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17 reviewsLymph node metastasis is crucial for esophageal squamous cell carcinoma (ESCC) malignancy. However, the molecular drivers andrelated mechanisms of lymph node metastasis in ESCC cells are unclear. In the present study, we found that the tyrosine kinasecomplex-focal adhesion kinase (FAK)/Src family kinase (SFK) axis specifically contributes to metabolic reprogramming by inducingthe phosphorylation of ATP-citrate synthase (ACLY) Tyr542, Tyr652, and fructose-bisphosphate aldolase A (ALDOA) Tyr174, Tyr302,or Tyr328 sites in both primary and metastatic ESCC cells. Mechanistically, activated ACLY and ALDOA and their metabolites drive atranscriptional program in primary tumors that induces cyclin-dependent kinase 7/9 (CDK7/9) complex-mediated expression ofDNA replication- and cell proliferation-related molecules. This process functions as an enabler of tumor malignancy. In metastatic1234567890();,:tumor cells, metabolic enzymes and their products facilitate the transcriptional activity of Yamanaka factors to induce the activationof downstream plasticity-related molecules, fueling ESCC cell survival within metastatic lymph nodes. FAK/SFK axis-controlled ACLYand ALDOA tyrosine phosphorylation and downstream transcription factors and effectors in primary and metastatic ESCC cells arestrongly associated with poor patient outcomes. We discovered a lead compound, quercetagitrin, that inhibits the phosphorylationof ALDOA at Tyr174, 302, and 328. Moreover, it has been shown to have antitumor effects alone or in combination with FAK/SFKinhibitors both in vivo and in vitro. The inhibition of tyrosine kinase-regulated metabolic enzyme activities and related signalingnetworks may be a potential strategy for the treatment and diagnosis of metastatic ESCC.