PT  - JOURNAL ARTICLE
AU  - SUNG-EUN HONG
AU  - HYEON-OK JIN
AU  - SEUNG-MI KIM
AU  - SE-KYEONG JANG
AU  - CHAN SUB PARK
AU  - MIN-KI SEONG
AU  - HYUN-AH KIM
AU  - WOO CHUL NOH
AU  - IN-CHUL PARK
TI  - miR-3188 Enhances Sensitivity of Breast Cancer Cells to Ionizing Radiation by Down-regulating Rictor
AID  - 10.21873/anticanres.15436
DP  - 2021 Dec 01
TA  - Anticancer Research
PG  - 6169--6176
VI  - 41
IP  - 12
4099  - http://ar.iiarjournals.org/content/41/12/6169.short
4100  - http://ar.iiarjournals.org/content/41/12/6169.full
SO  - Anticancer Res2021 Dec 01; 41
AB  - Background/Aim: Rictor is an adaptor protein essential for mTORC2, which regulates cell growth and survival. The aim of this study was to identify microRNAs (miR) that down-regulate Rictor and investigate their function on breast cancer cell survival. Materials and Methods: Trypan blue assay, MTT assay, polymerase chain reaction analysis, luciferase reporter assay and western blot analysis were carried out in breast cancer cell lines HCC1954, MDA-MB-231, SK-BR-3, and BT474. Results: miR-3188 overexpression suppressed the expression of Rictor and inhibited cell viability in HCC1954 and MDA-MB-231, highly Rictor-expressing breast cancer cells. In addition, miR-3188 overexpression decreased the protein level of p-AKT at Ser473, a substrate of mTORC2. Moreover, miRNA-3188 overexpression sensitized breast cancer cells to ionizing radiation (IR) by down-regulating Rictor and p-AKT. Conclusion: miR-3188 enhances IR sensitivity by affecting the mTORC2/AKT signalling pathway by altering the expression of Rictor, which could be a promising therapeutic strategy for the future treatment of breast cancer.