Correlation of P38 Mitogen-Activated Protein Kinase Expression to Clinical Stage in Nasopharyngeal Carcinoma

Farhat, Farhat; Daulay, Elvita Rahmi; Chrestella, Jessy; Asnir, Rizalina Arwinati; Yudhistira, Ashri; Susilo, Riko Radityatama

doi:10.3889/oamjms.2018.355

Cited by 8 publications

(6 citation statements)

References 38 publications

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“…As mentioned in Tables 1 and 2, increased expression of p38 MAPKs and JNKs has also been reported in NPC [59,78]. JNK and p38 MAPK activities have been evaluated in treatment-resistant NPC, of which the protein expressions of both JNK and p38 MAPK were found to be higher in cetuximab-resistant NPC [81].…”

Section: Jnk and P38 Mapk Activities Inhibit Pro-apoptotic Signaling ...mentioning

confidence: 91%

Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma

Pua

Chung

et al. 2022

IJMS

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c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) family members integrate signals that affect proliferation, differentiation, survival, and migration in a cell context- and cell type-specific way. JNK and p38 MAPK activities are found upregulated in nasopharyngeal carcinoma (NPC). Studies have shown that activation of JNK and p38 MAPK signaling can promote NPC oncogenesis by mechanisms within the cancer cells and interactions with the tumor microenvironment. They regulate multiple transcription activities and contribute to tumor-promoting processes, ranging from cell proliferation to apoptosis, inflammation, metastasis, and angiogenesis. Current literature suggests that JNK and p38 MAPK activation may exert pro-tumorigenic functions in NPC, though the underlying mechanisms are not well documented and have yet to be fully explored. Here, we aim to provide a narrative review of JNK and p38 MAPK pathways in human cancers with a primary focus on NPC. We also discuss the potential therapeutic agents that could be used to target JNK and p38 MAPK signaling in NPC, along with perspectives for future works. We aim to inspire future studies further delineating JNK and p38 MAPK signaling in NPC oncogenesis which might offer important insights for better strategies in diagnosis, prognosis, and treatment decision-making in NPC patients.

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Section: Jnk and P38 Mapk Activities Inhibit Pro-apoptotic Signaling ...mentioning

confidence: 91%

Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma

Pua

Chung

et al. 2022

IJMS

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“…In particular, MAPK demonstrated strong associations in our analysis. In fact, we found that many MAPK-associated signaling components were upregulated in NPC samples while SB203580, a small molecule MAPK inhibitor, was predicted to be inhibited; activity of these factors are known mediators of NPC tumorigenesis [56]. Specifically, SB203580 has been shown to down-regulate the p38 MAPK pathway, resulting in MMP-2 inhibition, another protein important for extracellular matrix breakdown, ultimately limiting NPC invasion [57,58].…”

Section: Plos Onementioning

confidence: 95%

Meta-Analysis illustrates possible role of lipopolysaccharide (LPS)-induced tissue injury in nasopharyngeal carcinoma (NPC) pathogenesis

et al. 2021

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Background Nasopharyngeal carcinoma (NPC) is a cancer of epithelial origin with a high incidence in certain populations. While NPC has a high remission rate with concomitant chemoradiation, recurrences are frequent, and the downstream morbidity of treatment is significant. Thus, it is imperative to find alternative therapies. Methods We employed a Search Tag Analyze Resource (STARGEO) platform to conduct a meta-analysis using the National Center for Biotechnology’s (NCBI) Gene Expression Omnibus (GEO) to define NPC pathogenesis. We identified 111 tumor samples and 43 healthy nasopharyngeal epithelium samples from NPC public patient data. We analyzed associated signatures in Ingenuity Pathway Analysis (IPA), restricting genes that showed statistical significance (p<0.05) and an absolute experimental log ratio greater than 0.15 between disease and control samples. Results Our meta-analysis identified activation of lipopolysaccharide (LPS)-induced tissue injury in NPC tissue. Additionally, interleukin-1 (IL-1) and SB203580 were the top upstream regulators. Tumorigenesis-related genes such as homeobox A10 (HOXA10) and prostaglandin-endoperoxide synthase 2 (PTGS2 or COX-2) as well as those associated with extracellular matrix degradation, such as matrix metalloproteinases 1 and 3 (MMP-1, MMP-3) were also upregulated. Decreased expression of genes that encode proteins associated with maintaining healthy nasal respiratory epithelium structural integrity, including sentan-cilia apical structure protein (SNTN) and lactotransferrin (LTF) was documented. Importantly, we found that etanercept inhibits targets upregulated in NPC and LPS induction, such as MMP-1, PTGS2, and possibly MMP-3. Conclusions Our analysis illustrates that nasal epithelial barrier dysregulation and maladaptive immune responses are key components of NPC pathogenesis along with LPS-induced tissue damage.

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“…Like other MAPKs, the functions of p38 have been well-established in tumor cells, directing any number of cell processes including differentiation, migration, and inflammation [58]. Accordingly, p38 overexpression is associated with poor responses to conventional therapy in several cancers including breast cancer, nasopharyngeal carcinoma, gastric, and pancreatic cancer [59][60][61][62].…”

Section: P38 Mapk Inhibitionmentioning

confidence: 99%

Mitogen-Activated Protein Kinase Inhibitors and T-Cell-Dependent Immunotherapy in Cancer

et al. 2020

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Mitogen-activated protein kinase (MAPK) signaling networks serve to regulate a wide range of physiologic and cancer-associated cell processes. For instance, a variety of oncogenic mutations often lead to hyperactivation of MAPK signaling, thereby enhancing tumor cell proliferation and disease progression. As such, several components of the MAPK signaling network have been proposed as viable targets for cancer therapy. However, the contributions of MAPK signaling extend well beyond the tumor cells, and several MAPK effectors have been identified as key mediators of the tumor microenvironment (TME), particularly with respect to the local immune infiltrate. In fact, a blockade of various MAPK signals has been suggested to fundamentally alter the interaction between tumor cells and T lymphocytes and have been suggested a potential adjuvant to immune checkpoint inhibition in the clinic. Therefore, in this review article, we discuss the various mechanisms through which MAPK family members contribute to T-cell biology, as well as circumstances in which MAPK inhibition may potentiate or limit cancer immunotherapy.

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Correlation of P38 Mitogen-Activated Protein Kinase Expression to Clinical Stage in Nasopharyngeal Carcinoma

Cited by 8 publications

References 38 publications

Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma

Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma

Meta-Analysis illustrates possible role of lipopolysaccharide (LPS)-induced tissue injury in nasopharyngeal carcinoma (NPC) pathogenesis

Mitogen-Activated Protein Kinase Inhibitors and T-Cell-Dependent Immunotherapy in Cancer

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