E-钙粘蛋白（一种上皮细胞粘附分子）的丢失通过介导上皮-间质转化（EMT）而与转移有关，从而促进癌细胞的侵袭和迁移。然而，最近的研究表明，E-钙粘蛋白支持转移性癌细胞的存活和增殖。在这里，我们通过上调丝氨酸从头合成途径（SSP）确定了 E-钙粘蛋白在乳腺癌中的代谢作用。上调的SSP为生物合成和抵抗氧化应激提供了代谢前体，使E-钙粘蛋白乳腺癌细胞能够实现更快的肿瘤生长和增强的转移。 PHGDH（SSP 中的限速酶）的抑制可显着且特异性地阻碍 E-钙粘蛋白乳腺癌细胞的增殖，并使它们容易受到氧化应激的影响，从而抑制其转移潜力。这些发现表明，E-钙粘蛋白重新编程细胞代谢，促进乳腺癌的肿瘤生长和转移。

The loss of E-cadherin, an epithelial cell adhesion molecule, has been implicated in metastasis by mediating the epithelial-mesenchymal transition (EMT), which promotes invasion and migration of cancer cells. However, recent studies have demonstrated that E-cadherin supports the survival and proliferation of metastatic cancer cells. Here, we identified a metabolic role for E-cadherin in breast cancer by upregulating the de novo serine synthesis pathway (SSP). The upregulated SSP provided metabolic precursors for biosynthesis and resistance to oxidative stress, enabling E-cadherin+ breast cancer cells to achieve faster tumor growth and enhanced metastases. Inhibition of PHGDH, a rate-limiting enzyme in the SSP, significantly and specifically hampered proliferation of E-cadherin+ breast cancer cells and rendered them vulnerable to oxidative stress, inhibiting their metastatic potential. These findings reveal that E-cadherin reprograms cellular metabolism, promoting tumor growth and metastasis of breast cancers.