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Del-1 and EMP2 are over-expressed in TNBC and show an inverse regulatory relationship. Del-1 knockdown promotes stemness features, while EMP2 knockdown reduces proliferation and increases chemosensitivity. These findings highlight the Del-1/EMP2 axis as a potential regulatory pathway in TNBC progression and resistance, suggesting that EMP2 may serve as a novel therapeutic target.
Lee et al. (Tue,) studied this question.