Protein Kinase Cι and Wnt/β-Catenin Signaling: Alternative Pathways to Kras/Trp53-Driven Lung Adenocarcinoma

Yin, Ning; Liu, Yi; Khoór, András; Wang, Xue; Thompson, E. Aubrey; Leitges, Michael; Justilien, Verline; Weems, Capella; Murray, Nicole R.; Fields, Alan P.

doi:10.1016/j.ccell.2019.11.007

Cited by 12 publications

(28 citation statements)

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“…While activated Wnt/β-catenin signaling alone cannot drive tumorigenesis of the bronchiolar epithelium, its activation in the setting of KrasG12D mutations accelerates disease progression 121 . Further, KrasG12D ; p53 fl/fl ; Prkci (KPI) lung adenocarcinoma (LADC) mouse model tumors arise from Tm4sf1 + Axin2+ ATII cells whereas KrasG12D ; p53 fl/fl (KP) tumors arise from BASCs 122 . In addition, KPI tumors are reliant on higher levels of Wnt/β-catenin signaling for their expansion, a signature that is also reflected in human patient tumors 122 .…”

Section: Disease Pathogenesismentioning

confidence: 99%

“…Further, KrasG12D ; p53 fl/fl ; Prkci (KPI) lung adenocarcinoma (LADC) mouse model tumors arise from Tm4sf1 + Axin2+ ATII cells whereas KrasG12D ; p53 fl/fl (KP) tumors arise from BASCs 122 . In addition, KPI tumors are reliant on higher levels of Wnt/β-catenin signaling for their expansion, a signature that is also reflected in human patient tumors 122 .…”

Section: Disease Pathogenesismentioning

confidence: 99%

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Wnt signaling in lung development, regeneration, and disease progression

2021

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The respiratory tract is a vital, intricate system for several important biological processes including mucociliary clearance, airway conductance, and gas exchange. The Wnt signaling pathway plays several crucial and indispensable roles across lung biology in multiple contexts. This review highlights the progress made in characterizing the role of Wnt signaling across several disciplines in lung biology, including development, homeostasis, regeneration following injury, in vitro directed differentiation efforts, and disease progression. We further note uncharted directions in the field that may illuminate important biology. The discoveries made collectively advance our understanding of Wnt signaling in lung biology and have the potential to inform therapeutic advancements for lung diseases.

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Section: Disease Pathogenesismentioning

confidence: 99%

Section: Disease Pathogenesismentioning

confidence: 99%

Wnt signaling in lung development, regeneration, and disease progression

2021

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“…Notwithstanding work in these ex vivo models, a lack of an absolute requirement for PKC family genes for cell division in vivo in the mouse (all knockouts are viable excepting PKCι and PKN2), suggests that for the controls operating to progress a ‘normal’ cell cycle, these proteins are not required. Furthermore, in the case of PKCι, conditional knockout in the adult does not prevent the transformation of AT2 cells in the lung by mutant Ras ( Yin et al, 2019 ), consistent with the lack of any fundamental requirement in the cell cycle. A similar argument can be made for PKN2 where the knockout appears to display selective defects in mesenchymal tissue ( Quetier et al, 2016 ).…”

Section: Introductionmentioning

confidence: 75%

A cancer-associated, genome protective programme engaging PKCε

Parker

Lockwood

Davis

et al. 2020

Advances in Biological Regulation

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Associated with their roles as targets for tumour promoters, there has been a long-standing interest in how members of the protein kinase C (PKC) family act to modulate cell growth and division. This has generated a great deal of observational data, but has for the most part not afforded clear mechanistic insights into the control mechanisms at play. Here, we review the roles of PKCε in protecting transformed cells from non-disjunction. In this particular cell cycle context, there is a growing understanding of the pathways involved, affording biomarker and interventional insights and opportunities.

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“…Also, some studies have shown that changes in the cell cycle [29]- [31], like the abnormal expression of cell cyclerelated molecules of topoisomerase (DNA) II alpha (TOP2A), cyclin-dependent kinase 1 (CDK1) may affect the occurrence and development of LUAD [32], [33]. Meanwhile, LUAD has been reported to be associated with abnormal signal pathways [34], [35], such as the Ras / Raf / MEK / ERK classic tumor signaling pathway [36], [37]. Surgery and postoperative chemotherapy are the gold standards for the treatment of advanced and metastatic nonsmall cell lung cancer, but as the effective rate of the current first-line treatment is no more than 20-30% [38], it is still essential to discover the molecular mechanism in the occurrence and development of LUAD.…”

Section: Related Workmentioning

confidence: 99%

Toward Identifying Key Gene Group in the Occurrence and Development of Lung Adenocarcinoma

Zhao

Liu

et al. 2021

IEEE Access

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Lung adenocarcinoma (LUAD) has become the most common pathological type of lung cancer in recent years. However, the molecular mechanism of LUAD remains unclear. To reveal the laws in the occurrence and development of LUAD, this paper first collects 676 differentially expressed genes related to LUAD and the corresponding proteins encoded by the genes, resulting in a complex proteinprotein interaction (PPI) network. The traditional analysis methods focus on the gene interaction relationships or the important genes separately, ignoring the fact that some important target genes may take effect jointly. In contrast, this paper adopts a new analysis method named the overlapping gene analysis method to screen out the closely interacted and important genes. Thereinto, the hub genes are first discovered according to the node importance index, and then the PPI network is divided into multiple communities. The overlapping genes are some genes belonging to both the hub genes and the genes in the same community, regarded as gene groups. Through experiments, 10 genes are identified as a gene group. Survival analyses to the gene group show that only PLK1, CCNB1, and CDK1 participate in the prognosis of LUAD, and relate to the pathological stage of LUAD. These demonstrate that the three genes are extremely important in the cell cycle, which is confirmed by the following enrichment analyses. Besides, some significant correlations are observed among the three genes, which provide a clue that the three genes may cooperate in the occurrence and development of LUAD. This finding provides possible clinical targets for the diagnosis and treatment of LUAD. INDEX TERMS complex protein network, hub gene analysis, community analysis, cell cycle, tumor and cancer.

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Protein Kinase Cι and Wnt/β-Catenin Signaling: Alternative Pathways to Kras/Trp53-Driven Lung Adenocarcinoma

Cited by 12 publications

References 0 publications

Wnt signaling in lung development, regeneration, and disease progression

Wnt signaling in lung development, regeneration, and disease progression

A cancer-associated, genome protective programme engaging PKCε

Toward Identifying Key Gene Group in the Occurrence and Development of Lung Adenocarcinoma

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