In conclusion, our data suggest that miR-182 might account for radioresistance in lung cancer and that miR-182-FOXO3 provides a novel radiosensitizing target.
In this work, a novel label-free strategy for the ultrasensitive detection of miRNA-182 (a typical biomarker for lung cancer) based on MoS<sub>2</sub>/Ti<sub>3</sub>C<sub>2</sub> nanohybrids was suggested.
Furthermore, miR-182 negatively regulated invadopodia function, and suppressed extracellular matrix(ECM) degradation in lung cancer cells by inhibiting cortactin.
Furthermore, high expression of miR-182-5p and low expression of <i>SESN2</i> mRNA tend to be associated with longer survival of glioma or lung cancer patients using public available gene expression datasets and online tools for prediction of clinical outcomes.
However, the role of miR-182 in the development of lung cancer remains largely unknown. miR-182 expression in tumor samples from 58 patients, normal lung tissue samples, and lung cancer cell lines were evaluated by qRT-PCR.
The miR-182-PDK4 axis regulates lung cancer cell growth by modulating the activity of PDH, the gatekeeping enzyme of pyruvate flux into acetyl-CoA, and subsequently de novo lipogenesis of cancer cells.
We performed methyl thiazolyl tetrazolium and colony formation assays to study the influence of miR-182 on proliferation of the lung cancer cell lines A549 and SPC-A-1.
Knockdown of miR-182 inhibited lung cancer cells growth, but enhanced the invasive and migratory abilities of these cells through increased N-cadherin expression.
We found that the serum levels of miR-21, miR-155, and miR-197 were significantly elevated in the patients with lung cancer and pneumonia whereas miR-182 and miR-197 levels were increased only in patients with lung cancer and TB, respectively, compared with controls.
Our results suggest that the expressions of miR-96, miR-182, and miR-183 in tumor and sera may be considered potential novel biomarkers for the diagnosis and prognosis of lung cancer.
In conclusion, endogenous mature miR-182 expression may have an important role in the pathogenesis of lung cancer through its interference with the target gene CTTN by epigenetic modification.