The miR-29 family (miR-29a, -29b, and -29c) suppresses the Wnt signaling pathway through demethylation of WIF-1 in non-small-cell lung cancer.

miR-29a suppress the growth, migration, and invasion of lung adenocarcinoma by binding 3'UTR CEACAM6.

Data suggest that expression of two microRNAs (MIRN19b-3p; MIRN29b-3p) by peripheral blood mononuclear cells may serve as biomarkers for early detection/diagnosis of non-small-cell lung carcinoma (with 72.62% sensitivity and 82.61% specificity).

Loss of tumor-suppressive miR29s enhanced cancer cell invasion in lung SCC through direct regulation of oncogenic LOXL2.

miR-29a-3p and miR-150-5p were identified as circulating biomarkers that correlated with delivered thoracic radiation dose in non-small cell lung cancer

Overexpression of LOXL2 and SERPINH1 was observed in clinical specimens of lung cancer and fibrotic lesions. Downregulation of miR-29a caused overexpression of LOXL2 and SERPINH1 in lung cancer and IPF, suggesting that these genes are involved in the pathogenesis of these two diseases.

miR-29 appears to mediate critical homeostatic functions, as decreased levels of this miRNA have been frequently noted in many respiratory disorders, including idiopathic pulmonary fibrosis (IPF), pulmonary hypertension, and lung cancer.

Our study provided the first evidence that miR-29a suppressed lung cancer cell growth through inhibition of NRAS

Similar levels of miR-29a and miR-185 were detected in Idiopathic pulmonary fibrosis and lung cancer while their common targets AKT1 and DNMT3b were not found to differ, suggesting potential pathogenetic similarities at the level of key epigenetic regulators.

MiR-29 regulates SETDB1 and indirectly Suv39h1 in the non-small cell lung cancer.expression levels of all the miR-29 family members are markedly down-regulated in non-small cell lung cancer.

MIR29a down-regulates MTSS1, a suppressor of tumor proliferation and invasion, which promotes the proliferation of non-small-cell lung carcinoma cells.