Biofield therapy inhibits pancreatic cancer invasion and metastasis by modulating multiple steps of metastatic cascade

Biofield therapies (BTs) are gaining attention as potential complementary treatments for cancer. Some devices have been developed to mimic the energetic or electromagnetic fields emitted by BT practitioners. We previously reported that BT significantly inhibited growth and invasiveness of pancreatic cancer cells in vitro and in relevant animal models. To identify which steps of the metastatic cascade are affected by BT and to elucidate potential antimetastatic mechanisms in pancreatic ductal adenocarcinoma (PDAC), we conducted in vivo studies using metastatic mouse models. In a KPCY orthotopic model, BT treatment significantly reduced the percentage of visible liver nodules by 61.3% and 54.6% compared with the colony control (CC) and sham control (SC) groups, respectively (p < 0.05). Imaging of YFP+ cells in the liver tissues revealed a significant reduction in disseminated tumor cells in the BT group relative to CC and SC groups (p < 0.05). In a tail-vein injection model, lung tissues from BT treated mice exhibited a significant 59.6% reduction in YFP+ signal intensity compared with SC mice, supporting the conclusion that BT suppresses metastatic dissemination of PDAC cells. BT treated mice bearing PANC-1 orthotopic tumors had significantly lower levels of tumor cell-free DNA (11.5 ± 4.6 ng/μl) compared with sham control (24.7 ± 7.9 ng/μl; p < 0.01), suggesting that BT treatment impairs tumor cell intravasation. This is consistent with our previous findings that BT inhibits EMT in human PDAC PANC-1 cells. Additionally, BT induced anoikis in PANC-1 cells, indicating that BT may also reduce PDAC cell survival in circulation. To investigate whether BT affects metastatic colonization, both PANC-1 and KPCY cells were exposed to BT and subjected to adhesion assay using phalloidin staining and fibronectin quantification, as fibronectin is a key regulator of cell adhesion. PANC-1 cells exposed to BT for 15 mins showed an average of 14 ± 4 adhered cells per field, compared with 96 ± 35 in the SC group (p < 0.0001). Similarly, fibronectin-based cell adhesion measurements showed a 58.3% decrease in BT-treated PANC-1 cells relative to SC (p < 0.001). BT also significantly reduced F-actin intensity in PANC-1 cells (p < 0.01), with similar results observed in KPCY cells after 30 min of treatment. Epigenetic profiling further revealed that BT modulated the expression of genes involved in actin cytoskeleton regulation. Collectively, these results demonstrated that biofield therapy suppressed multiple metastatic steps including cell invasion/migration, intravasation, survival in circulation, and colonization ultimately contributing to its antimetastatic effects in PDAC models. These processes may be mediated in part through alterations in cytoskeleton organization, particularly actin dynamics.