TSPAN2 is involved in cell invasion and motility during lung cancer progression.

In lung cancer progression, p53 mutations are more often observed in invasive tumors than in noninvasive tumors, suggesting that p53 is involved in tumor invasion and metastasis. To understand the nature of p53 function as a tumor suppressor, it is crucial to elucidate the detailed mechanism of the alteration in epithelial cells that follow oncogenic KRAS activation and p53 inactivation. Here, we report that KRAS activation induces epithelial-mesenchymal transition and that p53 inactivation is required for cell motility and invasiveness. Furthermore, a transmembrane protein, is responsible for cell motility and invasiveness elicited by p53 inactivation. is highly expressed in p53-mutated lung cancer cells, and high expression of Tduanyu1842N2 is associated with the poor prognosis of lung adenocarinomas. Tduanyu1842N2 knockdown suppresses metastasis to the lungs and liver, enabling prolonged survival. Tduanyu1842N2 enhances cell motility and invasiveness by assisting CD44 in scavenging intracellular reactive oxygen species.

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