Data show that loss of let-7 function enhances lung tumor formation in vivo, strongly supporting the hypothesis that let-7 is a tumor suppressor.

Let-7a miRNAs were under-expressed in the blood of non-small cell lung cancer (NSCLC) patients, as well as NSCLC cells and NSCLC tissues, compared to normal controls.

Loss of MicroRNA let-7a is associated with the proliferation and invasion of non-small cell lung cancer.

ur study demonstrated that disturbance of the let-7/LIN28 double-negative feedback loop is involved in the regulation of radio- and chemo-resistance, and that let-7 and LIN28 could be employed as predictive biomarkers of response to radiotherapy or chemotherapy in non-small-cell lung cancer patients.

NEAT1 regulates lung cancer cell progression by competing endogenous RNA network of NEAT1/let-7a/IGF2.

Low microRNAlet7a expression is associated with lung adenocarcinoma.

Results show that Let-7a-5p induced G1-phase cell cycle arrest in lung cancer cells. Let-7a-5p directly targeted the 3'UTR of CCND1 to inhibit its expression. These data suggest that let-7a- 5p act as a tumor suppressor by regulating cell cycle via CCND1 expression.

The lower expression of miR-let-7a in patients with lung cancer brain metastasis was closely related to unfavorable efficacy and prognosis of radiotherapy, and it may be an important predictive biomarker by regulation of DICER1

expression of let-7a-5p in pneumoconiosis is downregulated, while reduced let-7a-5p corresponds to high expression of BCL2L1 and poor survival of lung adenocarcinoma patients.

Circular RNA circ-CPA4/ let-7 miRNA/PD-L1 axis regulates cell growth, stemness, drug resistance and immune evasion in non-small cell lung cancer (NSCLC).