Peiying Yang, Daoyan Wei, Sharmistha Chakraborty, Phuong Nguyen, Andrew Cusimano, Defeng Deng, Shafaqmuhammad Iqbal, Monica Nelson, Meng Cui, Jianliang Dai, Mihai Gagea, Richard Wagner, Yisheng Li, Lorenzo Cohen
BACKGROUND: The high mortality of pancreatic ductal adenocarcinoma (PDAC) underscores the need for novel treatments. We investigated the potential role of human biofield therapy (BT) in modifying tumorigenic processes in murine and human PDAC cells through a series of in vitro and in vivo studies. METHODS: Cell viability and ultrastructure changes were examined by PrestoBlue assay and Transmission Electron Microscope, respectively. Cell voltage potentials were assessed using DiBAC4 staining. Both FOXM1 CRISPR KO and Tet-on FOXM1 overexpressing PDAC cells were used for the mechanistic studies. Antitumor efficacy was tested in orthotopic models using human PANC-1 and mouse KPCY cells. RESULTS: Multiple mouse and human PDAC cell lines exposed to BT (three different therapists using a standardized procedure) showed significantly reduced proliferation compared to sham control (SC) and incubator control (IC) cells across multiple studies. BT induced swollen mitochondria in PANC-1 cells and increased G1 cell cycle arrest in PANC-1, L3.7, and COLO357 cells. BT also downregulated key cell cycle regulators including FOXM1 in PANC-1 and L3.7 cells (p < 0.05). BT led to a 36.7% reduction of cell voltage potential measured in PANC-1 cells (p < 0.01), with similar effects in MiaPaCa-2 and KPCY cells. Furthermore, BT reduced the invasiveness in PANC-1, L3.7, and COLO357 cells, an effect influenced by FOXM1 gene expression. BT inhibited the primary tumor growth and liver metastasis of PANC-1 and KPCY cells in orthotopic mouse models (p < 0.05). CONCLUSIONS: These novel findings support the potential of BT to influence growth and metastasis of pancreatic cancer cells and warrant further investigation.