cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.12851846
title: 20-Hydroxyecdysone-responsive microRNAs of insects

description: 20-Hydroxyecdysone (20-HE) plays essential roles in coordinating developmental transitions of insects through responsive protein-coding genes and microRNAs (miRNAs). The involvement of single miRNAs in the ecdysone-signalling pathways has been extensively explored, but the interplay between ecdysone and the majority of miRNAs still remains largely unknown. Here, by small RNA sequencing, we systematically investigated the genome-wide responses of miRNAs to 20-HE in the embryogenic cell lines of <i>Bombyx mori</i> and <i>Drosophila melanogaster</i>. Over 60 and 70 20-HE-responsive miRNAs were identified in the BmE cell line and S2 cell line, respectively. The response of miRNAs to ecdysone exhibited a time-dependent pattern, and the response intensity increased with extending exposure to 20-HE. The relationship between ecdysone and the miRNAs was further explored through knockdown of ecdysone-signalling pathway genes. Specifically, ecdysone regulated the cluster miR-275 and miR-305 through the coordination of <i>BmEcR-B</i> and downstream <i>BmE75B</i>, and the interaction between <i>BmEcR</i> and miR-275 cluster was strengthened by the feedback regulation of <i>BmE75B</i>. Ecdysone induced miR-275-3p and miR-305-5p through the ecdysone response effectors (EcREs) at the upstream of the pre-miR-275 cluster. Overall, the results might help us further understand the relationship between ecdysone signalling pathways and small RNAs in the development and metamorphosis of insects.
DOI: 10.6084/m9.figshare.12851846.v1
title: 20-Hydroxyecdysone-responsive microRNAs of insects

description: 20-Hydroxyecdysone (20-HE) plays essential roles in coordinating developmental transitions of insects through responsive protein-coding genes and microRNAs (miRNAs). The involvement of single miRNAs in the ecdysone-signalling pathways has been extensively explored, but the interplay between ecdysone and the majority of miRNAs still remains largely unknown. Here, by small RNA sequencing, we systematically investigated the genome-wide responses of miRNAs to 20-HE in the embryogenic cell lines of <i>Bombyx mori</i> and <i>Drosophila melanogaster</i>. Over 60 and 70 20-HE-responsive miRNAs were identified in the BmE cell line and S2 cell line, respectively. The response of miRNAs to ecdysone exhibited a time-dependent pattern, and the response intensity increased with extending exposure to 20-HE. The relationship between ecdysone and the miRNAs was further explored through knockdown of ecdysone-signalling pathway genes. Specifically, ecdysone regulated the cluster miR-275 and miR-305 through the coordination of <i>BmEcR-B</i> and downstream <i>BmE75B</i>, and the interaction between <i>BmEcR</i> and miR-275 cluster was strengthened by the feedback regulation of <i>BmE75B</i>. Ecdysone induced miR-275-3p and miR-305-5p through the ecdysone response effectors (EcREs) at the upstream of the pre-miR-275 cluster. Overall, the results might help us further understand the relationship between ecdysone signalling pathways and small RNAs in the development and metamorphosis of insects.
DOI: 10.6084/m9.figshare.12851846.v3
title: 20-Hydroxyecdysone-responsive microRNAs of insects

description: 20-Hydroxyecdysone (20-HE) plays essential roles in coordinating developmental transitions of insects through responsive protein-coding genes and microRNAs (miRNAs). The involvement of single miRNAs in the ecdysone-signalling pathways has been extensively explored, but the interplay between ecdysone and the majority of miRNAs still remains largely unknown. Here, by small RNA sequencing, we systematically investigated the genome-wide responses of miRNAs to 20-HE in the embryogenic cell lines of <i>Bombyx mori</i> and <i>Drosophila melanogaster</i>. Over 60 and 70 20-HE-responsive miRNAs were identified in the BmE cell line and S2 cell line, respectively. The response of miRNAs to ecdysone exhibited a time-dependent pattern, and the response intensity increased with extending exposure to 20-HE. The relationship between ecdysone and the miRNAs was further explored through knockdown of ecdysone-signalling pathway genes. Specifically, ecdysone regulated the cluster miR-275 and miR-305 through the coordination of <i>BmEcR-B</i> and downstream <i>BmE75B</i>, and the interaction between <i>BmEcR</i> and miR-275 cluster was strengthened by the feedback regulation of <i>BmE75B</i>. Ecdysone induced miR-275-3p and miR-305-5p through the ecdysone response effectors (EcREs) at the upstream of the pre-miR-275 cluster. Overall, the results might help us further understand the relationship between ecdysone signalling pathways and small RNAs in the development and metamorphosis of insects.
DOI: 10.6084/m9.figshare.12851846.v2
title: 20-hydroxyecdysone-responsive microRNAs of insects

