Previously, we cloned a new gene termed 'tongue cancer resistance-associated 
protein 1' (TCRP1), which modulates tumorigenesis, enhances cisplatin (cDDP) 
resistance in cancers, and may be a potential target for reversing drug 
resistance. However, the mechanisms for regulating TCRP1 expression remain 
unclear. Herein, we combined bioinformatics analysis with luciferase reporter 
assay and ChIP assay to determine that c-Myc could directly bind to TCRP1 
promoter to upregulate its expression. TCRP1 upregulation in multidrug resistant 
tongue cancer cells (Tca8113/PYM) and cisplatin-resistant A549 lung cancer cells 
(A549/DDP) was accompanied by c-Myc upregulation, compared to respective 
parental cells. In tongue and lung cancer cells, siRNA-mediated knockdown of 
c-Myc led to decrease TCRP1 expression, whereas overexpression c-Myc did the 
opposite. Moreover, TCRP1 knockdown attenuated chemoresistance resulting from 
c-Myc overexpression, but TCRP1 overexpression impaired the effect of c-Myc 
knockdown on chemosensitivity. Additionally, in both human tongue and lung 
cancer tissues, c-Myc protein expression positively correlated with TCRP1 
protein expression and these protein levels were associated with worse prognosis 
for patients. Combined, these findings suggest that c-Myc could 
transcriptionally regulate TCRP1 in cell lines and clinical samples and 
identified the c-Myc-TCRP1 axis as a negative biomarker of prognosis in tongue 
and lung cancers.