JNK2 Is Required for the Tumorigenic Properties of Melanoma Cells

Du, Lili; Anderson, Anna Elizabeth; Nguyen, Khanh Thi-Thuy; Ojeda, Sandra S.; Ortiz-Rivera, Ivannie; Nguyen, Tran; Zhang, Tinghu; Kaoud, Tamer S.; Gray, Nathanael S.; Dalby, Kevin N.; Tsai, Kenneth Y.

doi:10.1021/acschembio.9b00083

Cited by 16 publications

(18 citation statements)

References 30 publications

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“…Furthermore, JNK activation was observed in the melanoma cells overexpressing JNK1WT, JNK2WT, and JNK1C116S but not JNK2C116S [170]. These data indicate that JNK2 is required for melanoma malignancy and resistance to BRAF inhibition [170].…”

Section: Jnk1 and Jnk2 In Melanoma Growth And Progressionmentioning

confidence: 85%

“…To investigate the role of JNK1 and JNK2, one group expressed wild type (WT) and C116S JNK1/2 mutants in melanoma cell lines, and it was found that JNK inhibition with the small molecule agent JNK-IN-8 enhanced proliferation and invasion in cell culture and subcutaneous xenografts expressing JNK2(C116S) mutant [170]. Furthermore, JNK activation was observed in the melanoma cells overexpressing JNK1WT, JNK2WT, and JNK1C116S but not JNK2C116S [170]. These data indicate that JNK2 is required for melanoma malignancy and resistance to BRAF inhibition [170].…”

Section: Jnk1 and Jnk2 In Melanoma Growth And Progressionmentioning

confidence: 99%

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The JNK Signaling Pathway in Inflammatory Skin Disorders and Cancer

Hammouda

Ford

Liu

et al. 2020

Cells

146

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The c-Jun N-terminal kinases (JNKs), with its members JNK1, JNK2, and JNK3, is a subfamily of (MAPK) mitogen-activated protein kinases. JNK signaling regulates a wide range of cellular processes, including cell proliferation, differentiation, survival, apoptosis, and inflammation. Dysregulation of JNK pathway is associated with a wide range of immune disorders and cancer. Our objective is to provide a review of JNK proteins and their upstream regulators and downstream effector molecules in common skin disorders, including psoriasis, dermal fibrosis, scleroderma, basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and melanoma.

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Section: Jnk1 and Jnk2 In Melanoma Growth And Progressionmentioning

confidence: 85%

Section: Jnk1 and Jnk2 In Melanoma Growth And Progressionmentioning

confidence: 99%

The JNK Signaling Pathway in Inflammatory Skin Disorders and Cancer

Hammouda

Ford

Liu

et al. 2020

Cells

146

View full text Add to dashboard Cite

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“…MAPK9 is a member of the MAP kinase family. A recent study has shown that MAPK9 activity played an indispensable part in invasiveness and BRAFi resistance of melanoma cell (47). As for USP10, decreased expression of USP10 has been proved to be an indicator of poor prognosis in lung cancer and epithelial ovarian cancer (48,49).…”

Section: Discussionmentioning

confidence: 99%

Development and Validation of Autophagy-Related Gene Signature and Nomogram for Predicting Survival in Oral Squamous Cell Carcinoma

et al. 2020

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Background: Autophagy, a highly conserved self-digesting process, has been deeply involved in the development and progression of oral squamous cell carcinoma (OSCC). However, the prognostic value of autophagy-related genes (ARGs) for OSCC still remains unclear. Our study set out to develop a multigene expression signature based on ARGs for individualized prognosis assessment in OSCC patients. Methods: Based on The Cancer Genome Atlas (TCGA) database, we identified prognosis-related ARGs through univariate COX regression analysis. Then we performed the least absolute shrinkage and selection operator (LASSO) regression analysis to identify an optimal autophagy-related multigene signature with the subsequent validation in testing set, GSE41613 and GSE42743 datasets. Results: We identified 36 prognosis-related ARGs for OSCC. Subsequently, the multigene signature based on 13 prognostic ARGs was constructed and successfully divided OSCC patients into low and high-risk groups with significantly different overall survival in TCGA training set (p < 0.0001). The autophagy signature remained as an independent prognostic factor for OSCC in univariate and multivariate Cox regression analyses. The area under the curve (AUC) values of the receiver operating characteristic (ROC) curves for 1, 3, and 5-year survival were 0.758, 0.810, 0.798, respectively. Then the gene signature was validated in TCGA testing set, GSE41613 and GSE42743 datasets. Moreover, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and single-sample gene set enrichment analysis (ssGSEA) revealed the underlying biological characteristics and signaling pathways associated with this signature in OSCC. Finally, we constructed a nomogram by combining the gene signature with multiple clinical parameters (age, gender, TNM-stage, tobacco, and alcohol history). The concordance index (C-index) and calibration plots demonstrated favorable predictive performance of our nomogram.

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“…Significant questions to address are how cells balance the pro-apoptotic and pro-survival/tumorigenic roles of JNK signaling and how differences in the regulation, enzymatic activities, and expression of the JNK isoforms impact their control of stemness. In addition to genetic approaches (e.g., RNA interference, CRISPR-Cas9, or genetically engineered mouse models), there needs to be an emphasis on a better understanding of the differential mechanisms of isoform regulation, the development of isoform-specific JNK inhibitors, as well as the utilization of chemical biology tools that allow for rapid downregulation of specific isoforms using pharmacological approaches [124,125]. Moreover, the crosstalk of the JNK signaling pathway with stemness-related pathways such as WNT and NOTCH, as described in several contexts above, is also largely unexplored and may be vital to unveiling the role of JNK signaling in regulating stemness.…”

Section: Discussionmentioning

confidence: 99%

JNK Signaling in Stem Cell Self-Renewal and Differentiation

Semba

Sammons

Wang

et al. 2020

IJMS

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C-JUN N-terminal kinases (JNKs), which belong to the mitogen-activated protein kinase (MAPK) family, are evolutionarily conserved kinases that mediate cell responses to various types of extracellular stress insults. They regulate physiological processes such as embryonic development and tissue regeneration, playing roles in cell proliferation and programmed cell death. JNK signaling is also involved in tumorigenesis and progression of several types of malignancies. Recent studies have shown that JNK signaling has crucial roles in regulating the traits of cancer stem cells (CSCs). Here we describe the functions of the JNK signaling pathway in self-renewal and differentiation, which are essential features of various types of stem cells, such as embryonic, induced pluripotent, and adult tissue-specific stem cells. We also review current knowledge of JNK signaling in CSCs and discuss its role in maintaining the CSC phenotype. A better understanding of JNK signaling as an essential regulator of stemness may provide a basis for the development of regenerative medicine and new therapeutic strategies against malignant tumors.

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JNK2 Is Required for the Tumorigenic Properties of Melanoma Cells

Cited by 16 publications

References 30 publications

The JNK Signaling Pathway in Inflammatory Skin Disorders and Cancer

The JNK Signaling Pathway in Inflammatory Skin Disorders and Cancer

Development and Validation of Autophagy-Related Gene Signature and Nomogram for Predicting Survival in Oral Squamous Cell Carcinoma

JNK Signaling in Stem Cell Self-Renewal and Differentiation

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