The Experts below are selected from a list of 522 Experts worldwide ranked by ideXlab platform
Evdokia Dimitriadis - One of the best experts on this subject based on the ideXlab platform.
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the long noncoding rna PTENP1 regulates human endometrial epithelial adhesive capacity in vitro implications in infertility
Biology of Reproduction, 2020Co-Authors: Masashi Takamura, Wei Zhou, Luk Rombauts, Evdokia DimitriadisAbstract:There is general consensus that the synchronous development of the embryo and endometrium is absolutely essential for successful implantation. Recent studies have strongly suggested that embryo-secreted factors are able to deliver into the endometrial cavity/endometrium and alter its protein profile in preparation for implantation. However, there is limited research focusing on long noncoding RNA (lncRNA) changes in the endometrium that brought about by the embryonic derived factors. It has been suggested that lncRNA has intricate interplay with microRNA (miR), small (~19-22 nucleotides), non-protein-coding RNA, to regulate protein production in the endometrium, thus controlling adhesive capacity. Here through microarray assays, we compare the lncRNA profile of the primary human endometrial epithelial cells (HEECs) that have been precultured with blastocyst-conditioned media (BCM) from embryos that implanted versus nonimplanted. Our data indicate a substantial change of lncRNA expression in HEECs, including 9 up-regulated and 12 down-regulated lncRNAs after incubation with implanted BCM. Selective knockdown of PTENP1, the most increased lncRNA after implanted BCM treatment in the HEECs, compromised the spheroid adhesion (P < 0.001). Characterization of PTENP1 confirmed its expression in the luminal epithelium with staining appeared most intense in the midsecretory phase. Furthermore, we have recorded a substantial change of miR profile upon PTENP1 knockdown in HEECs. Overexpression of miR-590-3p, a novel predicted target of PTENP1, impaired spheroid adhesion (P < 0.001). Collectively, these data have supported a novel regulation system that lncRNAs were able to participate in the regulation of implantation through association with miRs.
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The long noncoding RNA PTENP1 regulates human endometrial epithelial adhesive capacity in vitro: implications in infertility
Biology of reproduction, 2019Co-Authors: Masashi Takamura, Wei Zhou, Luk Rombauts, Evdokia DimitriadisAbstract:There is general consensus that the synchronous development of the embryo and endometrium is absolutely essential for successful implantation. Recent studies have strongly suggested that embryo-secreted factors are able to deliver into the endometrial cavity/endometrium and alter its protein profile in preparation for implantation. However, there is limited research focusing on long noncoding RNA (lncRNA) changes in the endometrium that brought about by the embryonic derived factors. It has been suggested that lncRNA has intricate interplay with microRNA (miR), small (~19-22 nucleotides), non-protein-coding RNA, to regulate protein production in the endometrium, thus controlling adhesive capacity. Here through microarray assays, we compare the lncRNA profile of the primary human endometrial epithelial cells (HEECs) that have been precultured with blastocyst-conditioned media (BCM) from embryos that implanted versus nonimplanted. Our data indicate a substantial change of lncRNA expression in HEECs, including 9 up-regulated and 12 down-regulated lncRNAs after incubation with implanted BCM. Selective knockdown of PTENP1, the most increased lncRNA after implanted BCM treatment in the HEECs, compromised the spheroid adhesion (P
Eileen M. Mcgowan - One of the best experts on this subject based on the ideXlab platform.
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PTEN/PTENP1: ‘Regulating the regulator of RTK-dependent PI3K/Akt signalling’, new targets for cancer therapy
Molecular cancer, 2018Co-Authors: Nahal Haddadi, Yiguang Lin, Glena Travis, Ann M. Simpson, Najah T. Nassif, Eileen M. McgowanAbstract:Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3 K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.
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pten PTENP1 regulating the regulator of rtk dependent pi3k akt signalling new targets for cancer therapy
Molecular Cancer, 2018Co-Authors: Nahal Haddadi, Yiguang Lin, Glena Travis, Ann M. Simpson, Najah T. Nassif, Eileen M. McgowanAbstract:Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3 K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.
Kevin V Morris - One of the best experts on this subject based on the ideXlab platform.
