PMID- 34983617 OWN - NLM STAT- MEDLINE DCOM- 20220316 LR - 20220531 IS - 1465-542X (Electronic) IS - 1465-5411 (Print) IS - 1465-5411 (Linking) VI - 24 IP - 1 DP - 2022 Jan 4 TI - Circular RNA circCCDC85A inhibits breast cancer progression via acting as a miR-550a-5p sponge to enhance MOB1A expression. PG - 1 LID - 10.1186/s13058-021-01497-6 [doi] LID - 1 AB - BACKGROUND: A growing body of evidence indicates that abnormal expression of circular RNAs (circRNAs) plays a crucial role by acting as molecular sponges of microRNAs (miRNAs) in various diseases, including cancer. In this study, we explored whether circCCDC85A could function as a miR-550a-5p sponge and influence breast cancer progression. METHODS: We detected the expression of circCCDC85A in breast cancer tissues and cells using fluorescence in situ hybridization (FISH) and quantitative reverse transcription polymerase chain reaction (qRT-PCR). CCK-8 and colony formation assay were used to detect the proliferative ability of breast cancer cells. Wound healing assay and transwell migration and invasion assays were used to detect the migrative and invasive abilities of breast cancer cells. We also examined the interactions between circCCDC85A and miR-550a-5p using FISH, RNA-binding protein immunoprecipitation (RIP), and luciferase reporter assay. Moreover, we performed luciferase reporter assay, qRT-PCR, and Western blot to confirm the direct targeting of miR-550a-5p to MOB1A. RESULTS: The expression of circCCDC85A in breast cancer tissues was obviously lower than that in normal breast tissues. Over-expression of circCCDC85A substantially inhibited the proliferative, migrative, and invasive ability of breast cancer cells, while knocking down of circCCDC85A enhanced the aforementioned properties of breast cancer cells. Moreover, enforced expression of circCCDC85A inhibits the oncogenic activity of miR-550a-5p and increases the expression of MOB1A targeted by miR-550a-5p. Further molecular mechanism research showed that circCCDC85A may act as a molecular sponge for miR-550a-5p, thus restoring miR-550a-5p-mediated targeting repression of tumor suppressor MOB1A in breast cancer cells. CONCLUSION: Our findings provide novel evidence that circCCDC85A inhibits the progression of breast cancer by functioning as a molecular sponge of miR-550a-5p to enhance MOB1A expression. CI - (c) 2021. The Author(s). FAU - Meng, Lingjiao AU - Meng L AD - Tumor Research Institute, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. AD - Research Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Chang, Sheng AU - Chang S AD - Tumor Research Institute, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Sang, Yang AU - Sang Y AD - Animal Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Ding, Pingan AU - Ding P AD - The Third Department of Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Wang, Liuxin AU - Wang L AD - Tumor Research Institute, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Nan, Xixi AU - Nan X AD - Tumor Research Institute, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Xu, Ruiyu AU - Xu R AD - Tumor Research Institute, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Liu, Fei AU - Liu F AD - Tumor Research Institute, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Gu, Lina AU - Gu L AD - Tumor Research Institute, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Zheng, Yang AU - Zheng Y AD - Tumor Research Institute, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. AD - Research Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Li, Ziyi AU - Li Z AD - Tumor Research Institute, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. FAU - Sang, Meixiang AU - Sang M AD - Tumor Research Institute, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. mxsang@hotmail.com. AD - Research Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China. mxsang@hotmail.com. LA - eng PT - Journal Article DEP - 20220104 PL - England TA - Breast Cancer Res JT - Breast cancer research : BCR JID - 100927353 RN - 0 (Adaptor Proteins, Signal Transducing) RN - 0 (MIRN550 microRNA, human) RN - 0 (MOB1A protein, human) RN - 0 (MicroRNAs) RN - 0 (RNA, Circular) SB - IM MH - Adaptor Proteins, Signal Transducing/*genetics MH - *Breast Neoplasms/genetics MH - Cell Movement/genetics MH - Cell Proliferation/genetics MH - Female MH - Gene Expression Regulation, Neoplastic MH - Humans MH - In Situ Hybridization, Fluorescence MH - *MicroRNAs/genetics MH - *RNA, Circular/genetics PMC - PMC8725284 OTO - NOTNLM OT - Breast cancer OT - Circular RNA OT - MOB1A OT - circCCDC85A OT - miR-550a-5p COIS- The authors declare that no competing interests exist. EDAT- 2022/01/06 06:00 MHDA- 2022/03/17 06:00 PMCR- 2022/01/04 CRDT- 2022/01/05 05:43 PHST- 2021/05/25 00:00 [received] PHST- 2021/12/15 00:00 [accepted] PHST- 2022/01/05 05:43 [entrez] PHST- 2022/01/06 06:00 [pubmed] PHST- 2022/03/17 06:00 [medline] PHST- 2022/01/04 00:00 [pmc-release] AID - 10.1186/s13058-021-01497-6 [pii] AID - 1497 [pii] AID - 10.1186/s13058-021-01497-6 [doi] PST - epublish SO - Breast Cancer Res. 2022 Jan 4;24(1):1. doi: 10.1186/s13058-021-01497-6.