LIN28B plays an important role in radiation responses of lung cancer cells through inhibiting let-7g microRNA processing and increasing translation of KRAS.

Genetic variants of LIN28B may be biomarkers for susceptibility to severe radiation pneumonitis in non-small cell lung cancer patients.

LIN28B was a direct target of miR-26a in ambient particulate matter-bound metal-triggered lung cancer.

The effects of acetylated Lin28B on let-7a-1 and let-7g are similar to that of stable knockdown of Lin28B in H1299 cells. The new role of PCAF in mediating Lin28B acetylation and the specific release of its target microRNAs in H1299 cells may shed light on the potential application of let-7 in the clinical treatment of lung cancer patients

Study investigated the effects of LIN28B expression on lung tumorigenesis using LIN28B transgenic overexpression in an autochthonous KRAS(G12V)-driven mouse model. LIN28B accelerates tumor initiation and enhances cell proliferation leading to a shortened overall survival. In addition, LIN28B expression is found in 24% of KRAS-mutated cases.

H19 depresses miR-196b to elevate LIN28B, resulting in accelerating cell proliferation in lung cancer.

Study provides evidence that cancer-testis (CT) genes LIN28B and was activated in lung adenocarcinoma (LUAD) patients. Its high expression is significantly associated with LUAD worse overall survival. Also, LIN28B promotes tumor proliferation and metastasis in vitro and in vivo.