a novel prognostic marker in non-small-cell lung cancer patients

Knockdown microRNA-34a decreased the rate of apoptosis caused by PRIMA-1 in lung cancer.

miR-34a was highly upregulated in the p53 wild-type lung cancer cells.

miR-34a may have a role in enhancing radiosensitivity of non-small cell lung cancer cells, partly by suppressing the LyGDI signaling pathway

these data support the involvement of miR-22, miR-24, and miR-34a in advanced non-small cell lung cancer

The relationship of miR-34a and erlotinib in non-small cell lung cancer cells with primary and acquired erlotinib resistance, was investigated.

miR-34a is a negative regulator of the tumorigenic properties of non-small cell lung cancer cells and CD44hi lung cancer stem cells.

overexpression of PEBP4, which we show to be a target of miR-34a, reduces the sensitivity of lung cancer cells to cisplatin

These results indicate cyclin E1 is downregulated by both miR-497 and miR-34a, which synergistically retard the growth of human lung cancer cells.

only miR-34a was prognostic for RFS (RR, 11.5; P = 0.027). miR-34a expression was inversely correlated with that of c-MET and CDK6 in non-small cell lung cancer , and had prognostic significance for RFS, especially in adenocarcinoma patients.

Negative feedback regulation of AXL by miR-34a modulates apoptosis in lung cancer cells by activating the transcription factor ELK1 via the JNK signaling pathway.

miR-34 loci methylation is associated with Non-Small-Cell lung cancer.

miR-34a and miR-34b/c promoter hypermethylation is a frequent event in lung adenocarcinoma (LAC) occurring in 68.7% and 35.3% of tested cases respectively; low miR-34b and miR-34c expression is associated with distant metastases formation in lung adenocarcinoma

in this review, we focus on two microRNAs centrally involved in lung cancer progression. MicroRNA-21 promotes and microRNA-34 inhibits cancer progression. We elucidate here involved pathways and imbed these antagonistic microRNAs in a network of interactions, stressing their cancer microRNA biology, followed by experimental and bioinformatics analysis of such microRNAs and their targets

PAI-1 was identified as the target gene of miR-34a and activated the Stat3 signaling pathway to promote epithelial-mesenchymal transition in non-small cell lung cancer cells.

the results of the present study revealed that LIMD2 promoted nonsmall cell lung cancer (NSCLC)progression and was regulated by miR34a.

In vitro binding experiments revealed that the RNA-recognition motifs within the SART3 sequence are responsible for selective pre-miR-34a binding. Our results provide evidence for a significant role of SART3 in miR-34a biogenesis and cell cycle progression in non-small-cell lung cancer (NSCLC) cells.

Cumulatively, these results reveal a novel mechanism of RBM38-mediated regulation of the HIF1A/miR-34a/SIRT1/p53 axis under hypoxia in non-small cell lung cancer cells.

Mechanism research of miR-34a regulates Axl in non-small-cell lung cancer with gefitinib-acquired resistance.

Integrative data modeling from lung and lymphatic cancer predicts functional roles for miR-34a and miR-16 in cell fate regulation.

LncRNA FEZF1-AS1 promotes non-small lung cancer cell migration and invasion through the up-regulation of NOTCH1 by serving as a sponge of miR-34a.

HCG18/miR-34a-5p/HMMR axis accelerates the progression of lung adenocarcinoma.

Long noncoding RNA TP73AS1 accelerates the progression and cisplatin resistance of nonsmall cell lung cancer by upregulating the expression of TRIM29 via competitively targeting microRNA34a5p.