PFN2 (Profilin)

PFN2 is an oncogenic driver that promotes OSCC progression through HDAC1-dependent transcriptional reprogramming. PFN2 may serve as a prognostic biomarker and predictor of response to HDAC-targeted therapy.

Our study revealed oncogene PFN2 promoted tumor angiogenesis in LUAD through regulating PKM2 nuclear translocation, providing novel molecular therapy targets for LUAD treatment.

This study unveils the roles of SIX2 in governing GC cell stemness, defining a novel SIX2/PFN2 regulatory loop responsible for this regulation. This suggests the potential of targeting the SIX2/PFN2 loop for GC treatment (Graphical Abstracts).

Overall, aberrant PFN2 expression is unreported in lung metastasis in colorectal cancer. In the present study, two PFN2 isoforms with differential tissue distribution were upregulated in metastatic cells, suggesting that they promote lung metastasis in colorectal cancer.

Collectively, these findings show that miR-1287-5p/PFN2 signaling was associated with downregulation of circ-SLC16A1 and reduced invasion and proliferation of NSCLC cells. So, circ-SLC16A1 is identified as a mediator of multiple pro-oncogenic signaling pathways in NSCLC and can be targeted to suppress tumor progression.

Additionally, downregulation of circ0020134 inhibited epithelial-mesenchymal transition (EMT) in CRC cells, which could be reversed by miR-183-5p inhibitor treatment. Collectively, our findings confirm that the circ0020134-miR-183-5p-PFN2-TGF-β/Smad axis induces EMT transformation within tumor cells, promoting CRC proliferation and metastasis, thus highlighting its potential as a therapeutic target for patients with CRC liver metastasis.

Upregulated PFN2 ultimately promotes tumorigenesis and invasion in SCLC. These findings provide novel prognostic indicators as well as promising new therapeutic targets for SCLC.