Cell Senescence and telomerase activity

Inhibition of deacetylation is one mechanism that can inhibit hTERT activation.

DNA shortens with each round of replication due to the loss of telomere (TTAGGG) sequences.

Hypermethylation can inhibit the activation of hTERT.

Normal cells become permanently growth arrested, a state known as replicative senescence.

The critical loss of telomeres triggers replicative senescence.

The promoter is inactive in normal cells due to epigenetic silencing mechanisms.

They lead to the activation of telomere immortalization.

A wide variety of small molecule telomerase inhibitors.

Telomerase is a large ribonucleoprotein complex responsible for the progressive synthesis of telomeric DNA repeats (TTAGGG) at the 3′ ends of linear chromosomes.

The Hayflick Limit refers to the intrinsic limit on the number of replications of normal fibroblasts in culture, typically between 50 to 70 divisions.

Telomerase is expressed in germ cells and stem cells, such as those in the bone marrow and the mucosa of the small intestine.

Des dysfonctionnements dans le processus d'époptose peuvent contribuer à des maladies comme le cancer, où les cellules échappent à la mort programmée.

Telomerase acts as a kind of reverse transcriptase, adding TTAGGG to the ends of chromosomes to lengthen telomeres.

The activity of telomerase is silenced by methylation of the promoter, similar to how oncofetal proteins are switched off.

Les mécanismes de l'époptose incluent l'activation de caspases, la dégradation de l'ADN et des changements morphologiques dans la cellule.

Immortality in rodent fibroblasts can be induced by carcinogens.

No, transformation is a multi-step process.

Limitations include lack of growth factors and the absence of a proper microenvironment, which affects cell survival and division.

It possesses a functional RNA component as well as a catalytic protein sub-unit.

Telomerase is significantly expressed in approximately 90% of human cancers.

The first step is the introduction of a carcinogen to make the cells immortal.

Transcription factors such as c-Myc, SP1, ETS family members, NF-kB, AP-2, and HIF-1 stimulate hTERT transcription.

L'époptose est un processus de mort cellulaire programmée qui joue un rôle crucial dans le développement et l'homéostasie des tissus.

Cancer cells are usually immortal and can continue dividing indefinitely in culture.

Telomerase adds repetitive sequences to telomeres, lengthening them and allowing stem cells to become immortal.

Human cells are exceptionally refractive to immortalization and malignant transformation.

During senescence, cells undergo changes that prevent them from dividing, which can contribute to aging and tissue dysfunction.

In normal cells, telomerase activity is low, leading to telomere shortening with each division, while in some cancer cells, telomerase is reactivated, allowing for unlimited division.

Immortalization is a prerequisite for malignant transformation.

Normal cells undergo senescence because they do not have telomerase to maintain telomere length, leading to critical telomere loss.

Combining two carcinogens can lead to cancer if the cell is already immortal, as H-ras can transform the cell into a malignant one.

The main mechanisms include mutations in the hTERT promoter, alterations in alternative splicing of hTERT pre-mRNA, hTERT amplification, epigenetic changes, and/or disruption of telomere position effect (TPE) machinery.

Telomerase maintains structures (telomeres) at the ends of chromosomes through the synthesis of characteristic telomeric (TTAGGG) sequences.

Further treatment of immortalized cells with additional carcinogens can produce cells with a malignant phenotype.

hTERT is regulated in normal cells through mechanisms that keep the telomerase gene silenced.

The telomerase gene is present in all cells, but its activity is silenced or switched off in normal cells.

Telomerase is dysregulated in virtually all cancers and is essential for the continued proliferation and clonal evolution of cancer cells.

Chromosomes lose about 200 base pairs with each cell division.

The second step involves treating the immortal cells with another carcinogen to produce malignancy.

Transcription factors such as P53, MAD, WT1, MZF-2, SIP1, and menin downregulate hTERT transcription.

For transformation to occur, there can be no more than one mutation, as there are backup mechanisms like tumor suppressor genes that resist transformation.

L'époptose aide à éliminer les cellules endommagées, à réguler le nombre de cellules et à prévenir le développement de tumeurs.

Telomerase is expressed in the majority of cancer cells.

Replicative senescence may have evolved as a tumor suppressive mechanism.

The enzyme telomerase was discovered, which is present in cancer cells but not in normal cells.

It constitutes a CpG island, suggesting epigenetic silencing of hTERT transcription in normal cells.

Yes, cancer stem cells also express hTERT.

When the replicative potential is reached, the cell undergoes apoptosis if it cannot repair significant DNA damage.

Methylation of the promoter leads to the silencing of telomerase activity in normal cells.

Telomerase is absent from the vast majority of normal human cells.

The anti-cancer benefit may be outweighed by side-effects arising from stem cell inhibition in other tissues.

Most, if not all, cancers arise from stem cells that already have active hTERT.

L'époptose est un processus régulé et contrôlé, tandis que la nécrose est une mort cellulaire non programmée souvent causée par des blessures ou des infections.

Cell senescence refers to the process where cells stop dividing and enter a state of permanent growth arrest.

Telomerase is an enzyme that can extend the telomeres of chromosomes, potentially delaying the aging process of cells by allowing them to divide more times.

The hTERT coding region contains 16 exons and 15 introns and spans 37kb of the genome.

Telomerase is not expressed in most normal cells, which is why it is active in most cancer cells.

De-repression of the telomerase gene in cancer cells is activated at the level of transcription.

First, cells must be immortal; second, another carcinogen causes the change from proto-oncogene to oncogene.

Low levels of telomerase activity are present in proliferative cells of self-renewing tissues such as bone marrow, trachea and bronchi, skin (basal layer), and gut (base of crypt).

Human cells are refractory to immortalization by carcinogen treatment due to very effective DNA repair and apoptosis mechanisms.

Telomerase activity can arise from mutational or epigenetic disruption of normal repressor genes, alterations in alternative splicing of hTERT pre-mRNA, or hTERT amplification.

In cancer cells, the silenced telomerase gene is reactivated, leading to telomerase activity.

Cancer stem cells have limited proliferative capacity, which prevents uncontrollable amounts of cells from forming.

H-ras can only induce malignant transformation in cells that are already immortalized.

Transfection of normal rodent cells with H-ras induces premature senescence rather than malignancy.

Histone deacetylase inhibitors activate hTERT in normal cells.

Methylation of the promoter silences hTERT transcription.

Rodent fibroblasts can be transformed by co-transfection with different oncogenes such as ras and myc, indicating that combinations of oncogenes are needed for immortalization and malignant transformation.

Activation of transcription of telomerase promotes cell division, while inhibition affects the immortality of cells, acting as a tumor suppressor gene.