description: 20-hydroxyecdysone (20-HE) plays essential roles in coordinating developmental transitions of insects through responsive protein-coding genes and microRNAs (miRNAs). The involvement of single miRNAs in the ecdysone-signalling pathways has been extensively explored, but the interplay between ecdysone and the majority of miRNAs still remains largely unknown. Here by small RNA sequencing, we systematically investigated the genome-wide responses of miRNAs to 20-HE in the embryogenic cell lines of <i>Bombyx mori</i> and <i>Drosophila melanogaster</i>. Over 60 and 70 20-HE-responsive miRNAs were identified in the BmE cell line and S2 cell line, respectively. The response of miRNAs to ecdysone exhibited a time-dependent pattern, and the response intensity increased with extending exposure to 20-HE. The relationship between ecdysone and the miRNAs was further explored through knockdown of ecdysone-signalling pathway genes. Specifically, ecdysone regulated the cluster miR-275 and miR-305 through the coordination of <i>BmEcR-B</i> and downstream <i>BmE75B</i>, and the interaction between <i>BmEcR</i> and miR-275 cluster was strengthened by the feedback regulation of <i>BmE75B</i>. Ecdysone induced miR-275-3p and miR-305-5p through the ecdysone response effectors (EcREs) at the upstream of the pre-miR-275 cluster. Overall, the results might help us further understand the relationship between ecdysone signaling pathways and small RNAs in the development and metamorphosis of insects.
DOI: 10.6084/m9.figshare.12851855
title: Epigenomics-based identification of oestrogen-regulated long noncoding RNAs in ER+ breast cancer

description: Breast cancer is one of the most prevalent cancers in women worldwide. Through the regulation of many coding and non-coding target genes, oestrogen (E<sub>2</sub> or 17β-oestradiol) and its nuclear receptor ERα play important roles in breast cancer development and progression. Despite the astounding advances in our understanding of oestrogen-regulated coding genes over the past decades, our knowledge on oestrogen-regulated non-coding targets has just begun to expand. Here we leverage epigenomic approaches to systematically analyse oestrogen-regulated long non-coding RNAs (lncRNAs). Similar to the coding targets of ERα, the transcription of oestrogen-regulated lncRNAs correlates with the activation status of ERα enhancers, measured by eRNA production, chromatin accessibility, and the occupancy of the enhancer regulatory components including P300, MED1, and ARID1B. Our 3D chromatin architecture analyses suggest that lncRNAs and their neighbouring E<sub>2</sub>-resonsive coding genes, exemplified by LINC00160 and RUNX1, might be regulated as a 3D structural unit resulted from enhancer-promoter interactions. Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the oestrogen-regulated LINC00160 and its neighbouring RUNX1 might represent potential biomarkers for ER+ breast cancers.
DOI: 10.6084/m9.figshare.12851855.v1
title: Epigenomics-based identification of oestrogen-regulated long noncoding RNAs in ER+ breast cancer

description: Breast cancer is one of the most prevalent cancers in women worldwide. Through the regulation of many coding and non-coding target genes, oestrogen (E<sub>2</sub> or 17β-oestradiol) and its nuclear receptor ERα play important roles in breast cancer development and progression. Despite the astounding advances in our understanding of oestrogen-regulated coding genes over the past decades, our knowledge on oestrogen-regulated non-coding targets has just begun to expand. Here we leverage epigenomic approaches to systematically analyse oestrogen-regulated long non-coding RNAs (lncRNAs). Similar to the coding targets of ERα, the transcription of oestrogen-regulated lncRNAs correlates with the activation status of ERα enhancers, measured by eRNA production, chromatin accessibility, and the occupancy of the enhancer regulatory components including P300, MED1, and ARID1B. Our 3D chromatin architecture analyses suggest that lncRNAs and their neighbouring E<sub>2</sub>-resonsive coding genes, exemplified by LINC00160 and RUNX1, might be regulated as a 3D structural unit resulted from enhancer-promoter interactions. Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the oestrogen-regulated LINC00160 and its neighbouring RUNX1 might represent potential biomarkers for ER+ breast cancers.
DOI: 10.6084/m9.figshare.12851855.v3
title: Epigenomics-based identification of oestrogen-regulated long noncoding RNAs in ER+ breast cancer

