precise differentiation in research and therapy. Furthermore, it discusses the revolutionary impact of CRISPR technology in identifying essential genes for cancer cell survival, which, while crucial, may not necessarily drive cancer. The complexities of epigenetic regulation and the discrepancies between mRNA and protein expression levels are also explored, emphasizing the necessity for integrated approaches that combine transcriptomics, proteomics, and computational models. This integrated perspective is vital for developing targeted therapies that address the multifaceted nature of gene expression and its regulation in cancer, aiming to refine therapeutic strategies and enhance clinical outcomes.
{"title":"Genetic expression in cancer research: Challenges and complexity","authors":"Hengrui Liu , Zheng Guo , Panpan Wang","doi":"10.1016/j.genrep.2024.102042","DOIUrl":"10.1016/j.genrep.2024.102042","url":null,"abstract":"<div><div>Cancer research is profoundly influenced by the complex interplay of gene expression, yet conventional studies often emphasize genes with high expression levels, potentially overlooking those that contribute subtly to tumorigenesis. This review challenges the standard paradigms by questioning the direct causality often attributed to high gene expression in cancer progression and underscores the importance of distinguishing correlation from causation. It highlights how traditional bulk data analysis might mask crucial cell-specific gene activities, a limitation increasingly addressed by emerging single-cell and spatial transcriptomics, albeit with their own inherent challenges. Additionally, the review delves into the critical roles of both oncogenes and tumor driver genes, advocating for a precise differentiation in research and therapy. Furthermore, it discusses the revolutionary impact of CRISPR technology in identifying essential genes for cancer cell survival, which, while crucial, may not necessarily drive cancer. The complexities of epigenetic regulation and the discrepancies between mRNA and protein expression levels are also explored, emphasizing the necessity for integrated approaches that combine transcriptomics, proteomics, and computational models. This integrated perspective is vital for developing targeted therapies that address the multifaceted nature of gene expression and its regulation in cancer, aiming to refine therapeutic strategies and enhance clinical outcomes.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":null,"pages":null},"PeriodicalIF":1.0,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142314809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-20DOI: 10.1016/j.genrep.2024.102038
Qingtao Ni , Yida Qian , Tongbo Yi , Jian Zhou , Kai Sang , Chi Pan
Introduction
MicroRNAs (miRNAs) are potential candidate clinical biomarkers for many diseases. This study explored the role and potential mechanisms of miR-16-5p in triple-negative breast cancer (TNBC).
Results
The expression of miR-16-5p was lower in wax block sections obtained from 47 TNBC patient samples. Overexpression of miR-16-5p decreased the migratory abilities and the cell proliferation in MDA-MB-231 cells. We found miR-16-5p modulated TP53 and LncRNA-NEAT1 in bioinformatics analysis. In transfection experiments, the higher expression of lncRNA-NEAT1 and TP53 were observed in miR-16-5p inhibitor group.
Conclusion
Our data demonstrated that miR-16-5p was lowly expressed and acted as a tumor suppressor in TNBC. Moreover, miR-16-5p regulated TNBC cell proliferation and migratory capacity by modulating TP53 and lncRNA-NEAT1 in vitro.
