miR-497 could play a role in both gastric and lung cancer cell lines at least in part by modulation of apoptosis via targeting BCL2

tumor samples from non-small cell lung cancers show an inverse relationship between microRNA-497 and hepatoma-derived growth factor (HDGF) levels; ectopic expression of miR-497 significantly inhibits tumor growth and angiogenesis in a xenograft model

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

miR-497 has a prominent role in suppression of VEGF-A-mediated non-small cell lung cancer cancer cell growth and invasion.

lnc-SNHG1 regulated the expression of the insulin-like growth factor 1 receptor (IGF1-R) by acting as a sponge of miR-497 in non-small cell lung cancer.

MIR-497-5p expression was downregulated in the non-small-cell lung cancer.MiR-497-5p regulates non-small-cell lung cancer cell proliferation, cell apoptosis, cell migration, and invasion.SOX5 is a direct target of miR-497-5P in the non-small-cell lung cancer cells.

MicroRNA-497 (miR-497) post-transcriptionally represses metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) while MALAT1 competes for miR-497 binding to its molecular target, EIF4E (eukaryotic translation initiation factor 4E) in adrenocortical carcinoma. Overexpression of miR-497 and silencing of MALAT1 suppress cellular proliferation and induce cell cycle arrest through downregulation of EIF4E expression.

Study demonstrated that miR497 was downregulated in nonsmall cell lung cancer (NSCLC) specimens and it served as a tumor suppressor to inhibit cancer cell proliferation and invasion, and increase radiosensitivity via targeting KDR.

The results of the present study identified miR497 as a potential tumor suppressor gene in nonsmall cell lung cancer that may function via repressing FGFR1 expression, and AKT and JNK signaling.

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.