description: Breast cancer is one of the most prevalent cancers in women worldwide. Through the regulation of many coding and non-coding target genes, oestrogen (E<sub>2</sub> or 17β-oestradiol) and its nuclear receptor ERα play important roles in breast cancer development and progression. Despite the astounding advances in our understanding of oestrogen-regulated coding genes over the past decades, our knowledge on oestrogen-regulated non-coding targets has just begun to expand. Here we leverage epigenomic approaches to systematically analyse oestrogen-regulated long non-coding RNAs (lncRNAs). Similar to the coding targets of ERα, the transcription of oestrogen-regulated lncRNAs correlates with the activation status of ERα enhancers, measured by eRNA production, chromatin accessibility, and the occupancy of the enhancer regulatory components including P300, MED1, and ARID1B. Our 3D chromatin architecture analyses suggest that lncRNAs and their neighbouring E<sub>2</sub>-resonsive coding genes, exemplified by LINC00160 and RUNX1, might be regulated as a 3D structural unit resulted from enhancer-promoter interactions. Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the oestrogen-regulated LINC00160 and its neighbouring RUNX1 might represent potential biomarkers for ER+ breast cancers.
DOI: 10.6084/m9.figshare.12851855.v2
title: Epigenomics-Based Identification of Estrogen-regulated Long Noncoding RNAs in ER+ Breast Cancer

description: Breast cancer is one of the most prevalent cancers in women worldwide. Through the regulation of many coding and non-coding target genes, estrogen (E<sub>2</sub> or 17β-estradiol) and its nuclear receptor ERα play important roles in breast cancer development and progression. Despite the astounding advances in our understanding of estrogen-regulated coding genes over the past decades, our knowledge on estrogen-regulated non-coding targets has just begun to expand. Here we leverage epigenomic approaches to systematically analyze estrogen-regulated long non-coding RNAs (lncRNAs).Similar to the coding targets of ERα, the transcription of estrogen-regulatedlncRNAs correlates with the activation status of ERα enhancers, measured by eRNA production, chromatin accessibility, and the occupancy of the enhancer regulatory components including P300, MED1, and ARID1B. Our 3D chromatin architecture analyses suggest that lncRNAs and their neighboring E<sub>2</sub>-resonsive coding genes, exemplified by LINC00160 and RUNX1, might be regulated as a 3D structural unit resulted from enhancer-promoter interactions. Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the estrogen-regulated LINC00160 and its neighboring RUNX1 might represent potential biomarkers for ER+ breast cancers.
DOI: 10.6084/m9.figshare.12851858
title: A newly identified duplex RNA unwinding activity of archaeal RNase J depends on processive exoribonucleolysis coupled steric occlusion by its structural archaeal loops

description: RNase J is a prokaryotic 5′-3′ exo/endoribonuclease that functions in mRNA decay and rRNA maturation. Here, we report a novel duplex unwinding activity of mpy-RNase J, an archaeal RNase J from <i>Methanolobus psychrophilus</i>, which enables it to degrade duplex RNAs with hairpins up to 40 bp when linking a 5′ single-stranded overhangs of ≥ 7 nt, corresponding to the RNA channel length. A 6-nt RNA-mpy-RNase J-S247A structure reveals the RNA-interacting residues and a steric barrier at the RNA channel entrance comprising two archaeal loops and two helices. Mutagenesis of the residues key to either exoribonucleolysis or RNA translocation diminished the duplex unwinding activity. Substitution of the residues in the steric barrier yielded stalled degradation intermediates at the duplex RNA regions. Thus, an exoribonucleolysis-driven and steric occlusion-based duplex unwinding mechanism was identified. The duplex unwinding activity confers mpy-RNase J the capability of degrading highly structured RNAs, including the bacterial REP RNA, and archaeal mRNAs, rRNAs, tRNAs, SRPs, RNase P and CD-box RNAs, providing an indicative of the potential key roles of mpy-RNase J in pleiotropic RNA metabolisms. Hydrolysis-coupled duplex unwinding activity was also detected in a bacterial RNase J, which may use a shared but slightly different unwinding mechanism from archaeal RNase Js, indicating that duplex unwinding is a common property of the prokaryotic RNase Js.
DOI: 10.6084/m9.figshare.12851858.v1
title: A newly identified duplex RNA unwinding activity of archaeal RNase J depends on processive exoribonucleolysis coupled steric occlusion by its structural archaeal loops

