Tridax procumbens promotes apoptosis and suppresses markers of proliferation, growth, and metastasis in pancreatic ductal adenocarcinoma cells

We assessed whether Tridax procumbens (TP) extracts could be used therapeutically against pancreatic cancer and remain nontoxic to normal cell types. The crude extract from TP (CETP) was fractionated using hexane, dichloromethane, and ethyl acetate to obtain fractions (NHF, DCMF, and EAF, respectively). The pancreatic ductal adenocarcinoma cell line (PANC-1) was cultured with (10, 20, 50, 100, and 250 μg/mL) dimethyl sulfoxide (DMSO) (control), CETP, and CETP-fractions for 24 or 48 h. As a normal cell type, we cultured E11.5d mouse pancreatic explants for five days before treating with the test samples (20 μg/mL) in DMSO for a further 48 h. Cytotoxicity assays (MTT and Live-Dead) were conducted, and the expression of cellular biomarkers, such as vimentin, Ki-67, p53, p21, and caspase-3, was evaluated. DCMF elicited PANC-1 cell death (IC₅₀ = 23.1 μg/mL) compared to CETP (IC₅₀ = 114.2 μg/mL). There were significant elevations in p53 (2.8-fold), caspase-3 (2.9-fold), catalase (4.0-fold), p21^Cip1/Wap−1 (4.4-fold), and ALP (5.0-fold) proteins in DCMF-treated cells compared to control. DCMF significantly suppressed PNA and GST-pi (2.3-fold), Ki-67 (2.7-fold), and vimentin (10.8-fold) in PANC-1 cells relative to control. Also, DCMF induced Bcl-2 perinuclear staining and cytoplasmic translocation of APC in treated cells. Phenotype morphogenesis was observed in DCMF-treated embryonic pancreas with immunopositivity for insulin, vimentin, and amylase (1.3-fold), cytokeratin-7 (1.5-fold), PNA (1.9-fold), and glucagon (2.8-fold). In conclusion, Tridax procumbens appear to exert its anticancer effect via induction of apoptosis, antioxidant enzymes, and suppression of growth, proliferation, and invasiveness in PANC-1 cells without any observable toxicity on the normal embryonic pancreas.