Characters of KRT80 and its roles in neoplasms diseases.


Journal

Cancer medicine
ISSN: 2045-7634
Titre abrégé: Cancer Med
Pays: United States
ID NLM: 101595310

Informations de publication

Date de publication:
07 2023
Historique:
revised: 12 04 2023
received: 14 01 2023
accepted: 23 04 2023
medline: 21 7 2023
pubmed: 22 5 2023
entrez: 22 5 2023
Statut: ppublish

Résumé

KRT80 is a human epithelial intermediate filament type II gene; its expression product is a component of intracellular intermediate filaments (IFs) and is involved in the assembly of the cytoskeleton. There is evidence that IFs form a dense network mainly in the perinuclear area, but they can also reach the cortex. They are essential for mechanical cushioning of cells, organelle positioning, cell apoptosis, migration, adhesion, and interactions with other cytoskeletal components. Humans possess 54 functional keratin genes, and KRT80 is one of the more unique genes. It is widely expressed in almost all epithelial cells, although it is structurally more similar to type II hair keratins than to type II epithelial keratins. In this review, we summarize the basic facts about the keratin family and KRT80, the essential role of KRT80 in neoplasms, and its potential as a therapeutic target. We hope that this review will inspire researchers to at least partially focus on this area. In many neoplastic diseases, the high expression status of KRT80 and its role in regulating the biological functions of cancer cells have been well established. KRT80 can effectively enhance the proliferation, invasiveness and migration of cancer cells. However, the effects of KRT80 on prognosis and clinically relevant indices in patients with various cancers have not been extensively studied, and even opposite conclusions have been reached in different studies of the same cancer. Based on this, we should add more clinically relevant studies to clarify the prospect of clinical application of KRT80. Many researchers have made great progress in studying the mechanism of action of KRT80. However, their studies should be extended to more cancers to find common regulators and signaling pathways of KRT80 in different cancers. KRT80 may have far-reaching effects on the human body, and this marker may play a crucial role in the function of cancer cells and the prognosis of cancer patients, so it has a promising future in the field of neoplasms. In neoplastic diseases, KRT80 is overexpressed in many cancers and plays an essential role in promoting proliferation, migration, invasiveness and poor prognosis. The mechanisms of KRT80 functions in cancer have been partially elucidated, suggesting that KRT80 is a potentially useful cancer therapeutic target. However, more systematic, in-depth and comprehensive studies are still needed in this field.

Sections du résumé

BACKGROUND
KRT80 is a human epithelial intermediate filament type II gene; its expression product is a component of intracellular intermediate filaments (IFs) and is involved in the assembly of the cytoskeleton. There is evidence that IFs form a dense network mainly in the perinuclear area, but they can also reach the cortex. They are essential for mechanical cushioning of cells, organelle positioning, cell apoptosis, migration, adhesion, and interactions with other cytoskeletal components. Humans possess 54 functional keratin genes, and KRT80 is one of the more unique genes. It is widely expressed in almost all epithelial cells, although it is structurally more similar to type II hair keratins than to type II epithelial keratins.
AIM
In this review, we summarize the basic facts about the keratin family and KRT80, the essential role of KRT80 in neoplasms, and its potential as a therapeutic target. We hope that this review will inspire researchers to at least partially focus on this area.
RESULT
In many neoplastic diseases, the high expression status of KRT80 and its role in regulating the biological functions of cancer cells have been well established. KRT80 can effectively enhance the proliferation, invasiveness and migration of cancer cells. However, the effects of KRT80 on prognosis and clinically relevant indices in patients with various cancers have not been extensively studied, and even opposite conclusions have been reached in different studies of the same cancer. Based on this, we should add more clinically relevant studies to clarify the prospect of clinical application of KRT80. Many researchers have made great progress in studying the mechanism of action of KRT80. However, their studies should be extended to more cancers to find common regulators and signaling pathways of KRT80 in different cancers. KRT80 may have far-reaching effects on the human body, and this marker may play a crucial role in the function of cancer cells and the prognosis of cancer patients, so it has a promising future in the field of neoplasms.
CONCLUSION
In neoplastic diseases, KRT80 is overexpressed in many cancers and plays an essential role in promoting proliferation, migration, invasiveness and poor prognosis. The mechanisms of KRT80 functions in cancer have been partially elucidated, suggesting that KRT80 is a potentially useful cancer therapeutic target. However, more systematic, in-depth and comprehensive studies are still needed in this field.

