Tubulin epsilon and delta complex 2 enhances malignancy in non-small cell lung cancer by activating the hedgehog signaling pathway to promote tumor cell stemness.

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, accounting for approximately 85 % of cases, and is associated with high incidence and mortality rates. The presence of cancer stem cells (CSCs) contributes significantly to treatment resistance and poor patient prognosis. This study investigates the role of tubulin epsilon and delta complex 2 (TEDC2) in the progression and stemness of NSCLC. We found that TEDC2 was aberrantly overexpressed in various solid tumors, specifically in lung adenocarcinoma (LUAD), and its expression negatively correlated with patient prognosis. Functional assays demonstrated that the knockdown of TEDC2 inhibited the proliferation, migration, and maintenance of stemness in tumor cells, primarily through the inhibition of the Hedgehog (Hh) signaling pathway. Additionally, TEDC2 knockdown enhanced the sensitivity of NSCLC cells to chemotherapy drug cisplatin (DDP). In vivo animal models further demonstrated that knockdown of TEDC2 could inhibit tumor cell stemness and enhance the therapeutic efficacy of DDP. These findings highlight TEDC2 as a critical regulator promoting NSCLC progression, which may serve as a potential therapeutic target. Targeting TEDC2 could enhance the efficacy of existing treatment strategies, providing a new avenue for improving clinical outcomes of NSCLC patients.