description: RNase J is a prokaryotic 5′-3′ exo/endoribonuclease that functions in mRNA decay and rRNA maturation. Here, we report a novel duplex unwinding activity of mpy-RNase J, an archaeal RNase J from <i>Methanolobus psychrophilus</i>, which enables it to degrade duplex RNAs with hairpins up to 40 bp when linking a 5′ single-stranded overhangs of ≥ 7 nt, corresponding to the RNA channel length. A 6-nt RNA-mpy-RNase J-S247A structure reveals the RNA-interacting residues and a steric barrier at the RNA channel entrance comprising two archaeal loops and two helices. Mutagenesis of the residues key to either exoribonucleolysis or RNA translocation diminished the duplex unwinding activity. Substitution of the residues in the steric barrier yielded stalled degradation intermediates at the duplex RNA regions. Thus, an exoribonucleolysis-driven and steric occlusion-based duplex unwinding mechanism was identified. The duplex unwinding activity confers mpy-RNase J the capability of degrading highly structured RNAs, including the bacterial REP RNA, and archaeal mRNAs, rRNAs, tRNAs, SRPs, RNase P and CD-box RNAs, providing an indicative of the potential key roles of mpy-RNase J in pleiotropic RNA metabolisms. Hydrolysis-coupled duplex unwinding activity was also detected in a bacterial RNase J, which may use a shared but slightly different unwinding mechanism from archaeal RNase Js, indicating that duplex unwinding is a common property of the prokaryotic RNase Js.
DOI: 10.6084/m9.figshare.12851885
title: Long non-coding RNA <i>TUG1</i> and its molecular mechanisms in polycystic ovary syndrome

description: Polycystic ovary syndrome (PCOS) causes anovulatory infertility in women of reproductive age, but etiopathogenesis of PCOS remains undetermined. Taurine up-regulated 1 (<i>TUG1</i>), an evolutionarily conserved long non-coding RNA, performs various biological functions; however, the role of <i>TUG1</i> in PCOS remains unclear. Herein, <i>TUG1</i> expression was assayed in granulosa cells (GCs) of 100 patients with PCOS and 100 control participants. Receiver operating characteristic (ROC) curve analysis was conducted to determine the diagnostic value of <i>TUG1</i> in PCOS. <i>TUG1</i> expression was also silenced in KGN cells to explore the role of <i>TUG1</i> in cellular proliferation, apoptosis, cell-cycle progression, autophagy, and steroidogenesis. We found that <i>TUG1</i> levels were dramatically increased in the PCOS group compared with those of the control group; this increased expression was related to a rising antral follicle count (R = 0.209, P &lt; 0.001 versus control). The ROC curve indicated a significant separation between PCOS group and the control group (AUC: 0.702; 95% CI: 0.630–0.773; P &lt; 0.001). <i>TUG1</i> showed a predominantly nuclear localization in human GCs. <i>TUG1</i> knockdown reduced cellular proliferation, and promoted MAPKs pathway-dependent apoptosis and P21-dependent autophagy, but may not affect cell-cycle progression. <i>TUG1</i> knockdown increased aromatase expression and oestradiol biosynthesis. Our results indicate that increased <i>TUG1</i> expression in PCOS GCs may contribute to excessive follicular activation and growth, and may disrupt the selection of dominant follicle. Our study shows that <i>TUG1</i> can be used as a diagnostic biomarker for PCOS.
DOI: 10.6084/m9.figshare.12851885.v1
title: Long non-coding RNA <i>TUG1</i> and its molecular mechanisms in polycystic ovary syndrome

description: Polycystic ovary syndrome (PCOS) causes anovulatory infertility in women of reproductive age, but etiopathogenesis of PCOS remains undetermined. Taurine up-regulated 1 (<i>TUG1</i>), an evolutionarily conserved long non-coding RNA, performs various biological functions; however, the role of <i>TUG1</i> in PCOS remains unclear. Herein, <i>TUG1</i> expression was assayed in granulosa cells (GCs) of 100 patients with PCOS and 100 control participants. Receiver operating characteristic (ROC) curve analysis was conducted to determine the diagnostic value of <i>TUG1</i> in PCOS. <i>TUG1</i> expression was also silenced in KGN cells to explore the role of <i>TUG1</i> in cellular proliferation, apoptosis, cell-cycle progression, autophagy, and steroidogenesis. We found that <i>TUG1</i> levels were dramatically increased in the PCOS group compared with those of the control group; this increased expression was related to a rising antral follicle count (R = 0.209, P &lt; 0.001 versus control). The ROC curve indicated a significant separation between PCOS group and the control group (AUC: 0.702; 95% CI: 0.630–0.773; P &lt; 0.001). <i>TUG1</i> showed a predominantly nuclear localization in human GCs. <i>TUG1</i> knockdown reduced cellular proliferation, and promoted MAPKs pathway-dependent apoptosis and P21-dependent autophagy, but may not affect cell-cycle progression. <i>TUG1</i> knockdown increased aromatase expression and oestradiol biosynthesis. Our results indicate that increased <i>TUG1</i> expression in PCOS GCs may contribute to excessive follicular activation and growth, and may disrupt the selection of dominant follicle. Our study shows that <i>TUG1</i> can be used as a diagnostic biomarker for PCOS.
DOI: 10.6084/m9.figshare.12851885.v3
title: Long non-coding RNA <i>TUG1</i> and its molecular mechanisms in polycystic ovary syndrome

