PTK2 and neoplasm: ECM1a modulated CDDP resistance and tumor formation by activating the AKT/FAK/Paxillin/Rac/cytoskeletal axis and stimulating the CD326 via various mechanisms such as alternative splicing through hnRNPLL, enhancing tumor cell stemness via ABCG1, and interacting with integrin αXβ2 through the Gly-Pro-Arg (GPR) motif.