METTL16-mediated upregulation of LINC00665 inhibits the apoptosis of breast cancer via regulating miR-28-5p/GLG1 axis.

BACKGROUND

Long non-coding RNAs (lncRNAs) are intensively involved in the progression of breast cancer. This study aimed to investigate the potential of LINC00665 in breast cancer.

METHODS

RNA expression was determined by quantitative reverse transcriptase polymerase chain reaction. The binding sites between miR-28-5p and LINC00665/golgi glycoprotein 1 (GLG1) was predicted by Starbase3. The bindings sites were confirmed by luciferase assay. N6-methyladenosine (m6A) modification of LINC00665 was determined by methylated RNA immunoprecipitation assay. Cell viability was determined by Cell Counting Kit-8 assay. Cell migration was detected by wound healing assay. Cell invasion was detected by transwell assay. Cell apoptosis was detected using flow cytometry.

RESULTS

We found that methyltransferase-like 16 (METTL16)-mediated m6A modification drove the upregulation of LINC00665 in breast cancer. However, LINC00665 knockdown inhibited the proliferation, migration and invasion of breast cancer cells, as well as promoted cell apoptosis. Furthermore, LINC00665 sponged miR-28-5p to upregulate GLG1. GLG1 overexpression alleviated the effects of LINC00665 knockdown and mediated malignant behaviors of breast cancer cells.

CONCLUSIONS

Taken together, LINC00665 promotes the progression of breast cancer via regulating miR-28-5p/GLG1 axis.