p53 Interference and Growth Inhibition in p53-Mutant and Overexpressing Endometrial Cancer Cell Lines

Janicek, Mike F.; Angioli, Roberto; Ünal, Ayçe; Sevin, Bernd‐Uwe; Madrigal, Marilu; Estape, Ricardo; Averette, Hervy E.

doi:10.1006/gyno.1997.4713

Cited by 4 publications

(2 citation statements)

References 16 publications

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“…The RL95-2 cell line presents a mutant P53 expression with a codon deletion in exon 6 [ 49 ], a condition that leads to a loss of function of wild-type P53 [ 50 ]. Furthermore, in cancer cells, mutations leading to a P53 inactivation could entail an enhancement of stemness-associated markers, as well as the capacity for sphere forming [ 50 ], as our results demonstrate.…”

Section: Discussionmentioning

confidence: 99%

Influence of Aldehyde Dehydrogenase Inhibition on Stemness of Endometrial Cancer Stem Cells

Serambeque,

Mestre,

Correia-Barros

et al. 2024

Cancers

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Endometrial cancer is one of the most common gynaecological malignancies. Although often diagnosed at an early stage, there is a subset of patients with recurrent and metastatic disease for whom current treatments are not effective. Cancer stem cells (CSCs) play a pivotal role in triggering tumorigenesis, disease progression, recurrence, and metastasis, as high aldehyde dehydrogenase (ALDH) activity is associated with invasiveness and chemotherapy resistance. Therefore, this study aimed to evaluate the effects of ALDH inhibition in endometrial CSCs. ECC-1 and RL95-2 cells were submitted to a sphere-forming protocol to obtain endometrial CSCs. ALDH inhibition was evaluated through ALDH activity and expression, sphere-forming capacity, self-renewal, projection area, and CD133, CD44, CD24, and P53 expression. A mass spectrometry-based proteomic study was performed to determine the proteomic profile of endometrial cancer cells upon N,N-diethylaminobenzaldehyde (DEAB). DEAB reduced ALDH activity and expression, along with a significant decrease in sphere-forming capacity and projection area, with increased CD133 expression. Additionally, DEAB modulated P53 expression. Endometrial cancer cells display a distinct proteomic profile upon DEAB, sharing 75 up-regulated and 30 down-regulated proteins. In conclusion, DEAB inhibits ALDH activity and expression, influencing endometrial CSC phenotype. Furthermore, ALDH18A1, SdhA, and UBAP2L should be explored as novel molecular targets for endometrial cancer.

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Section: Discussionmentioning

confidence: 99%

Influence of Aldehyde Dehydrogenase Inhibition on Stemness of Endometrial Cancer Stem Cells

Serambeque,

Mestre,

Correia-Barros

et al. 2024

Cancers

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“…30 The mechanisms for the nonspecific effects of ODNs could be related to (1) the structure of the ODN itself, (2) hybridization to DNA or mRNA other than the target sequence, with subsequent RNase cleavage, (3) binding to proteins or other molecules, and/or (4) ODN degradation products, which in themselves can affect cellular functions. 2,3,6,8,16,17,20,30,45,64,65 Phosphorothioated ODNs have been shown to be inherently growth-inhibitory, 66 particularly those having four adjacent guanosine bases. 30,39,67 As polyanions, ODNs have been shown to nonspecifically bind proteins such as bFGF, VEGF, PKC, and protein tyrosine receptors including the epidermal growth factor receptor.…”

Section: Non-antisense Effects Of Odn Treatmentmentioning

confidence: 99%

Antisense Oligodeoxynucleotide Technology: Potential Use for the Treatment of Malignant Brain Tumors

Engelhard

1998

Cancer Control

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BACKGROUND: Antisense oligodeoxynucleotides (ODNs) have been proposed as a new therapy for patients with cancer, including malignant brain tumors. Antisense ODNs are taken up by tumor cells and selectively block gene expression. Use of ODNs for brain tumors is attractive due to their theoretical specificity, relative ease of production and, to date, paucity of reported adverse effects. This article presents current information regarding antisense ODNs and their possible future use for the treatment of brain tumors. METHODS: The available published experimental and clinical information regarding antisense ODN treatment of glioblastoma cells and administration into the central nervous system (CNS) was reviewed. Other clinically relevant information pertaining to the molecular biology of antisense ODNs was also collected and summarized. RESULTS: Targets for antisense ODN therapy in malignant glioma cells have included c-myc, c-myb, c-sis, c-erb B, CD44, p34cdc2, bFGF, PDGF, TGF-beta, IGF-1, PKC-alpha tumor necrosis factor, urokinase, and S100beta protein. Few in vivo studies of ODN treatment of brain tumors have yet been reported. Systemically administered ODNs enter the brain only in extremely small quantities; therefore, microinfusion into the brain has been recommended. CONCLUSIONS: Antisense ODNs have been used successfully to block glioblastoma gene expression in vitro and expression of multiple genes within the CNS of experimental animals. Upcoming clinical trials will address the safety of antisense ODN use against malignant brain tumors.

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Brain Tumor Therapy with Antisense Oligonucleotides

Schneider

2009

Therapeutic Ribonucleic Acids in Brain Tumors

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p53 Interference and Growth Inhibition in p53-Mutant and Overexpressing Endometrial Cancer Cell Lines

Cited by 4 publications

References 16 publications

Influence of Aldehyde Dehydrogenase Inhibition on Stemness of Endometrial Cancer Stem Cells

Influence of Aldehyde Dehydrogenase Inhibition on Stemness of Endometrial Cancer Stem Cells

Antisense Oligodeoxynucleotide Technology: Potential Use for the Treatment of Malignant Brain Tumors

Brain Tumor Therapy with Antisense Oligonucleotides

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