results suggest that hsa-miR-145 is a key player in protecting a cell against EGFR mutation; restoration of hsa-miR-145 successfully inhibits growth in lung adenocarcinoma cells with EGFR mutation

miR-145 inhibits proliferation of non-small cell lung cancer cells through c-Myc

miR-145 can impair the proliferation of human lung adenocarcinoma-initiating cells by targeting OCT4

MiR-145 can inhibit the proliferation of lung cancer stem cells in A549 cell line via down-regulating OCT4 expression.

miR-145 and miR-367 may have roles in relapse in surgically treated nonsmall cell lung cancer

Low miR-145 expression is associated with lung cancer.

These results suggest that miR-145 may have a cell type-specific function and play important roles in the process of brain metastases from lung adenocarcinoma.

EGFR activation is involved in the downregulation of miR-145 in lung cancer cells

Data indicate that the expression level of miR-145 was downregulated in lung adenocarcinoma tissues.

miR145 inhibited lung cancer cell metastasis and EMT via targeting the Oct4 mediated Wnt/betacatenin signaling pathway.

higher expression in cisplatin-resistant non-small-cell lung carcinoma

These preliminary data suggest that serum miR-125a-5p, miR-145 and miR-146a may be useful noninvasive biomarkers for the clinical diagnosis of Non-small-cell lung cancer.

DNA hyper-methylation in the miR-145 promoter region reduced its expression in lung adenocarcinoma and miR-145 expression level might serve as a novel prognostic biomarker.

This prompts for further studies on the mechanisms behind the TP53-induced regulation of SOX2 expression and the possible importance of hsa-miR-145 in lung cancer.

miR-145-3p functions as a tumor-suppressor as well as miR-145-5p in lung squamous cell carcinoma cells.

Studied the roles of MIRN145 in lung adenocarcinoma (LAC) and its targeting of N-cadherin. Knockdown of N-cadherin inhibited invasion and migration of LAC cell lines similar to overexpression of MIRN45.

Results show that mir-145 expression level is dowregulated in non-small cell lung cancer (NSCLC) and may inhibit cell growth, motility, and chemotaxis in NSCLC by targeting PDK1 through suppressing the mTOR pathway.

These results suggested that RIOK2 and NOB1 may be potential targets in the treatment of Non-small cell lung cancer (NSCLC), and miR145 may be considered a therapeutic inhibitor of both genes.

Genes regulated by anti-tumor miR-145-5p and miR-145-3p are closely involved in the molecular pathogenesis of lung adenocarcinoma.

the present study demonstrated that miR145 regulates the EGFR/PI3K/AKT signaling pathway in patients with nonsmall cell lung cancer.

Increased miR-145 expression exerted a critical role in subsiding the growth, survival and migration of a lung cancer cell line.

The expression of miRNA-145 is higher in the normoxic conditions than hypoxic conditions in breast, prostate and lung cancer cell lines. This result shows that hypoxia, a metastasis-inducing factor, down regulates miR-145 expression.

Long non-coding RNA JPX correlates with poor prognosis and tumor progression in non-small-cell lung cancer by interacting with miR-145-5p and CCND2.

miR-145 rs3733846 polymorphism is associated with an increased lung adenocarcinoma risk among nonsmoking females residing in northeast China.

Nonenzymatic function of Aldolase A downregulates miR-145 to promote the Oct4/DUSP4/TRAF4 axis and the acquisition of lung cancer stemness.

The long non-coding RNA PVT1/miR-145-5p/ITGB8 axis regulates cell proliferation, apoptosis, migration and invasion in non-small cell lung cancer cells.

CircRNA BIRC6 promotes non-small cell lung cancer cell progression by sponging microRNA-145.

The expression and clinical significance of B7-H3 and miR-145 in lung cancer patients with malignant pleural effusion.

Loss of miR-145-5p Causes Ceruloplasmin Interference with PHD-Iron Axis and HIF-2alpha Stabilization in lung Adenocarcinoma-Mediated Angiogenesis.