Although metastasis-associated lung adenocarcinoma transcript (MALAT)-1 is known to be consistently upregulated in several epithelial malignancies, little is known about its function or regulation. We therefore examin...Although metastasis-associated lung adenocarcinoma transcript (MALAT)-1 is known to be consistently upregulated in several epithelial malignancies, little is known about its function or regulation. We therefore examined the relationship between MALAT-1 expression and candidate modulators such as DNA tumor virus oncoproteins human papillomavirus (HPV)-16 E6 and E7, BK virus T antigen (BKVTAg), mouse polyoma virus middle T antigen (MPVmTAg) and tumor suppressor genes p53 and pRb. Using suppressive subtractive hybridization (SSH) and real-time reverse transcriptase polymerase chain reaction (RT-PCR) assays, MALAT-1 was shown to be increased in viral oncongene-expressing salivary gland biopsies from humans and mice. The results also indicated that MALAT-1 transcripts and promoter activity were increased in vitro when viral oncongene-expressing plasmids were introduced into different cell types. These same viral oncogenes in addition to increasing MALAT-1 transcription have also been shown to inhibit p53 and/or pRb function. In p53 mutant or inactive cell lines MALAT-1 was also shown to be highly upregulated. We hypothesize that there is a correlation between MALAT-1 over-expression and p53 deregulation. In conclusion, we show that disruption of p53, by both polyoma and papilloma oncoproteins appear to play an important role in the up-regulation of MALAT-1. MALAT-1 might therefore represent a biomarker for p53 deregulation within malignancies.展开更多
BK virus(BKV) is a polyomavirus that is able to cause renal dysfunction in transplanted grafts via BK virusassociated nephritis(BKVAN).This condition was misdiagnosed in the past due to clinical and histopthological s...BK virus(BKV) is a polyomavirus that is able to cause renal dysfunction in transplanted grafts via BK virusassociated nephritis(BKVAN).This condition was misdiagnosed in the past due to clinical and histopthological similarities with acute rejection.Due to the prevalence of the virus in the population,it is an important pathogen in this context,and so it is important to understand how this virus functions and its' relationship with the pathogenesis of BKVN.Screening for BKV often reveals viruria and/or viremia,which then manifests as BKVN,which can be asymptomatic or result in clinical features namely renal dysfunction.The pathogenesis of BKV infection is still unclear and needs to be further investigated; nevertheless there are a variety of hypotheses that indicate that there are a host of factors that play important roles.Treatments for BKVAN include a reduction in immunosuppression,the use of antiviral therapy or the combination of both treatment options.展开更多
文摘Although metastasis-associated lung adenocarcinoma transcript (MALAT)-1 is known to be consistently upregulated in several epithelial malignancies, little is known about its function or regulation. We therefore examined the relationship between MALAT-1 expression and candidate modulators such as DNA tumor virus oncoproteins human papillomavirus (HPV)-16 E6 and E7, BK virus T antigen (BKVTAg), mouse polyoma virus middle T antigen (MPVmTAg) and tumor suppressor genes p53 and pRb. Using suppressive subtractive hybridization (SSH) and real-time reverse transcriptase polymerase chain reaction (RT-PCR) assays, MALAT-1 was shown to be increased in viral oncongene-expressing salivary gland biopsies from humans and mice. The results also indicated that MALAT-1 transcripts and promoter activity were increased in vitro when viral oncongene-expressing plasmids were introduced into different cell types. These same viral oncogenes in addition to increasing MALAT-1 transcription have also been shown to inhibit p53 and/or pRb function. In p53 mutant or inactive cell lines MALAT-1 was also shown to be highly upregulated. We hypothesize that there is a correlation between MALAT-1 over-expression and p53 deregulation. In conclusion, we show that disruption of p53, by both polyoma and papilloma oncoproteins appear to play an important role in the up-regulation of MALAT-1. MALAT-1 might therefore represent a biomarker for p53 deregulation within malignancies.
文摘BK virus(BKV) is a polyomavirus that is able to cause renal dysfunction in transplanted grafts via BK virusassociated nephritis(BKVAN).This condition was misdiagnosed in the past due to clinical and histopthological similarities with acute rejection.Due to the prevalence of the virus in the population,it is an important pathogen in this context,and so it is important to understand how this virus functions and its' relationship with the pathogenesis of BKVN.Screening for BKV often reveals viruria and/or viremia,which then manifests as BKVN,which can be asymptomatic or result in clinical features namely renal dysfunction.The pathogenesis of BKV infection is still unclear and needs to be further investigated; nevertheless there are a variety of hypotheses that indicate that there are a host of factors that play important roles.Treatments for BKVAN include a reduction in immunosuppression,the use of antiviral therapy or the combination of both treatment options.
