Most tumor cells reprogram their glucose metabolism as a result of mutations in oncogenes
and tumor suppressors, leading to the constitutive activation of signaling pathways involved …

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 …

The JNKs are master protein kinases that regulate many physiological processes, including
inflammatory responses, morphogenesis, cell proliferation, differentiation, survival and …

Abstract p16INK4a, located on chromosome 9p21. 3, is lost among a cluster of neighboring
tumor suppressor genes. Although it is classically known for its capacity to inhibit cyclin …

Abstract Integrin beta 4 (ITGB4) overexpression in cancer cells contributes to cancer
progression. However, the role of stromal ITGB4 expression in cancer progression remains …

Most tumour cells use aerobic glycolysis (the Warburg effect) to support anabolic growth and
evade apoptosis. Intriguingly, the molecular mechanisms that link the Warburg effect with the …

Long non-coding RNAs (lncRNAs) have been shown to be implicated in the complex
network of cancer including malignant melanoma and play important roles in tumorigenesis …

Regulation of cell survival is a key part of the pathogenesis of multiple myeloma (MM). Jun N-
terminal kinase (JNK) signaling has been implicated in MM pathogenesis, but its function is …

Abnormal energy metabolism, as one of the important hallmarks of cancer, was induced by
multiple carcinogenic factors and tumor-specific microenvironments. It comprises aerobic …

JNKs (c-Jun N-terminal kinases) belong to mitogen-activated protein kinases' family and
become activated by several growth factors, stress, radiation, and other extracellular signals …