Anti-STAT3 (C-terminal) polyclonal antibody

Cancer stem cells (CSCs) play an important role in shaping the invasive cancer phenotype by contributing to tumor initiation, metastasis, relapse, and therapeutic resistance in non-small cell lung cancer (NSCLC). The Aryl hydrocarbon receptor (AhR), a ligand activated transcription factor, which is well known for mediating the toxicity and tumorigenesis of a variety of environmental pollutants, has been extensively recognized as an important mediator in NSCLC development. Here, evidence showed that AhR was overexpressed in NSCLC tissues, and a high AhR protein level was associated with an aggressive tumor phenotype. Knockdown of AhR suppressed cell proliferation, invasion and migration, as well as CSC-like properties, while upregulation and activation of AhR enhanced CSC-like properties and increased stem cell-associated gene expression in NSCLC cells. Elevated and activated AhR leads to phosphorylation of janus kinase 2 (Jak2), as well as its downstream effector, activator of transcription 3 (STAT3), while inhibition of Jak2/STAT3 signaling by pharmacologic approach attenuates the effects of AhR-mediated NSCLC cell stemness, suggesting a role for the Jak2/STAT3 pathway in AhR-regulated NSCLC stemness. In summary, our study uncovers a transcriptional-independent mechanism of AhR through which AhR mediates NSCLC stemness via Jak2/STAT3 signaling pathway, indicating a promising target for the treatment of NSCLC.

Gastric cancer is one of the most lethal cancers worldwide. FYN, a gene that is differentially expressed in gastric cancer, is considered a critical metastasis regulator in several solid tumors, but its role in gastric cancer is still unclear. This study aimed to evaluate the role of FYN and test whether FYN promotes migration and invasion of gastric cancer cells in vitro and in vivo via STAT3 signaling. FYN was overexpressed in gastric cancer and positively correlated with metastasis. FYN knockdown significantly decreased cancer cell migration and invasion, whereas FYN overexpression increased cancer migration and invasion. Genetic inhibition of FYN decreased the number of metastatic lung nodules in vivo. Several epithelial-mesenchymal transition markers were positively correlated with FYN expression, indicative of FYN involvement in this transition. Furthermore, gene set enrichment analysis of a Cancer Genome Atlas dataset revealed that the STAT3 signaling pathway was positively correlated with FYN expression. STAT3 inhibition reversed the FYN-mediated epithelial-mesenchymal transition and suppressed metastasis. In conclusion, FYN promotes gastric cancer metastasis possibly by activating STAT3-mediated epithelial mesenchymal transition and may be a novel therapeutic target for gastric cancer.