Jianchao Gao1, Sisi Wang2, Zhisheng Zhang1, Jun Li3. 1. Department of Breast Surgery, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei Province, 075000, People's Republic of China. 2. Department of Obstetrics and Gynecology, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei Province, 075000, People's Republic of China. 3. Department of Radiotherapy, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, and The Affiliated Cancer Hospital of Nanjing Medical University, Room 803, Building 19, Jinyu Zhongyang 2 Block, Shogunate West Road, Gulou District, Nanjing City, Jiangsu Province, 210009, People's Republic of China. ej5027@163.com.
Abstract
BACKGROUND: BRE-AS1 is a recently identified tumor suppressor in non-small cell lung cancer. It role in other human diseases remains elusive. METHODS: Differential expression of BRE-AS1 in with triple-negative breast cancer (TNBC) patients (n = 74, patient group) and healthy volunteers (n = 58, control group) was studied with RT-qPCR. The direct interaction between BRE-AS1 and premature microRNA-21 (miR-21) was assessed by RNA pull-down assay. The interactions among BRE-AS1, miR-21 and PTEN were evaluated by overexpression assays. CCK-8 assay and Transwell assay were used to evaluate cell behaviors. RESULTS: BRE-AS1 was downregulated in TNBC, while miR-21 was highly expressed in TNBC. Low expression levels of lncRNA BRE-AS1 and high expression levels of miR-21 were significantly correlated with unfavorable survival outcomes. BRE-AS1 and miRNA-21 were inversely correlated across TNBC samples, not control samples. BRE-AS1 decreased miR-21 expression and increased PTEN expression while miR-21showed no role in BRE-AS1 expression. RNA pull-down assay illustrated that BRE-AS1 may sponge premature miR-21 to suppress it maturation. Overexpression of BRE-AS1 decreased cell behaviors, while overexpression of miR-21 promoted cell behaviors. MiR-21 suppressed the role of BRE-AS1 in cancer cell behaviors. CONCLUSION: Therefore, BRE-AS1 may inhibit TNBC by downregulating miR-21.
BACKGROUND:BRE-AS1 is a recently identified tumor suppressor in non-small cell lung cancer. It role in other human diseases remains elusive. METHODS: Differential expression of BRE-AS1 in with triple-negative breast cancer (TNBC) patients (n = 74, patient group) and healthy volunteers (n = 58, control group) was studied with RT-qPCR. The direct interaction between BRE-AS1 and premature microRNA-21 (miR-21) was assessed by RNA pull-down assay. The interactions among BRE-AS1, miR-21 and PTEN were evaluated by overexpression assays. CCK-8 assay and Transwell assay were used to evaluate cell behaviors. RESULTS:BRE-AS1 was downregulated in TNBC, while miR-21 was highly expressed in TNBC. Low expression levels of lncRNA BRE-AS1 and high expression levels of miR-21 were significantly correlated with unfavorable survival outcomes. BRE-AS1 and miRNA-21 were inversely correlated across TNBC samples, not control samples. BRE-AS1 decreased miR-21 expression and increased PTEN expression while miR-21showed no role in BRE-AS1 expression. RNA pull-down assay illustrated that BRE-AS1 may sponge premature miR-21 to suppress it maturation. Overexpression of BRE-AS1 decreased cell behaviors, while overexpression of miR-21 promoted cell behaviors. MiR-21 suppressed the role of BRE-AS1 in cancer cell behaviors. CONCLUSION: Therefore, BRE-AS1 may inhibit TNBC by downregulating miR-21.
Entities:
Keywords:
Survival; Triple-negative breast cancer; lncRNA BRE-AS1; miR-21
Authors: Ryan Charles Pink; Priya Samuel; Davide Massa; Daniel Paul Caley; Susan Ann Brooks; David Raul Francisco Carter Journal: Gynecol Oncol Date: 2015-01-08 Impact factor: 5.482
Authors: Cornelia Liedtke; Chafika Mazouni; Kenneth R Hess; Fabrice André; Attila Tordai; Jaime A Mejia; W Fraser Symmans; Ana M Gonzalez-Angulo; Bryan Hennessy; Marjorie Green; Massimo Cristofanilli; Gabriel N Hortobagyi; Lajos Pusztai Journal: J Clin Oncol Date: 2008-02-04 Impact factor: 44.544
Authors: Shaokun Shu; Charles Y Lin; Housheng Hansen He; Robert M Witwicki; Doris P Tabassum; Justin M Roberts; Michalina Janiszewska; Sung Jin Huh; Yi Liang; Jeremy Ryan; Ernest Doherty; Hisham Mohammed; Hao Guo; Daniel G Stover; Muhammad B Ekram; Jonathan Brown; Clive D'Santos; Ian E Krop; Deborah Dillon; Michael McKeown; Christopher Ott; Jun Qi; Min Ni; Prakash K Rao; Melissa Duarte; Shwu-Yuan Wu; Cheng-Ming Chiang; Lars Anders; Richard A Young; Eric Winer; Antony Letai; William T Barry; Jason S Carroll; Henry Long; Myles Brown; X Shirley Liu; Clifford A Meyer; James E Bradner; Kornelia Polyak Journal: Nature Date: 2016-01-06 Impact factor: 49.962