MAP2K7 (Mitogen-Activated Protein Kinase Kinase 7)

Our findings suggest that UPM exposure alone elicited limited stress-adaptive antioxidant responses without effective cytoprotection. In contrast, araliadiol treatment independently activated robust antioxidant and cytoprotective signaling. Moreover, under UPM exposure, araliadiol further enhanced cellular defense through the activation of the Nrf2 and JNK-AP-1 signaling pathways. These results highlight the therapeutic potential of araliadiol as a dermoprotective agent derived from Centella asiatica, particularly in mitigating pollutant-induced skin damage.

Moreover, elevated MAPK8 gene expression was linked to an increased incidence of regional lymph node metastasis. Furthermore, bioinformatics analysis confirmed that MAP2K7 and MAPK8 appear to promote tumor aggressiveness and metastasis, whereas MAPK9 and MAP2K4 may have a protective or regulatory role in early stages of the disease.

This study establishes UBE2M as a critical tumor suppressor in melanoma through the MKK7 neddylation-JNK-EGR1 axis and highlights its potential as a therapeutic target.

MiR-331-3p could be recognized as a promising inhibitor for the ERK/MAPK signal pathway in NSCLC cells since it has an interfering effect on MAP2K7 protein. These results cast a meaningful insight into the shadow regarding molecular mechanisms underlying NSCLC and the potential therapeutic perspective of circRNA methylation.

Here, we performed unbiased genome-wide CRISPR/Cas9 knockout screens using endocrine sensitive ER+ breast cancer cells to identify novel drivers of resistance to combination endocrine therapy (tamoxifen) and CDK4/6 inhibitor (palbociclib) treatment. Overall, we demonstrate that suppression of JNK signalling enables persistent growth during combined endocrine therapy and CDK4/6 inhibition. Our data provides the pre-clinical rationale to stratify patients based on JNK pathway activity prior to receiving combination endocrine therapy and CDK4/6 inhibition.

We identified MAP2K1 to 7 as potential diagnostic markers, and MAP2K2 to 7 as prognostic markers, of LIHC. Our future work will promote the use of MAP2Ks in the diagnosis and treatment of LIHC.

Our findings establish a multi-layered regulatory mechanism of TNF-α signaling in astrocytic tumors. These data highlight the TNF-α/IL-1β/MAP3K8 axis as a critical driver of glioma aggressiveness and a potential therapeutic target.

Meanwhile, MAP2K7 is the most potential target for sensitizing PTT. By integrating ARS with PTT agents, the serine-MAPK axis in CAFs is successfully modulated, thereby overcoming PTT resistance in TNBC therapy.

POLG and MAP2K7 demonstrate crucial roles in the progression from AA to MDS and, ultimately, to AML. These genes regulate more than 20 immune regulatory pathways through MIF-mediated communication, thereby influencing disease progression.

The heterogeneity of ATGs expression was dependent on cell subsets, pathologic conditions, and challenges, as well as varied among cellular phenotypes, functions, and behaviors, and the severity of lung diseases. In conclusion, our data might provide new insights into the roles of ATGs in epithelial biology and pulmonary disease pathogenesis, with implications for disease progression and prognosis.

The tumor was completely excised with negative margins. The patient is doing well at 17 months follow-up with no signs of recurrence.

Despite some progress, further research is needed to fully comprehend the role of MAP2K7 in cancer and assess the potential use of kinase inhibitors in cancer therapy. This review examines the role of MAP2K7 in cancer and the development of small-molecule inhibitors.