PMID- 33539023
OWN - NLM
STAT- MEDLINE
DCOM- 20210215
LR  - 20210412
IS  - 0065-2598 (Print)
IS  - 0065-2598 (Linking)
VI  - 1275
DP  - 2021
TI  - A Crosstalk Between Dual-Specific Phosphatases and Dual-Specific Protein Kinases 
      Can Be A Potential Therapeutic Target for Anti-cancer Therapy.
PG  - 357-382
LID - 10.1007/978-3-030-49844-3_14 [doi]
AB  - While protein tyrosine kinases (PTKs) play an initiative role in growth 
      factor-mediated cellular processes, protein tyrosine phosphatases (PTPs) 
      negatively regulates these processes, acting as tumor suppressors. Besides 
      selective tyrosine dephosphorylation of PTKs via PTPs may affect oncogenic 
      pathways during carcinogenesis. The PTP family contains a group of 
      dual-specificity phosphatases (DUSPs) that regulate the activity of 
      Mitogen-activated protein kinases (MAPKs), which are key effectors in the control 
      of cell growth, proliferation and survival. Abnormal MAPK signaling is critical 
      for initiation and progression stages of carcinogenesis. Since depletion of 
      DUSP-MAPK phosphatases (MKPs) can reduce tumorigenicity, altering MAPK signaling 
      by DUSP-MKP inhibitors could be a novel strategy in anti-cancer therapy. 
      Moreover, Cdc25A is, a DUSP and a key regulator of the cell cycle, promotes cell 
      cycle progression by dephosphorylating and activating cyclin-dependent kinases 
      (CDK). Cdc25A-CDK pathway is a novel mechanism in carcinogenesis. Besides the 
      mammalian target of rapamycin (mTOR) kinase inhibitors or mammalian target of 
      rapamycin complex 1 (mTORC1) inhibition in combination with the dual 
      phosphatidylinositol 3 kinase (PI3K)/mTOR or AKT kinase inhibitors are more 
      effective in inhibiting the phosphorylation of eukaryotic translation initiation 
      factor 4E-binding protein 1 (4E-BP1) and cap-dependent translation. Dual 
      targeting of the Akt and mTOR signaling pathways regulates cellular growth, 
      proliferation and survival. Like the Cdc2-like kinases (CLK), dual-specific 
      tyrosine phosphorylation-regulated kinases (DYRKs) are essential for the 
      regulation of cell fate. The crosstalk between dual-specific phosphatases and 
      dual- specific protein kinases is a novel drug target for anti-cancer therapy. 
      Therefore, the focus of this chapter involves protein kinase modules, critical 
      biochemical checkpoints of cancer therapy and the synergistic effects of protein 
      kinases and anti-cancer molecules.
FAU - Celtikci, Basak
AU  - Celtikci B
AD  - Hacettepe University, Faculty of Medicine, Department of Medical Biochemistry, 
      Ankara, Turkey. basakceltics@gmail.com.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Adv Exp Med Biol
JT  - Advances in experimental medicine and biology
JID - 0121103
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 3.1.3.2 (Phosphoric Monoester Hydrolases)
SB  - IM
MH  - *Phosphatidylinositol 3-Kinases/metabolism
MH  - *Phosphoric Monoester Hydrolases
MH  - Phosphorylation
MH  - Protein-Tyrosine Kinases
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Signal Transduction
OTO - NOTNLM
OT  - AKT
OT  - CDK
OT  - Carcinogenesis
OT  - Cdc25A
OT  - DUSP
OT  - Kinases
OT  - MAPK
OT  - PI3K
OT  - Phosphatases
OT  - mTOR
EDAT- 2021/02/05 06:00
MHDA- 2021/02/16 06:00
CRDT- 2021/02/04 12:17
PHST- 2021/02/04 12:17 [entrez]
PHST- 2021/02/05 06:00 [pubmed]
PHST- 2021/02/16 06:00 [medline]
AID - 10.1007/978-3-030-49844-3_14 [doi]
PST - ppublish
SO  - Adv Exp Med Biol. 2021;1275:357-382. doi: 10.1007/978-3-030-49844-3_14.