TP53 is the most common gene mutated in human cancers, including in cholangiocarcinoma (CCA). The gain‑of‑function properties of p53 variants are often involved in cancer progression. The present study demonstrated that a truncated del p53 variant, del p53M213, exhibited gain‑of‑function properties and was highly expressed in the invasive liver fluke Opisthorchis viverrini‑associated CCA cell line, KKU‑M213. The del p53M213 variant lacked exons 7‑9 and contained a V31I substitution (p53‑p72‑Δ225‑331‑V31I). Stably transfected p53‑null human non‑small cell lung H1299 cells exhibited a del p53M213 localization in both the cell cytosol and nucleus. Del p53M213 lacked anti‑growth functions, and instead enhanced migration and invasiveness. In addition, this p53 variant downregulated claudin‑1 expression and promoted Cdc42 activation, consistent with the roles of claudin‑1 and Cdc42 in inhibiting cell‑cell dissociation and promoting cell migration, respectively. On the whole, although del p53M213 is an important driver of cancer cell migration and invasiveness, other properties related to its novel gain‑of‑function properties require further investigation in order to develop effective treatment strategies for cancers bearing this truncated TP53 allele.