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The aim of this study was to determine whether the polymorphic expression of NB1 GP is due to CD177 gene deletions and duplications. Quantitative real-time PCR determined the number of copies of exon 2 of CD177, an exon that is unique to this gene, and the number of copies of exon 9 of CD177, an exon that is present in both CD177 and pseudogene. In 7 of the 12 subjects, the ratio between the number of copies of sequences homologous to CD177 exon 9 was 1. 5 or greater, indicating that both CD177 and the homologous pseudogene were present. In the other 5 subjects, the ratio of exon 9 to exon 2 varied from 1 to exon 2, indicating that the pseudogene was not present in these subjects.
Source link: https://doi.org/10.21307/immunohematology-2019-492
This report examines the remarkably high prevalence of multiple pseudogene expression in the rat ovary during the cascade of functional gene expression in the rat ovary in reaction to an ovulation-stimulating dose of gonadotropin. The 12-h ovulatory process was started by 10 IU chorionic gonadotropin subcutaneously by Immature Wistar rats, and 48 h later, the 12-h ovulatory process was initiated by 10 IU hCG subcutaneously. Gene expression in the ovarian tissue was found by RT-PCR differentiation analysis, which was used for RT-PCR discrimination analysis. 12 of the 22 clones tested here share high sequence similarity to Cyp21a1-ps' cytochrome P450 pseudogene Cyp21a1-ps, while 5 of the five clones have high sequence similarity to both the Cyp21a1-ps and the aldo reductase gene Akr1c6. The remaining five clones were clones of the endogenous retrovirus SC1 (which has prominently infested the rat genome).
Source link: https://doi.org/10.1677/joe-08-0108
ABSTRACT Four hirsute females from a family with an idiopathic dominant hirsutism family were investigated. Basal blood pressures of u0394 5 and 44% were within the normal range, but ACTH stimulation led to rises in 17-hydroxypregnenolone and dehydroepiandrosterone, both at dangerous levels that were significantly above control levels. A novel homologue of exon 3 of 3 b2-HSD was found in a study of PCR amplification products by denaturing gradient gel electrophoresis and sequencing results. The novel homologue of one of the patients' was used to create a genomic library in u03bb gem11 and clones containing the novel homologue were obtained and partially sequenced. Both patient and control were identical and homologous to exons 2u20134 of human 3b2-HSD types I and II. In the PCR primer sites flanking the exon 3 homologue that resulted in its detection on DGGE gels, there was no difference.
Source link: https://doi.org/10.1677/jme.0.0150167
We hypothesized that NANOGP8 transcription in prostate cancer cells could be controlled by its 5u2019-flanking sequences, and that cells with activation of these sequences should have NANOGP8 functions in cell growth and tumor formation, according to this research. To replace the CMV promoter, we cloned a 5kb piece of NANOGP8's 5kb region of 5u2019-flanking area of 5Kb from a PAC clone containing the entire NANOGP8 gene and inserted the fragment into the pEGFP vector. In the two populations, the EGFP positive cells were isolated from EGFP negative cells by flow cytometry, and the expression of NANOG was determined by real-time RT-PCR. In EGFP positive cells, the RNA expression of NANOG was 3. 5 fold higher than in EGFP negative cells. In the EGFP negative subset, the colony formation in the EGFP positive DU145 subset was 24% relative to 13. 4%. In the EGFP positive DU145 sub-subject, sphere formation in the EGFP positive sub-subjective subscript was 40% higher than that in the EGFP negative subpoena. A tumor was discovered in all 14 mice after 15 weeks, after 15 weeks, with EGFP negative cells; however, a tumor was found in 11 of 14 mice. Tumor volume and weight were 5. 3 and 7. 5 fold higher than in EGFP negative cells, respectively, according to a review of tumor volume and weight. All analyzed tumor samples from mice injected with EGFP negative cells became EGFP positive, according to the further investigation of EGFP expression in collected xenograph tumors.
