In the present analysis, emetine affected both CAF and the tumor cells in vitro; it inhibited CAF-mediated support of tumor cell survival and it inhibited glycolysis due to the suppression of HIF-1α and key enzymes of glycolysis including HK2 and PDK1 in tumor cells, leading to the accumulation of intracellular ROS and the induction of apoptosis. Here, PDK1 is linked to neoplasm.