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. 2020 Jul 24;12(8):2037. doi: 10.3390/cancers12082037

Figure 2.

Figure 2

S100 signalling in lung cancer. Extracellular S100A4 inhibits autophagy and induces Wnt signalling by interacting with the receptor for advanced glycation end products (RAGE) and intracellular S100A4 additionally activates β-catenin, resulting in increased proliferation and enhanced viability of lung cancer cells. S100A4 also induces the expression of (MMP9) by activating nuclear factor “kappa-light-chain-enhancer” of activated B-cells (NF-κB), thereby promoting invasion and metastasis. S100A7 is most likely involved in adenocarcinoma (ADC) to squamous cell carcinoma (SSC) transdifferentiation of lung cancer cells, by upregulating the SSC marker DNp63 and downregulation of the ADC markers thyroid transcription factor 1 (TTF1) and aspartic proteinase napsin (napsin A). In this context, an inverse correlation of S100A7 and yes-associated protein (YAP) was observed. Moreover, S100A7 seems to activate NF-κB-dependent cell proliferation. Within lung cancer-derived brain metastasis cells, S100B was shown to upregulate the expression of B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma extra-large (Bcl-xL), indicating that S100B is capable of suppressing apoptosis.