{"title":"miR-16-5p may modulate migration and proliferation through TP53 and LncRNA-NEAT1 in triple-negative breast cancer","authors":"Qingtao Ni , Yida Qian , Tongbo Yi , Jian Zhou , Kai Sang , Chi Pan","doi":"10.1016/j.genrep.2024.102038","DOIUrl":"10.1016/j.genrep.2024.102038","url":null,"abstract":"<div><h3>Introduction</h3><div>MicroRNAs (miRNAs) are potential candidate clinical biomarkers for many diseases. This study explored the role and potential mechanisms of miR-16-5p in triple-negative breast cancer (TNBC).</div></div><div><h3>Results</h3><div>The expression of miR-16-5p was lower in wax block sections obtained from 47 TNBC patient samples. Overexpression of miR-16-5p decreased the migratory abilities and the cell proliferation in MDA-MB-231 cells. We found miR-16-5p modulated TP53 and LncRNA-NEAT1 in bioinformatics analysis. In transfection experiments, the higher expression of lncRNA-NEAT1 and TP53 were observed in miR-16-5p inhibitor group.</div></div><div><h3>Conclusion</h3><div>Our data demonstrated that miR-16-5p was lowly expressed and acted as a tumor suppressor in TNBC. Moreover, miR-16-5p regulated TNBC cell proliferation and migratory capacity by modulating TP53 and lncRNA-NEAT1 in vitro.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":null,"pages":null},"PeriodicalIF":1.0,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142310856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-19DOI: 10.1016/j.genrep.2024.102041
Burçin Erkal Çam , Tuğba Elgün , Tuğba Kul Köprülü , Arzu Çoban , Şenay Vural Korkut
Introduction
Multiple Sclerosis (MS) is an autoimmune disease that affects the central nervous system (CNS), characterized by chronic inflammation, demyelination, and neurodegeneration. In recent years, among non-coding RNAs miRNA have emerged as key regulators of different biological processes and it has been suggested that they play an important role in the mechanisms underlying MS pathogenesis. Through in silico methods, miR-629-5p and miR-98-5p were identified as significant factors in MS pathology. The aim of this study was to examine the levels of expression of miR-629-5p and miR-98-5p in blood samples obtained from patients with relapsing–remitting MS. Methods: Total blood were recruited from RRMS and control group and qPCR analysis was used for evaluating of target miRNAs expression. The mirDIP database was utilized to identify the target genes. Hub genes were identified with the Cytoscape and target pathways were identified using the STRING. Results: Expression analysis revealed a significant upregulation of miR-629-5p and miR-98-5p (FC ≥ 1.5 and p < 0.05) in patients with RRMS. PI3K-Akt, Rap1, MAPK and FoxO signaling pathways were found as target. Discussion: The discovery of these miRNAs suggests that they may have a notable impact on MS patients by intervening on pathways involved in both the immune and nervous systems.
{"title":"miR-98 and miR-629 can be used as a potential biomarker on relapsing-remitting multiple sclerosis patients","authors":"Burçin Erkal Çam , Tuğba Elgün , Tuğba Kul Köprülü , Arzu Çoban , Şenay Vural Korkut","doi":"10.1016/j.genrep.2024.102041","DOIUrl":"10.1016/j.genrep.2024.102041","url":null,"abstract":"<div><h3>Introduction</h3><div>Multiple Sclerosis (MS) is an autoimmune disease that affects the central nervous system (CNS), characterized by chronic inflammation, demyelination, and neurodegeneration. In recent years, among non-coding RNAs miRNA have emerged as key regulators of different biological processes and it has been suggested that they play an important role in the mechanisms underlying MS pathogenesis. Through in silico methods, miR-629-5p and miR-98-5p were identified as significant factors in MS pathology. The aim of this study was to examine the levels of expression of miR-629-5p and miR-98-5p in blood samples obtained from patients with relapsing–remitting MS. Methods: Total blood were recruited from RRMS and control group and qPCR analysis was used for evaluating of target miRNAs expression. The mirDIP database was utilized to identify the target genes. Hub genes were identified with the Cytoscape and target pathways were identified using the STRING. Results: Expression analysis revealed a significant upregulation of miR-629-5p and miR-98-5p (FC ≥ 1.5 and <em>p</em> < 0.05) in patients with RRMS. PI3K-Akt, Rap1, MAPK and FoxO signaling pathways were found as target. Discussion: The discovery of these miRNAs suggests that they may have a notable impact on MS patients by intervening on pathways involved in both the immune and nervous systems.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":null,"pages":null},"PeriodicalIF":1.0,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142314810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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