Cyclin-dependent kinase inhibitors (CDKIs) and the DNA damage response: The link between signaling pathways and cancer

Amani, Jafar; Gorjizadeh, Nassim; Younesi, Simin; Najafi, Meysam; Ashrafi, Arash M.; Irian, Saeed; Gorjizadeh, Negar; Azizian, Khalil

doi:10.1016/j.dnarep.2021.103103

Cited by 13 publications

(8 citation statements)

References 162 publications

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“…In breast cancer, the cell cycle is deregulated at multiple levels. The P21/WAF1 is a cyclin‐dependent kinase inhibitor similar to p27 and p57, and it plays a critical role in cell cycle arrest after DNA damage (Amani et al, 2021). The overexpression of p21 leads to G1, G2, or S‐phase cell cycle arrest.…”

Section: Novel Drug Candidates Obtained From Natural Sources With Egf...mentioning

confidence: 99%

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Targeting epidermal growth factor receptor and its downstream signaling pathways by natural products: A mechanistic insight

Damare,

Engle,

Kumar

2024

Phytotherapy Research

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The epidermal growth factor receptor (EGFR) is a transmembrane receptor tyrosine kinase (RTK) that maintains normal tissues and cell signaling pathways. EGFR is overactivated and overexpressed in many malignancies, including breast, lung, pancreatic, and kidney. Further, the EGFR gene mutations and protein overexpression activate downstream signaling pathways in cancerous cells, stimulating the growth, survival, resistance to apoptosis, and progression of tumors. Anti‐EGFR therapy is the potential approach for treating malignancies and has demonstrated clinical success in treating specific cancers. The recent report suggests most of the clinically used EGFR tyrosine kinase inhibitors developed resistance to the cancer cells. This perspective provides a brief overview of EGFR and its implications in cancer. We have summarized natural products‐derived anticancer compounds with the mechanistic basis of tumor inhibition via the EGFR pathway. We propose that developing natural lead molecules into new anticancer agents has a bright future after clinical investigation.

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Section: Novel Drug Candidates Obtained From Natural Sources With Egf...mentioning

confidence: 99%

“…The transition of G2 to the mitosis phase is regulated via the phosphorylation of cell division cycle 2 (Cdc2) kinase/cyclin B kinase (activated by Cdc25C). DNA damage inhibits Cdc25C; thus, cell cycle arrest at the G2/M boundary (Amani et al, 2021; Fischer et al, 2015).…”

Section: Novel Drug Candidates Obtained From Natural Sources With Egf...mentioning

confidence: 99%

Targeting epidermal growth factor receptor and its downstream signaling pathways by natural products: A mechanistic insight

Damare,

Engle,

Kumar

2024

Phytotherapy Research

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“…Compared to tubulin inhibitors, DNA inhibitors can act on the whole cell cycle by destroying DNA through double-strand breakage, alkylation, chimerism, crosslinking, etc., causing cytotoxic effects, and having a good therapeutic effect on solid tumors 76 . In addition, DNA inhibitors have far fewer targets than tubulin inhibitors, and DNA inhibitors can show a better killing effect when ADCs carry the same amount of payloads into the cells.…”

Section: The Various Payloads Of Adcmentioning

confidence: 99%

Antibody–drug conjugates: Recent advances in payloads

Wang

Gou

et al. 2023

Acta Pharmaceutica Sinica B

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“…This increases the stability of P27KIP1, enabling it to trigger cell cycle arrest. Additionally, P27 promotes the accumulation of RAD51 during double-strand break repair (DSBR), allowing efficient DNA repair [ 15 ]. MYC protein can combat replication stress.…”

Section: Cdk/myc and Ddrmentioning

confidence: 99%

Cyclin-Dependent Kinase Synthetic Lethality Partners in DNA Damage Response

Kciuk

Gielecińska

Mujwar

et al. 2022

IJMS

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Cyclin-dependent kinases (CDKs) are pivotal mediators and effectors of the DNA damage response (DDR) that regulate both the pathway components and proteins involved in repair processes. Synthetic lethality (SL) describes a situation in which two genes are linked in such a way that the lack of functioning of just one maintains cell viability, while depletion of both triggers cell death. Synthetic lethal interactions involving CDKs are now emerging, and this can be used to selectively target tumor cells with DNA repair defects. In this review, SL interactions of CDKs with protooncogene products MYC, poly (ADP-ribose) polymerase (PARP-1), and cellular tumor antigen p53 (TP53) are discussed. The individual roles of each of the SL partners in DDR are described.

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Cyclin-dependent kinase inhibitors (CDKIs) and the DNA damage response: The link between signaling pathways and cancer

Cited by 13 publications

References 162 publications

Targeting epidermal growth factor receptor and its downstream signaling pathways by natural products: A mechanistic insight

Targeting epidermal growth factor receptor and its downstream signaling pathways by natural products: A mechanistic insight

Antibody–drug conjugates: Recent advances in payloads

Cyclin-Dependent Kinase Synthetic Lethality Partners in DNA Damage Response

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