Source link: https://doi.org/10.1158/1538-7445.am2013-4903
Since recent studies have shown that POU5F1B mRNA is present in several types of cancer tissues, the oncogenic role remains unclear. POU5F1B, which is located on the side of the MYC gene on 8q24, has been regularly involved in MYC amplicons in gastric cancer, according to We discovered that POU5F1B, which is located on the other side of the MYC gene on 8q24, was often involved in MYC amplicons in gastric cancer. In several gastric cancer cell lines, POU5F1B and MYC genes were highly amplified, according to gene copy number analysis. In addition, the POU5F1B mRNA expression levels were upregulated using PCR and sequencing analyses. We hypothesized that gene amplification of POU5F1B mediates certain biological functions in cancer cells, as shown by the following. We integrated POU5F1B gene into SNU-16 or TU-KATO III gastric cancer cell lines and established stable cell lines SNU-16/GFP, TU-KATO III/GFP, and /POU5F1B. Interestingly, we discovered that POU5F1B's increasing gene copy number in 180 cases of gastric cancer.
Source link: https://doi.org/10.1158/1538-7445.am2012-424
qRT-PCR was performed in 15 breast cancer cell lines using custom-designed SYBR assays. In 44 normal and breast tumour tissues from patients recruited from the University of Chicago Breast SPORE using custom-designed TaqMan CNV assays, physiological copy number alterations were investigated in 44 normal and breast tumour tissues from patients recruited from the U. Chicago Breast SPORE. In bioengineered breast cancer cells with BRCA1P1 over-expression, cell proliferation and invasion assays were carried out. Results: We investigated the genome of a pseudogene of breast cancer susceptibility protein1 duplicated from the functional gene but with only three exons apiece. In the exon 1a, comparison of DNA sequences revealed that BRCA1P1 is a fusion pseudogene with 343 bp sequences of 60S acidic ribosomal protein inserted in the exon 1a. BRCA1P1 is ubiquitously transcribed in human normal tissues and highly expressed in breast cancer cell lines, and is also present in breast cancer cell lines. BRCA1P1 amplification events were recorded in breast tumor DNAs, although no amplification was observed in normal breast tissue tissues. BRCA1P1 amplification may have a role in breast cancer rises, according to the results. In cells that had BRCA1P1 over-expression relative to cells transfected with control vectors, a substantial rise in cell proliferation was observed. To clarify cell proliferation regulation by BRCA1P1 and other miRNAs, we're currently doing microarray as well as investigating the pseudogene interaction with BRCA1, RPLP1, or other miRNAs. A better understanding of pseudogenes and elucidation of pathways triggered by BRCA1P1 pseudogene could advance the field of cancer biology and may reveal new targets for preventive and therapeutic interventions of human breast cancer.
Source link: https://doi.org/10.1158/1538-7445.am2012-200
We've re-sequenced the exon regions of wild type POU5F1 on chromosome 6, 8, 10, and 12, as well as six of its six closest cousin pseudogenes, including POU5F1P1, 8, 10, and 12, as well as identifying sequence variants unique to POU5F1P1 for which we have developed and confirmed expression of the POU5F1P1 transcript on 8q24, and reported sequence variants on chromosome 6 and confirmed and reported sequence variantsed sed the exon regions of wild type POU5F1P1's 1, 8, 10, 8, 10 and its six chromosome 6 and 12 and 12 on chromosome 6 and 12 on chromosome 6 on chromosome 6C1P1P1P1P1P1P1P1P1P1P1P1P1P1P1P1P1 transcript on 8q1P1P1 POU5F1P1P1P1P1 and confirmed expression of POU5F1P1P POU5F1 and pseudogene POU5F1P1 is approximately 97% homologous. We discovered uncommon copy number variants throughout this region by using TaqMan DNA copy number variation assays. Both POU5F1P1 and POU5F1P1were were further tested in 14 colon cancer cell lines, of which two, DLD-1 and KM12, expressed POU5F1P1 but no wild type POU5F1. We knocked down POU5F1P1 expression in DLD-1 and KM12, which resulted in a decrease in colon cancer cell proliferation and anchorage-independent growth of colon cancer cells using shRNA technology.
