Long noncoding RNALINC00963promotes breast cancer progression by functioning as a molecular sponge for microRNA-625 and thereby upregulating HMGA1
Authors: Shanping Sun
Xin Wang
Wei Wang
Yang Zhang
Yongkun Wang
Yumin Yao
Zhen Wu
Zhongxi Ren
Journal: Cell Cycle (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: High mobility group AT-hook 1; LINC00963; breast cancer; microRNA-625.
Affiliations: Department of Breast and Thyroid Surgery, Liaocheng People's Hospital, Liaocheng, Shandong, P.R. China.

Abstract:  Extensive research has shown that LINC00963 is aberrantly expressed in human cancers, and that dysregulation of LINC00963 is implicated in the initiation and progression of human cancers. The expression and functions of LINC00963 in breast cancer are still unclear. Our aims were to measure the expression of LINC00963 in breast cancer, determine its effects on malignant behaviors of tumor cells, and uncover the molecular events underlying the actions of LINC00963 in breast cancer. Herein, LINC00963 was found to be overexpressed in breast cancer samples, and its overexpression was correlated with lymph node metastasis, TNM stage and differentiation grade. Patients with breast cancer harboring higher LINC00963 expression showed shorter overall survival than did the patients with lower LINC00963 expression. Functional experiments revealed that depletion of LINC00963 inhibited breast cancer cell proliferation, migration, and invasion and facilitated apoptosis in vitro and impaired tumor growth in vivo. Mechanism investigation revealed that LINC00963 can interact with microRNA-625 (miR-625). LINC00963 worked as a competitive endogenous RNA for miR-625 to weaken the suppressive effect of miR-625 on high mobility group AT-hook 1 (HMGA1) in breast cancer cells. Furthermore, miR-625 inhibition and HMGA1 restoration both abrogated the effects of LINC00963 silencing on breast cancer cells. Our findings indicate that the LINC00963-miR-625-HMGA1 pathway plays an important role in the malignancy of breast cancer in vitro and in vivo. Hence, targeting this pathway may be a novel strategy against breast cancer. 

Retracted: No

PubPeer comments:
 Pointed out by a reader. * Red boxes: Figure 2A of this paper (rutile TiO2) looks identical to Figure 4 from another paper by the same group, where it represents rutile TiO2 doped with an upconversion luminescence agent. That other paper is: Jun Wang et al., Water Research (2006), DOI: 10.1016 j.watres.2006.04.009 Can the authors please clarify if the photo represents the exact same catalyst? ![file] , 
 Two more occurrences of these photos, but not always showing the same thing. The four papers that include the same photo(s) now are: * Jun Wang et al., Journal of Molecular Catalysis A: Chemical (2007), DOI: 10.1016 j.molcata.2007.03.018 - https: pubpeer.com publications F5E2CBCB64CC30E4E1CC9F24EC665C * Jun Wang et al., Water Research (2006), DOI: 10.1016 j.watres.2006.04.009 - https: pubpeer.com publications 2F926D1A987CE4C9255A960859A213 * Jun Wang et al., Journal of Chemical Technology and Biotechnology (2007), DOI: 10.1002 jctb.1709 - https: pubpeer.com publications 18CFB27B21493C5DD3AE15F117CE0F * Jun Wang et al., Environmental Progress (2008), DOI: 10.1002 ep.10256 - https: pubpeer.com publications 9E4866F5E2BEE27391E9BF6B171573 ![file] ![file] ,