Identifiants

pubmed: 37211956
doi: 10.1002/cam4.6040
pmc: PMC10358247
doi:

Substances chimiques

Keratins 68238-35-7
KRT80 protein, human 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

13991-14003

Informations de copyright

© 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

Références

Oncogene. 2015 Apr 23;34(17):2156-66
pubmed: 25347742
Oncol Rep. 2010 Sep;24(3):607-12
pubmed: 20664964
J Cell Sci. 2003 Dec 15;116(Pt 24):4977-84
pubmed: 14625391
Mol Biol Cell. 2011 Jul 1;22(13):2282-9
pubmed: 21562225
Int J Cancer. 2009 Oct 15;125(8):1842-50
pubmed: 19582876
Cell Physiol Biochem. 2011;28(2):185-98
pubmed: 21865726
Exp Mol Pathol. 2022 Apr;125:104756
pubmed: 35339455
Int J Mol Sci. 2019 Sep 11;20(18):
pubmed: 31514295
Biomed Pharmacother. 2021 Dec;144:112325
pubmed: 34656065
Anticancer Res. 2022 Apr;42(4):1707-1717
pubmed: 35346989
Science. 1998 Jan 23;279(5350):514-9
pubmed: 9438837
Mol Cell Biochem. 2015 Jan;399(1-2):269-78
pubmed: 25348361
Annu Rev Biochem. 1994;63:345-82
pubmed: 7979242
Oncotarget. 2016 Jan 5;7(1):860-72
pubmed: 26497212
FEBS Lett. 2008 Jun 18;582(14):2140-8
pubmed: 18502206
Cell Death Discov. 2022 Feb 2;8(1):45
pubmed: 35110531
Biomed Pharmacother. 2020 Jun;126:109941
pubmed: 32169757
BMC Med Genomics. 2021 Feb 27;14(1):60
pubmed: 33639954
Annu Rev Biochem. 2004;73:749-89
pubmed: 15189158
Cancer Res. 2015 Jun 1;75(11):2316-2325
pubmed: 25858145
Exp Cell Res. 2005 Apr 15;305(1):110-21
pubmed: 15777792
Nat Commun. 2015 Nov 27;6:10044
pubmed: 26610607
CA Cancer J Clin. 2021 May;71(3):209-249
pubmed: 33538338
J Invest Dermatol. 2005 Mar;124(3):536-44
pubmed: 15737194
Cell. 2016 Feb 25;164(5):911-21
pubmed: 26875866
Curr Opin Cell Biol. 2013 Feb;25(1):47-56
pubmed: 23270662
Cancer Med. 2023 Jul;12(13):13991-14003
pubmed: 37211956
Oncol Rep. 2020 Feb;43(2):581-590
pubmed: 31789399
J Hum Genet. 2020 Nov;65(11):1019-1034
pubmed: 32623445
J Cell Sci. 2011 Mar 15;124(Pt 6):865-72
pubmed: 21378307
J Mol Biol. 1999 Mar 12;286(5):1403-20
pubmed: 10064706
Cells. 2019 Apr 18;8(4):
pubmed: 31003495
Front Cell Dev Biol. 2017 Sep 14;5:81
pubmed: 28959689
Eur Respir J. 2017 Oct 19;50(4):
pubmed: 29051268
BMJ. 2013 Feb 05;346:e5793
pubmed: 23386361
Differentiation. 2004 Dec;72(9-10):527-40
pubmed: 15617563
J Oncol. 2021 Sep 27;2021:2042114
pubmed: 34616452
Am J Physiol Cell Physiol. 2000 Jul;279(1):C188-94
pubmed: 10898730
J Cell Sci. 2001 Jul;114(Pt 14):2569-75
pubmed: 11683385
Cell. 2009 Nov 25;139(5):871-90
pubmed: 19945376
J Cell Biol. 2006 Jul 17;174(2):169-74
pubmed: 16831889
J Cancer. 2021 Sep 24;12(22):6835-6850
pubmed: 34659572
Nat Commun. 2019 May 9;10(1):2115
pubmed: 31073170
Biol Open. 2015 Sep 14;4(10):1290-7
pubmed: 26369929
Cell Death Dis. 2018 Sep 27;9(10):1009
pubmed: 30262880
J Struct Biol. 2002 Jan-Feb;137(1-2):128-45
pubmed: 12064940
Cancer Sci. 2006 Mar;97(3):167-74
pubmed: 16542212
Proc Natl Acad Sci U S A. 2006 Oct 31;103(44):16206-11
pubmed: 17050693
Biochem Biophys Res Commun. 2014 Sep 12;452(1):106-11
pubmed: 25152407
Exp Ther Med. 2020 Dec;20(6):176
pubmed: 33101466
Biomedicines. 2021 Sep 27;9(10):
pubmed: 34680448
Trends Cell Biol. 2008 Jan;18(1):28-37
pubmed: 18083519
J Invest Dermatol. 2016 Jan;136(1):202-13
pubmed: 26763440
Gene. 2018 Sep 25;672:195-201
pubmed: 29890311
J Invest Dermatol. 2015 Jun;135(6):1609-1620
pubmed: 25668239
Cell Signal. 2010 Jan;22(1):88-96
pubmed: 19781633
J Biol Chem. 2010 Nov 19;285(47):36909-21
pubmed: 20843789

Auteurs

Xin-Yuan Wei (XY)

Lanzhou University Second Hospital, Lanzhou, Gansu, China.

Jie Zhao (J)

Department of oncology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.

Hao-Bin Tong (HB)

Lanzhou University Second Hospital, Lanzhou, Gansu, China.

Shang-Jie Cheng (SJ)

Lanzhou University Second Hospital, Lanzhou, Gansu, China.

Na He (N)

Department of oncology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.

Fei-Xue Song (FX)

Department of oncology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH