Modulation of Proliferation and Tumorigenic Potential of Cervical-Carcinoma Cells by the Expression of Sense and Antisense P53

Velasco, Ja; Stevens, Cw; Esteban, Jm; Ruthsatz, Mkj; Ramsamooj, Priya; Dritschilo, Anatoly; Notario,

doi:10.3892/ijo.7.4.883

Cited by 2 publications

(4 citation statements)

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“…We have cloned and characterized the 5'-¯anking region of the PARP gene from EWS (A4573) cells. Our data show that PARP promoter strength correlates with the high levels of PARP mRNA and protein expression in EWS cell lines (Prasad et al, 1990;Velasco et al, 1995) and strongly suggest that transcription factor availability, rather than nucleotide sequence di erences or mRNA stability, is the main determinant for PARP expression levels. Previous studies also indicated that PARP is an inducible gene (Cesarone et al, 1990;Negroni and Bertazzoni, 1993) and that its promoter responds to extracellular signals such as cAMP and phorbol esters (Yokoyama et al, 1990).…”

Section: Inhibition Of Ets1 Expression Enhances Growth Retardation Ofsupporting

confidence: 62%

“…Figure 2a shows that, in agreement with previous reports (Prasad et al, 1990), EWS cell lines (A4573, TC 106, SK-ES-1) express enhanced levels of PARP protein relative to other human tumor cell lines tested. Previously we reported that EWS cell lines also contain high levels of PARP mRNA (Thraves et al, 1989;Prasad et al, 1990;Velasco et al, 1995) and suggested the possibility that the up-regulation of PARP in these cells was a transcriptional e ect. Furthermore, treatment of EWS cells, A549 human lung adenocarcinoma cells and SQ-20B cells with actinomycin D followed by Northern analysis of RNA prepared after various treatment periods demonstrated that increased PARP mRNA stability is not the determinant of the elevated PARP expression levels in EWS cells (data not shown).…”

Section: Functional Analysis Of the Parp Promoter From Ews Cellsmentioning

confidence: 87%

“…Therefore, EWS cells represent a unique model to investigate PARP transcriptional regulation with regard to the identi®cation of the transcription e ectors responsible for the unusually high levels of PARP in these primitive neuroectodermal tumor cells. Recently, we utilized EWS cells to demonstrate that the dbl proto-oncogene participates in mechanisms which regulate the endogenous levels of PARP in mammalian cells (Velasco et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

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Regulation of the human poly(ADP-ribose) polymerase promoter by the ETS transcription factor

et al. 1999

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Ewing's sarcoma (EWS) cells accumulate elevated steady-state levels of poly (ADP-ribose) polymerase (PARP) mRNA and protein. To understand the molecular mechanisms underlying PARP upregulation, we cloned and analysed the 5'-¯anking region of the PARP gene from EWS cells. Nucleotide sequence analysis demonstrated no variations in the PARP promoter region in EWS cells. The PARP promoter encompasses multiple binding motifs for the ETS transcription factor. We have also observed that there is a coordinated up-regulation of the expression of both PARP and ETS1, relative to cells of other human tumor types expressing lower levels of PARP. Transient coexpression of ETS1 in EWS cells resulted in a strong enhancement of PARP-promoter activity. The participation of ETS in the regulation of PARP gene expression was further demonstrated in EWS cells stably transfected with Ets1 antisense cDNA constructs. Antisensemediated down-regulation of endogenous ETS1 resulted in the inhibition of PARP expression in EWS cells, and sensitized these cells to ionizing radiation. These data provide support for ETS regulation of PARP expression levels, and implicate ETS transcription factors in the radiation response of EWS cells.

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Section: Inhibition Of Ets1 Expression Enhances Growth Retardation Ofsupporting

confidence: 62%

Section: Functional Analysis Of the Parp Promoter From Ews Cellsmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

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Regulation of the human poly(ADP-ribose) polymerase promoter by the ETS transcription factor

et al. 1999

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“…The first report to hint that HPV infection might be associated with senescence induction was provided in studies by Velasco et al, which described p53 upregulation in HPV-positive cells [ 169 ]. Subsequently, the Shay laboratory showed that HPV16 E6 and E7, through their modulation of the tumor suppressors p53 and pRb, are necessary for human diploid fibroblast cells to evade cellular senescence [ 170 , 171 ].…”

Section: Human Papilloma Virus (Hpv)-induced Senescencementioning

confidence: 99%

Senolytic Therapy: A Potential Approach for the Elimination of Oncogene-Induced Senescent HPV-Positive Cells

Saleh

Khasawneh

Himsawi

et al. 2022

IJMS

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Senescence represents a unique cellular stress response characterized by a stable growth arrest, macromolecular alterations, and wide spectrum changes in gene expression. Classically, senescence is the end-product of progressive telomeric attrition resulting from the repetitive division of somatic cells. In addition, senescent cells accumulate in premalignant lesions, in part, as a product of oncogene hyperactivation, reflecting one element of the tumor suppressive function of senescence. Oncogenic processes that induce senescence include overexpression/hyperactivation of H-Ras, B-Raf, and cyclin E as well as inactivation of PTEN. Oncogenic viruses, such as Human Papilloma Virus (HPV), have also been shown to induce senescence. High-risk strains of HPV drive the immortalization, and hence transformation, of cervical epithelial cells via several mechanisms, but primarily via deregulation of the cell cycle, and possibly, by facilitating escape from senescence. Despite the wide and successful utilization of HPV vaccines in reducing the incidence of cervical cancer, this measure is not effective in preventing cancer development in individuals already positive for HPV. Accordingly, in this commentary, we focus on the potential contribution of oncogene and HPV-induced senescence (OIS) in cervical cancer. We further consider the potential utility of senolytic agents for the elimination of HPV-harboring senescent cells as a strategy for reducing HPV-driven transformation and the risk of cervical cancer development.

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Modulation of Proliferation and Tumorigenic Potential of Cervical-Carcinoma Cells by the Expression of Sense and Antisense P53

Cited by 2 publications

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Regulation of the human poly(ADP-ribose) polymerase promoter by the ETS transcription factor

Regulation of the human poly(ADP-ribose) polymerase promoter by the ETS transcription factor

Senolytic Therapy: A Potential Approach for the Elimination of Oncogene-Induced Senescent HPV-Positive Cells

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