circulating miR-142-3p was found to be associated with a high risk of recurrence in early-stage lung adenocarcinoma patients, and a putative serum marker for risk assessment.

Functional enrichment analysis identified MIR-142-5p and miR-9 as being involved in squamous lung cancer by regulating cell cycle genes.

data demonstrate that miR-142-3p influences the proliferation of non-small cell lung cancer cells through repression of TGFbetaR1

Suggest that miR-142-3p may function as a tumor suppressor through the downregulation of HMGB1 in non-small-cell lung carcinoma.

These findings shed light on the therapeutic potential of miR-142-3p in combating acquired Non-small-cell lung cancer chemo-resistance.

The inhibition of PTEN also reduced the cancer effects of CD4+ T cells on non-small cell lung cancer (NSCLC) cell lines following miR-142-5p downregulation. Therefore, our study demonstrated that miR-142-5p regulated CD4+ T cells in human NSCLC through PD-L1 expression via the PTEN pathway.

miR-142-3p inhibits lung adenocarcinoma cell proliferation, migration and invasion, and enhances cell apoptosis by targeting NR2F6.

ur study revealed that TTN-AS1 played an important role in lung adenocarcinoma (LUAD) progression. TTN-AS1/miR-142-5p/CDK5 regulatory axis may serve as a novel therapeutic target in the treatment of LUAD.

MiR-142 inhibits lung cancer cell proliferation and promotes apoptosis by targeting XIAP.

LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1.