PMID- 31623973
OWN - NLM
STAT- MEDLINE
DCOM- 20210127
LR  - 20210127
IS  - 2212-4934 (Electronic)
IS  - 2212-4926 (Linking)
VI  - 75
DP  - 2020 Jan
TI  - Oncogenic protein kinase Ciota signaling mechanisms in lung cancer: Implications for 
      improved therapeutic strategies.
PG  - 100656
LID - S2212-4926(19)30077-6 [pii]
LID - 10.1016/j.jbior.2019.100656 [doi]
AB  - Protein Kinase Ciota (PKCiota) is a major oncogene involved in the initiation, 
      maintenance and progression of numerous forms of human cancer. In the lung, PKCiota 
      is necessary for the maintenance of the transformed phenotype of the two major 
      forms of non-small cell lung cancer (NSCLC), lung adenocarcinoma (LADC) and lung 
      squamous cell carcinoma (LSCC). In addition, PKCiota is necessary for both LADC and 
      LSCC tumorigenesis by establishing and maintaining a highly aggressive stem-like, 
      tumor-initiating cell phenotype. Interestingly however, while PKCiota signaling in 
      these two major lung cancer subtypes shares some common elements, it also drives 
      distinct, sub-type specific pathways. Furthermore, recent analysis has revealed 
      both PKCiota-dependent and PKCiota-independent pathways to LADC development. Herein, we 
      discussion our current knowledge of oncogenic PKCiota signaling in LADC and LSCC, 
      and discuss these findings in the context of how they may inform strategies for 
      improved therapeutic intervention in these deadly diseases.
CI  - Copyright (c) 2019. Published by Elsevier Ltd.
FAU - Yin, Ning
AU  - Yin N
AD  - From the Department of Cancer Cell Biology, Mayo Clinic Florida, Jacksonville, 
      FL, 32224, USA.
FAU - Liu, Yi
AU  - Liu Y
AD  - From the Department of Cancer Cell Biology, Mayo Clinic Florida, Jacksonville, 
      FL, 32224, USA.
FAU - Murray, Nicole R
AU  - Murray NR
AD  - From the Department of Cancer Cell Biology, Mayo Clinic Florida, Jacksonville, 
      FL, 32224, USA.
FAU - Fields, Alan P
AU  - Fields AP
AD  - From the Department of Cancer Cell Biology, Mayo Clinic Florida, Jacksonville, 
      FL, 32224, USA. Electronic address: fields.alan@mayo.edu.
LA  - eng
GR  - R01 CA081436/CA/NCI NIH HHS/United States
GR  - R01 CA202697/CA/NCI NIH HHS/United States
GR  - R01 CA140290/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20190925
PL  - England
TA  - Adv Biol Regul
JT  - Advances in biological regulation
JID - 101572336
RN  - 0 (Isoenzymes)
RN  - 0 (Neoplasm Proteins)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 2.7.11.13 (protein kinase C lambda)
SB  - IM
MH  - *Adenocarcinoma of Lung/enzymology/genetics
MH  - *Carcinoma, Non-Small-Cell Lung/enzymology/genetics
MH  - Humans
MH  - *Isoenzymes/genetics/metabolism
MH  - *Lung Neoplasms/enzymology/genetics
MH  - *Neoplasm Proteins/genetics/metabolism
MH  - *Protein Kinase C/genetics/metabolism
MH  - *Signal Transduction
OTO - NOTNLM
OT  - Genetically-engineered mouse models
OT  - Lung adenocarcinoma
OT  - Lung squamous cell carcinoma
OT  - Oncogenic signaling pathways
OT  - Protein kinase Ciota
COIS- Declaration of competing interest The authors have no conflicts of interest to 
      declare.
EDAT- 2019/10/19 06:00
MHDA- 2021/01/28 06:00
CRDT- 2019/10/19 06:00
PHST- 2019/09/03 00:00 [received]
PHST- 2019/09/19 00:00 [revised]
PHST- 2019/09/21 00:00 [accepted]
PHST- 2019/10/19 06:00 [pubmed]
PHST- 2021/01/28 06:00 [medline]
PHST- 2019/10/19 06:00 [entrez]
AID - S2212-4926(19)30077-6 [pii]
AID - 10.1016/j.jbior.2019.100656 [doi]
PST - ppublish
SO  - Adv Biol Regul. 2020 Jan;75:100656. doi: 10.1016/j.jbior.2019.100656. Epub 2019 
      Sep 25.