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A pseudogene long-noncoding-RNA network regulates PTEN transcription and translation in human cells
Nature Structural & Molecular Biology, 2013Co-Authors: Per Johnsson, Linda Vidarsdottir, Amanda Ackley, Weng-onn Lui, Martin Corcoran, Dan Grandér, Kevin V MorrisAbstract:PTEN is a tumor-suppressor gene that has been shown to be under the regulatory control of a PTEN pseudogene expressed noncoding RNA, PTENpg1. Here, we characterize a previously unidentified PTENpg1-encoded antisense RNA (asRNA), which regulates PTEN transcription and PTEN mRNA stability. We find two PTENpg1 asRNA isoforms, α and β. The α isoform functions in trans, localizes to the PTEN promoter and epigenetically modulates PTEN transcription by the recruitment of DNA methyltransferase 3a and Enhancer of Zeste. In contrast, the β isoform interacts with PTENpg1 through an RNA-RNA pairing interaction, which affects PTEN protein output through changes of PTENpg1 stability and microRNA sponge activity. Disruption of this asRNA-regulated network induces cell-cycle arrest and sensitizes cells to doxorubicin, which suggests a biological function for the respective PTENpg1 expressed asRNAs. The PTEN tumor-suppressor gene is regulated by the PTENpg1 long noncoding RNA. A new study investigating a previously uncharacterized PTENpg1-encoded antisense RNA (asRNA) now reveals that the asRNA α isoform functions as a negative regulator of PTEN transcription by recruiting chromatin remodelers and catalyzing H3K27me3 formation, whereas the asRNA β isoform interacts with PTENpg1, thereby affecting PTEN levels post-transcriptionally.
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a pseudogene long noncoding rna network regulates pten transcription and translation in human cells
Nature Structural & Molecular Biology, 2013Co-Authors: Per Johnsson, Linda Vidarsdottir, Amanda Ackley, Martin Corcoran, Dan Grandér, Kevin V MorrisAbstract:The PTEN tumor-suppressor gene is regulated by the PTENpg1 long noncoding RNA. A new study investigating a previously uncharacterized PTENpg1-encoded antisense RNA (asRNA) now reveals that the asRNA α isoform functions as a negative regulator of PTEN transcription by recruiting chromatin remodelers and catalyzing H3K27me3 formation, whereas the asRNA β isoform interacts with PTENpg1, thereby affecting PTEN levels post-transcriptionally.
Ping Xue - One of the best experts on this subject based on the ideXlab platform.
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Correction to: Exosomal miR-21 regulates the TETs/PTENP1/PTEN pathway to promote hepatocellular carcinoma growth.
Molecular cancer, 2020Co-Authors: Liang-qi Cao, Xue-wei Yang, Yu-bin Chen, Da-wei Zhang, Xiao-feng Jiang, Ping XueAbstract:Following the publication of article [1], the authors found that the images of Transwell Matrigel invasion (Fig. 7d) are incorrect.
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Exosomal miR-21 regulates the TETs/PTENP1/PTEN pathway to promote hepatocellular carcinoma growth.
Molecular cancer, 2019Co-Authors: Liang-qi Cao, Xue-wei Yang, Yu-bin Chen, Da-wei Zhang, Xiao-feng Jiang, Ping XueAbstract:As an important means of communication, exosomes play an important role in the development of hepatocellular carcinoma (HCC). Bioinformatics analysis, dual-luciferase reporter assays, methylation-specific quantitative PCR, and ChIP-PCR analysis were used to gain insight into the underlying mechanism of miR-21 in HCC. The detection of miRNAs in exosomes of HCC showed that miR-21 expression in exosomes was positively correlated with the expression level of miR-21 in cells and negatively correlated with the expression of its target genes PTEN, PTENP1 and TETs. HCC cell-derived exosomes could increase miR-21 and p-Akt expression in HCC cells and downregulate the expression of PTEN, PTENP1 and TETs. MiR-21 inhibitors or PTENP1 overexpression vectors could weaken the effect of the abovementioned exosomes and simultaneously weaken their role in promoting cell proliferation and migration and inhibiting apoptosis. Further studies showed that miR-21 not only directly regulated the expression of PTEN, PTENP1 and TETs but also increased the methylation level of the PTENP1 promoter by regulating the expression of TETs, thereby inhibiting the expression of PTENP1 and further downregulating the expression of PTEN. Exosomal miR-21 can regulate the expression of the tumor suppressor genes PTEN and PTENP1 in various ways and affect the growth of HCC cells.
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correction to exosomal mir 21 regulates the tets PTENP1 pten pathway to promote hepatocellular carcinoma growth
Molecular Cancer, 2019Co-Authors: Liang-qi Cao, Xue-wei Yang, Yu-bin Chen, Da-wei Zhang, Xiao-feng Jiang, Ping XueAbstract:Following the publication of article [1], the authors found that the images of Transwell Matrigel invasion (Fig. 7d) are incorrect.
Nahal Haddadi - One of the best experts on this subject based on the ideXlab platform.
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PTEN/PTENP1: ‘Regulating the regulator of RTK-dependent PI3K/Akt signalling’, new targets for cancer therapy
Molecular cancer, 2018Co-Authors: Nahal Haddadi, Yiguang Lin, Glena Travis, Ann M. Simpson, Najah T. Nassif, Eileen M. McgowanAbstract:Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3 K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.
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pten PTENP1 regulating the regulator of rtk dependent pi3k akt signalling new targets for cancer therapy
Molecular Cancer, 2018Co-Authors: Nahal Haddadi, Yiguang Lin, Glena Travis, Ann M. Simpson, Najah T. Nassif, Eileen M. McgowanAbstract:Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3 K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.