Measuring plasma levels of miR-195 and miR-122 may especially be useful in EGFR mutant patients with lung adenocarcinoma

Data indicate that insulin-like growth factor 1 receptor (IGF1R) was a target of miR-195 in non-small cell lung cancer (NSCLC)cells.

Data indicate that hepatoma-derived growth factor (HDGF) was a target of miR-195 in non-small cell lung cancer (NSCLC) cells.

Suggest that miR-195, a tumor suppressor miRNA, contributes to the lung metastasis of HCC by negatively regulating FGF2 and VEGFA expression.

Results found miR-195 to directly targets the 3' untranslated region of HMGA2 messenger RNA and suppress its expression in lung cancer.

Overexpression or induced expression of miR-195 in lung tumors slows tumor growth and that repression of miR-195 accelerates tumor growth. Knockout of miR-195 promotes cancer cell growth.

Data indicate the importance of miR-195 in regulating the response of non-small cell lung cancer (NSCLC) cells to MTAs and underline the potential application of miR-195 as a biomarker for response to microtubule-targeting agents (MTAs), and as a therapeutic adjuvant to MTA treatment.

CYTOR played an oncogenic role in Nonsmall cell lung cancer (NSCLC) progression through sponging miR-195. Together, our study elucidates the role of CYTOR as a microRNA sponge in NSCLC, and CYTOR may be used as a promising therapeutic target for NSCLC treatment

Low miR195 expression is correlated with Non-small Cell lung cancer.

MiR-195 is downregulated in lung adenocarcinoma tissues and cell lines and negatively correlated with poor prognosis and apelin expression. Its overexpression inhibits the proliferation and suppresses the migration and invasion of lung adenocarcinoma cells by targeting apelin.

Data suggest that circular RNA VANGL1 (circVANGL1) functions as an oncogene to promote non-small cell lung cancer (NSCLC) progression partly through miR-195/BCL2 apoptosis regulator (Bcl-2) axis, which might be a therapeutic target for NSCLC patients.

miR1955p acted as a tumor suppressor in squamous cell lung cancer (SQCLC) cells. The expression levels of miR195 were decreased in two SQCLC cell lines (H520 and SKMes1) compared with a normal lung cell line, and miR195 directly targeted the 3'untranslated region of vascular endothelial growth factor (VEGF) in SQCLC cells.

hese findings demonstrate that miR-195 and miR-497 act as a tumor suppressor by suppressing ubiquitination-mediated degradation of TGF-beta receptors through SMURF2, and suggest that miR-195 and miR-497 are potential therapeutic targets for lung cancer.

Silencing of LINC00461 enhances radiosensitivity of lung adenocarcinoma cells by down-regulating HOXA10 via microRNA-195.

miR-195-5p Suppresses lung cancer Cell Proliferation, Migration, and Invasion Via FOXK1.