Cyclin-Dependent Kinase Synthetic Lethality Partners in DNA Damage Response

被引：10

作者：

Kciuk, Mateusz ^{[1
,2
]}

Gielecinska, Adrianna ^{[1
]}

Mujwar, Somdutt ^{[3
]}

Mojzych, Mariusz ^{[4
]}

Kontek, Renata ^{[1
]}

机构：

[1] Univ Lodz, Dept Mol Biotechnol & Genet, Banacha 12-16, PL-90237 Lodz, Poland

[2] Univ Lodz, Doctoral Sch Exact & Nat Sci, Banacha St 12-16, PL-90237 Lodz, Poland

[3] Maharishi Markandeshwar Deemed Univ Mullana, MM Coll Pharm, Ambala 133207, India

[4] Siedlce Univ Nat Sci & Humanities, Dept Chem, 3 Maja 54, PL-08110 Siedlce, Poland

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2022年 / 23卷 / 07期

关键词：

cyclin-dependent kinase (CDK); DNA damage response (DDR); inhibitor; MYC oncogene; poly (ADP-ribose) polymerase 1 (PARP-1); synthetic lethality; POLY(ADP-RIBOSE) POLYMERASE PARP; C-MYC; GENOMIC INSTABILITY; BREAST-CANCER; CELL LYMPHOMA; P53; REPLICATION; INHIBITION; CDK1; APOPTOSIS;

D O I：

10.3390/ijms23073555

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页数：16

共 50 条

[41] Cyclin-dependent kinase subunit (Cks) 1 or Cks2 overexpression overrides the DNA damage response barrier triggered by activated oncoproteins
Liberal, Vasco
Martinsson-Ahlzen, Hanna-Stina
Liberal, Jennifer
Spruck, Charles H.
Widschwendter, Martin
McGowan, Clare H.
Reed, Steven I.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2012, 109 (08) : 2754 - 2759
[42] Synthetic lethality of cyclin-dependent kinase inhibitor Dinaciclib with VHL-deficiency allows for selective targeting of clear cell renal cell carcinoma
Nelson, Luke J.
Castro, Kyleen E.
Xu, Binzhi
Li, Junyi
Dinh, Nguyen B.
Thompson, Jordan M.
Woytash, Jordan
Kipp, Kevin R.
Razorenova, Olga, V
CELL CYCLE, 2022, 21 (10) : 1103 - 1119
[43] Cyclin-dependent kinase inhibitors for treating cancer
Toogood, PL
MEDICINAL RESEARCH REVIEWS, 2001, 21 (06) : 487 - 498
[44] Cyclin-dependent kinase inhibition in mesothelioma.
Kratzke, Marian
Kren, Betsy
Porter, Stephen
Scaria, George
Klein, Mark A.
CANCER RESEARCH, 2021, 81 (13)
[45] The cyclin-dependent kinase pathway moves forward
Bornfeldt, KE
CIRCULATION RESEARCH, 2003, 92 (04) : 345 - 347
[46] Mechanisms of cyclin-dependent kinase inactivation by progestins
Musgrove, EA
Swarbrick, A
Lee, CSL
Cornish, AL
Sutherland, RL
MOLECULAR AND CELLULAR BIOLOGY, 1998, 18 (04) : 1812 - 1825
[47] Direct regulation of Treslin by cyclin-dependent kinase is essential for the onset of DNA replication
Kumagai, Akiko
Shevchenko, Anna
Shevchenko, Andrej
Dunphy, William G.
JOURNAL OF CELL BIOLOGY, 2011, 193 (06): : 995 - 1007
[48] Cyclin-Dependent Kinase Inhibitors as Anticancer Drugs
Krystof, Vladimir
Uldrijan, Stjepan
CURRENT DRUG TARGETS, 2010, 11 (03) : 291 - 302
[49] Cyclin-dependent kinase-5 in neurodegeneration
Shelton, SB
Johnson, GVW
JOURNAL OF NEUROCHEMISTRY, 2004, 88 (06) : 1313 - 1326
[50] Cyclin-dependent kinase control of motile ciliogenesis
Vladar, E. K.
Stratton, M. B.
Stearns, T.
Axelrod, J. D.
MOLECULAR BIOLOGY OF THE CELL, 2015, 26

← 1 2 3 4 5 →