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Background  Previous research has revealed that Krüppel‐like factor 5 ( KLF5 ) may affect DNA damage repair pathways; however, the associated molecular mechanisms are unclear.    Methods  The expression of  KLF5  was studied by immunohistochemical staining in paired tumour and normal tissues from 90 patients with ESCC. We studied the effects of  KLF5  knockdown on cell proliferation and apoptosis with or without cisplatin treatment in A549 and H1299 cell lines. Moreover, we examined the effect of  KLF5  on the DNA damage response.    Results   KLF5  was significantly overexpressed in non‐small cell lung cancer (NSCLC) tissues, and high  KLF5  expression predicted poor prognosis for NSCLC patients. The inhibition of  KLF5  markedly augmented cisplatin‐induced cell apoptosis. In addition, we observed that  KLF5  knockdown could decrease DNA repair potential by inhibiting H2AX S139 phosphorylation in response to cisplatin. Moreover, silencing of  KLF5  in NSCLC cell lines inhibited the phosphorylation of checkpoint kinases Chk1 S345 and Chk2 T68.  KLF5  knockdown permits cells with broken or damaged DNA strands to enter mitosis by inhibiting the activation of H2AX, Chk1 and Chk2, resulting in mitotic catastrophe.    Conclusion   KLF5  plays a significant role in the DNA damage response by regulating DNA damage checkpoint proteins. Inhibition of  KLF5  may be a potential therapeutic target for NSCLC patients with cisplatin resistance.

Knockdown of KLF5 promotes cisplatin‐induced cell apoptosis via regulating DNA damage checkpoint proteins in non‐small cell lung cancer