Extracellular Vesicles: A New Perspective in Tumor Therapy.

In recent years, the study of extracellular vesicles has been booming across various industries. Extracellular vesicles are considered one of the most important physiological endogenous carriers for the specific delivery of molecular information (nucleonic acid, cytokines, enzymes, etc.) between cells.

Ursolic Acid Attenuates TGF-β1-Induced Epithelial-Mesenchymal Transition in NSCLC by Targeting Integrin αVβ5/MMPs Signaling.

Transforming growth factor-β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) of non-small cell lung cancer (NSCLC) may contribute to tumor metastasis. TGF-β1-induced EMT in H1975 cells (a human NSCLC cell line) resulted in the adoption of mesenchymal responses that were predominantly mediated via the TGF-β1-integrin signaling pathway. Ursolic acid has been previously reported to inhibit tumor growth and metastasis in several cancers.

Epithelial-mesenchymal transition: potential regulator of ABC transporters in tumor progression.

Epithelial-mesenchymal transition (EMT) can directly contribute to some malignant phenotypes of tumor cells including invasion, metastasis and resistance to chemotherapy. Although EMT is widely demonstrated to play a critical role in chemoresistance and metastasis, the potential signaling network between EMT and drug resistance is still unclear. The distribution of drugs in the internal and external environment of the tumor cells is tightly linked with ATP-binding cassette (ABC) transporters.

CCNA2 facilitates epithelial-to-mesenchymal transition via the integrin αvβ3 signaling in NSCLC.

Non-small cell lung carcinoma (NSCLC) is the most common malignancy with the highest morbidity and mortality. Studies have demonstrated that the abnormal expression of cyclin-A2 (CCNA2) is associated with multiple malignancies, yet its functional role in NSCLC metastasis remains to be elucidated. In the present study, we investigated the role of CCNA2 in regulating migration and invasion of NSCLC cells by establishing NSCLC cell strains with constitutively silenced or elevated CCNA2 expression.