Inhibitors of Cell Growth
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Cell growth is an elegantly coordinated series of steps; any of these steps are subject to interference by drugs and chemicals. Specifically, alcohol disrupts neural stem cell growth and division. Alcohol causes cells to progress more slowly through the cell cycle. The cycle consists of 4 major stages, during which cells grow and produce new proteins G1 , synthesize DNA S , produce new organelles G2 and divide by mitosis M. The most susceptible stage of the cell cycle is the G1 phase where alcohol inhibits the transcription and translation of genes that regulate the remaining steps of the cell cycle.
With a reduction in cell proliferation, the loss of neurons within the hippocampus can lead to significant learning and memory problems. The loss of neurons may explain the smaller hippocampus observed in the brains of adolescents with alcohol use disorder read on! Figure 3. Alcohol disrupts the duplication of DNA in S phase, leading to reduced mitosis. Insulin-like growth factor-1 receptor and ligand targeting in head and neck squamous cell carcinoma.
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Open Access Review. See all authors and affiliations. Abstract Genetic, epigenetic and somatic changes deregulate the expression of growth factor receptors GFRs , leading to cancer initiation and progression.
Growth factor receptors: promising drug targets in cancer
Table 1 Involvement of GFRs in cancer progression. Table 2 GFR expression in cancer. Vascular endothelial growth factor receptor This family consists of three membrane receptors VEGFR , predominantly expressed on endothelial cells and few additional cell types. Targeting GFR-mediated signals with cancer therapeutics Accumulated understanding over the last 30 years of signaling pathways mediated by different GFRs and their relationship with cancer progression has led to the development of targeted agents for cancer treatment.
Protein kinase inhibitors Structural and functional analyses have paved the way to discovery and development of numerous protein kinase inhibitors, especially tyrosine kinase inhibitors TKIs that inhibit the cytoplasmic kinase activity of growth receptors and subsequently their downstream signaling cascades into the cells.
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Nucleic acid-based therapeutics to block GFR expression The clinical applications of current chemotherapeutic drugs are often limited by their toxic effects on healthy dividing cells. References 1. DOI 2. DOI PubMed 3. VEGF targets the tumour cell. DOI PubMed 5. DOI PubMed 6. DOI PubMed DOI DOI PubMed. Recommended Articles Mechanisms of acquired resistance to fibroblast growth factor receptor targeted therapy David K.
Table of Contents. This results in the invasion of surrounding tissues, their metastasis to nearby organs, and eventually tumorigenesis. Cells of naked mole rats , a species in which cancer has never observed, show hypersensitivity to contact inhibition.
Furthermore, recent studies have further revealed some mechanisms of contact inhibition of proliferation and its potential implications in cancer therapy. Furthermore, it has been shown that cell-cell adhesion formation not only restricts growth and proliferation by imposing physical constraints such as cell area, but also by triggering signaling pathways that downregulate proliferation.
One such pathway is the Hippo-YAP signaling pathway, which is largely responsible for inhibiting cell growth in mammals. This pathway consists primarily of a phosphorylation cascade involving serine kinases and is mediated by regulatory proteins, which regulate cell growth by binding to growth-controlling genes. The phosphorylation of YAP serves to export it from the nucleus and prevent it from activating growth-promoting genes; this is how the Hippo-YAP pathway inhibits cell growth.
For example, cadherins are transmembrane proteins that form cellular junctions via homophilic binding  and thus act as detectors for cell-cell contact. However, it is important to note that contact-inhibited cells undergo cell cycle arrest, but do not senesce. In fact, it has been shown that contact-inhibited cells resume normal proliferation and mitogen signaling upon being replated in a less confluent culture.
Thus, contact inhibition of proliferation may be viewed as a reversible form of cell cycle arrest.
Furthermore, to transition from cell cycle arrest to senescence, contact-inhibited cells must activate growth-activating pathways such as mTOR. This has crucial implications in cancer therapy; even though cancer cells are not contact-inhibited, confluent cancer cell cultures still suppress their senescence machinery. Therefore, this may be a plausible explanation why senescence-inducing cancer therapy drugs are ineffective. In most cases, when two cells collide they attempt to move in a different direction to avoid future collisions; this behavior is known as contact inhibition of locomotion.
This is accomplished via a multistep, multi-faceted mechanism that involves the formation of a cell-cell adhesion complex upon collision. The disassembly of this complex is thought to be driven largely by tension in the cells and ultimately results in the colliding cells' changing directions. First, motile cells collide and touch via their respective lamellae , whose actin exhibit high retrograde flow.
A cellular adhesion forms between the lamellae, reducing the actins' retrograde flow rate in the area immediately surrounding the adhesion. Consequently, the cells' velocity and motility are reduced. This then allows actin stress fibers and microtubules to form and align with each other in both colliding partners. The alignment of these stress fibers locally accumulates elastic tension in the lamellae. Eventually, the tension buildup becomes too great, and the cell adhesion complex dissociates, collapses the lamellae protrusions, and releases the cells in different directions in an effort to alleviate the elastic tension.
A possible alternate event that also leads to the assembly dissociation is that upon stress fiber alignment, the cells' leading edges repolarize away from the contiguous lamellae.