10 Therapeutic strategies Top Targeting of cancer stem cells and Biology Diagrams Cell-cycle-targeting drugs have the advantages of high specificity, low toxicity, low side effects, and low drug resistance. Aberrant angiogenic signaling pathways: accomplices in ovarian cancer progression and treatment. Cell Signal 120, 111240. 10.1016/j.cellsig.2024.111240 [Google Scholar] Articles from Frontiers in Pharmacology are Cell cycle inhibitors such as CDK and checkpoint kinase inhibitors are often used in combination with chemotherapy to target cell cycle factors for cancer treatment [21, 124, 140, 141]. In addition to CDKs, checkpoint kinases like Aurora A/B and PLKs are other targets for cancer therapy. Abnormal activity of the core cell-cycle machinery is seen in essentially all tumor types and represents a driving force of tumorigenesis. Recent studies revealed that cell-cycle proteins regulate a wide range of cellular functions, in addition to promoting cell division. With the clinical success of CDK4/6 inhibitors, it is becoming increasingly clear that targeting individual cell-cycle
Cell cycle regulation has an important influence on the proliferation, metastasis, and recurrence of tumor cells . In the current cancer treatment, the regulation of the cell cycle is mainly to control the expression of related genes and the activity of intracellular enzymes, proteins, or signal factors [5,6,7].
Targeted Cancer Therapies Biology Diagrams
A cardinal feature of cancer cells is the deregulation of cell cycle controls. Targeted drug therapy is designed to take advantage of specific genetic alterations that distinguish tumor cells from their normal counterparts. Mutated oncogenes and inactivated tumor suppressors can increase the dependency of cancer cells on G1-phase cyclin-dependent kinases, augment replication stress and DNA Proteins regulating cell cycle progression are involved in the formation of most cancer types. This Review discusses the role of cell cycle proteins in cancer, the rationale for targeting them in
To date, cancer patients have been treated with therapies targeting cell cycle progression (Table 1), most of them used in combination to achieve the higher effect over cancer cells with the minimum impact over normal proliferating cells. However, in the light of the coordinative mechanisms described above it is possible to suggest new Further research into combinatorial therapies and biomarkers for patient selection may enhance the efficacy of cell cycle modulators as cancer treatments. More clinical trials are warranted to fully assess the safety, efficacy, and long-term outcomes of targeting the cell cycle machinery across diverse cancer types and molecular subtypes.
