Open AccesslncRNA‐ NKILA / NF ‐ κ B feedback loop modulates laryngeal cancer cell proliferation, invasion, and radioresistance
Author(s) -
Yang Tao,
Li Shisheng,
Liu Jiajia,
Yin Danhui,
Yang Xinming,
Tang Qinglai
Publication year - 2018
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1405
Subject(s) - radioresistance , cancer , cancer research , gene knockdown , cancer cell , suppressor , nf κb , viability assay , cell growth , chemistry , downregulation and upregulation , cytotoxicity , cell , apoptosis , biology , radiation therapy , medicine , biochemistry , in vitro , gene
Laryngeal cancer is one of the most common head and neck malignant tumors and is commonly resistant to X‐ray‐based radiotherapy. NF ‐ κ B interacting lncRNA ( NKILA ) has been reported to serve as a tumor suppressor in several cancers through combining with NF ‐ κ B: I κ B complex thereby inhibiting NF ‐ κ B activation. Herein, we demonstrated a low NKILA expression in laryngeal cancer and its correlation with shorter overall survival in patients with laryngeal cancer. NKILA serves as a tumor suppressor in laryngeal cancer by suppressing laryngeal cancer cell viability and migration, whereas promoting cell apoptosis; NKILA knockdown reverses the cytotoxicity of X‐ray radiation on laryngeal cancer cells through combining with NF ‐ κ B: I κ B complex to inhibit I κ B phosphorylation, inhibit p65 nuclear translocation, and finally inhibit NF ‐ κ B activation. NF ‐ κ B binds to the promoter region of NKILA to activate its transcriptional activity, upregulated NKILA then inhibits I κ B phosphorylation and NF ‐ κ B activation, thus forming a negative feedback loop to sensitize laryngeal cancer cell to X‐ray radiation. In conclusion, NKILA can serve as a promising agent of enhancing the cytotoxicity of X‐ray radiation on laryngeal cancer and addressing the radioresistance of laryngeal cancer.