description: Polycystic ovary syndrome (PCOS) causes anovulatory infertility in women of reproductive age, but etiopathogenesis of PCOS remains undetermined. Taurine up-regulated 1 (<i>TUG1</i>), an evolutionarily conserved long non-coding RNA, performs various biological functions; however, the role of <i>TUG1</i> in PCOS remains unclear. Herein, <i>TUG1</i> expression was assayed in granulosa cells (GCs) of 100 patients with PCOS and 100 control participants. Receiver operating characteristic (ROC) curve analysis was conducted to determine the diagnostic value of <i>TUG1</i> in PCOS. <i>TUG1</i> expression was also silenced in KGN cells to explore the role of <i>TUG1</i> in cellular proliferation, apoptosis, cell-cycle progression, autophagy, and steroidogenesis. We found that <i>TUG1</i> levels were dramatically increased in the PCOS group compared with those of the control group; this increased expression was related to a rising antral follicle count (R = 0.209, P &lt; 0.001 versus control). The ROC curve indicated a significant separation between PCOS group and the control group (AUC: 0.702; 95% CI: 0.630–0.773; P &lt; 0.001). <i>TUG1</i> showed a predominantly nuclear localization in human GCs. <i>TUG1</i> knockdown reduced cellular proliferation, and promoted MAPKs pathway-dependent apoptosis and P21-dependent autophagy, but may not affect cell-cycle progression. <i>TUG1</i> knockdown increased aromatase expression and oestradiol biosynthesis. Our results indicate that increased <i>TUG1</i> expression in PCOS GCs may contribute to excessive follicular activation and growth, and may disrupt the selection of dominant follicle. Our study shows that <i>TUG1</i> can be used as a diagnostic biomarker for PCOS.
DOI: 10.6084/m9.figshare.12851885.v2
title: Long non-coding RNA <i>TUG1</i> and its molecular mechanisms in polycystic ovary syndrome

description: Polycystic ovary syndrome (PCOS) causes anovulatory infertility in women of reproductive age, but etiopathogenesis of PCOS remains undetermined. Taurine up-regulated 1 (<i>TUG1</i>), an evolutionarily conserved long non-coding RNA, performs various biological functions; however, the role of <i>TUG1</i> in PCOS remains unclear. Herein, <i>TUG1</i> expression was assayed in granulosa cells (GCs) of 100 patients with PCOS and 100 control participants. Receiver operating characteristic (ROC) curve analysis was conducted to determine the diagnostic value of <i>TUG1</i> in PCOS. <i>TUG1</i> expression was also silenced in KGN cells to explore the role of <i>TUG1</i> in cellular proliferation, apoptosis, cell-cycle progression, autophagy, and steroidogenesis. We found that <i>TUG1</i> levels were dramatically increased in the PCOS group compared with those of the control group; this increased expression was related to a rising antral follicle count (R = 0.209, P &lt; 0.001 versus control). The ROC curve indicated a significant separation between PCOS group and the control group (AUC: 0.702; 95% CI: 0.630–0.773; P &lt; 0.001). <i>TUG1</i> showed a predominantly nuclear localization in human GCs. <i>TUG1</i> knockdown reduced cellular proliferation, and promoted MAPKs pathway-dependent apoptosis and P21-dependent autophagy, but may not affect cell-cycle progression. <i>TUG1</i> knockdown increased aromatase expression and estradiol biosynthesis. Our results indicate that increased <i>TUG1</i> expression in PCOS GCs may contribute to excessive follicular activation and growth, and may disrupt the selection of dominant follicle. Our study shows that <i>TUG1</i> can be used as a diagnostic biomarker for PCOS.