Integrated bioinformatics analysis reveals the bidirectional effects of TSPAN6 for cisplatin resistance in lung cancer.

ABSTRACT

Cisplatin-based chemotherapy is frequently employed as the primary therapeutic approach for advanced lung cancer. Nevertheless, a significant proportion of patients may develop resistance to cisplatin, leading to diminished efficacy of chemotherapy. Through analysis of Gene Expression Omnibus databases, TSPAN6 has been identified as a key factor in conferring resistance to cisplatin, attributed to its activation of the NF-κB signaling pathway. Knockdown of TSPAN6 using siRNA resulted in decreased expression levels of NF-κB in A549 cells. This indicates that TSPAN6 may have dual effects on lung cancer cisplatin resistance and could serve as a promising therapeutic target for individuals with cisplatin resistance.