Source link: https://doi.org/10.1158/1538-7445.am2012-117
We hypothesized that NANOGP8 transcription could be controlled by a promoter-like region in its 5th-flanking sequences and cells with activation of these sequences, resulting in increased cell growth and sphere formation in this study. We first established if the expressed NANOG in prostate cancer comes from NANOGP8 to test this theory. RT-PCR was carried out using RNA obtained from prostate cell lines PC3 and DU145, and primary culture of normal and cancerous prostate cells with primers spanning both the whole code region and the 3u2019UTR. In cancer cells and normal prostate cells, the 1. 6kb PCR products were sequenced, showing that the NANOG RNA was transcribed from NANOGP8 and not from NANOG. Following generation with G418, the EGFP positive cells were separated from EGFP negative cells by flow cytometry and expression of NANOG were analyzed by real-time RT-PCR in the two populations. The RNA expression of NANOG in EGFP positive DU145 and PC3 cells was 3. 5 fold and 1. 5 fold higher than in EGFP negative cells, respectively. The colony growth in the EGFP positive subset was 24% relative to 13. 4% in the EGFP negative subset, according to a DU145 stably transfected cell line. Similarly, sphere formation in the EGFP positive DU145 cell subset was 40% higher than that in the EGFP negative subset. The 5u2019-flanking sequence of NANOGP8 may have a role in the expression of the NANOGP8 gene in prostate cancer cells and in the regulation of cancer stem cell stem cells.
Source link: https://doi.org/10.1158/1538-7445.am2011-500
The PTEN pseudogene has been shown to function as a decoy adsorbing micro RNAs attacking PTEN for degradation in prostate cancer cells. PTENP1's potential involvement in PTEN enforcement of breast cancer has not been investigated systematically. Method: We treated murine C3HBA breast cancer cells lacking endogenous PTENP1 with a lentiviral PTENP1 construct to see the effect of the pseudogene on PTEN and Akt-mTOR downstream signaling, global gene expression, as well as in vitro and in vivo tumor growth characteristics. PTENP1 transfection in the murine C3HBA breast cancer cell line resulted in elevated endogenous PTEN, p53 and AP-2u03b3 protein levels, leading to tumor growth inhibition. PTEN, p53, and activating protein 2 gamma, as well as tumor formation in murine breast cancer rises.
Source link: https://doi.org/10.1158/1538-7445.am2015-3986
The purpose of this research was to investigate PTENP1 gene and its influence on PTEN expression and PI3K-Akt-mTOR signaling in human breast cancer. PTEN and PTENP1 expression was found in 30 patients with locally advanced breast cancer before and after surgery, and the results were correlated to tumor response rates. In addition, the human PTENP1 positive MDA-MB231 and the murine PTENP1 negative C3HBA breast cancer cell lines were lentivirally transfected with PTENP1 to determine the effects of PTENP1 overexpression in vitro, tumor formation in mice, as well as its influence on PTEN and PI3K-MTOR signaling. PTEN and PTENP1 mRNA expression was concordant in the breast cancer samples before and after 16 weeks of doxorubicin therapy. Tumor samples from patients with progressive disease had the lowest PTEN mRNA levels, but tumors with stable disease or partial response had higher PTEN levels, according to a censor. After surgery, PD tumors had a minor change in PTEN and PTENP1 levels, while PTEN and PTENP1 increased in SD and PR tumors, while PTEN and PTENP1 increased in PTEN and PTENP1 increased in PTEN and PTENP1. PTENP1 did not influence PTEN mRNA expression in MDA-MB231 tumors, but PTEN protein expression increased slightly, but PTEN protein expression increased slightly. Although PTEN had an effect on PTEN gene and protein expression, it had no effect on MDA-MB231, targeting miRNAs in MDA-MB231. Therefore, the mechanism behind PTEN control in breast cancer that is mediated by PTENP1 remains to be elaborated on further.
Source link: https://doi.org/10.1158/1538-7445.am2014-3539
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