MiR-26b-5p inhibits cell proliferation and EMT by targeting MYCBP in triple-negative breast cancer

Abstract

Background The study was designed to elucidate the association and functional roles of miR-26b-5p and c-MYC binding protein (MYCBP) in triple-negative breast cancer (TNBC). Method Luciferase reporter assay was used to confirm the relationship between miR-26b-5p and MYCBP in TNBC cells. The expression levels of miR-26b-5p and MYCBP in tissue specimens and cell lines were determined using reverse transcription-quantitative PCR. Cell proliferation, migration and invasion were assessed using CCK-8 assay, colony formation and transwell assay. Results We first observed that miR-26b-5p directly targets the 3′-UTR of MYCBP to inhibit MYCBP expression in MDA-MB-468 and BT-549 cells. The expression of miR-26b-5p was inversely correlated with MYCBP expression in TNBC tissues. We further demonstrated that MYCBP knockdown suppressed the proliferation, migration and invasion of TNBC cells. Furthermore, MYCBP overexpression counteracted the suppressive effect of miR-26b-5p on TNBC cell behaviors. Western blot analysis demonstrated that the E-cadherin protein level was increased, while protein levels of N-cadherin and vimentin were decreased in cells transfected with miR-26b-5p, which were all reversed by ectopic expression of MYCBP. Conclusions In summary, our findings revealed the tumor suppressive role of miR-26b-5p in regulating TNBC cell proliferation and mobility, possibly by targeting MYCBP.

Down-regulation of EVA1A by miR-103a-3p promotes hepatocellular carcinoma cells proliferation and migration

“…The epithelial-mesenchymal transition (EMT) is the critical factor for cancer cell metastasis [ 25 , 26 ]. Recently, we have reported that EVA1A could inhibit EMT in HCC cells, by upregulating epithelial marker E-cadherin levels and downregulating mesenchymal markers N-cadherin and Vimen levels [ 10 ].…”

Identification of lncRNA, miRNA and mRNA expression profiles and ceRNA Networks in small cell lung cancer

“…The miRNA miR-26b-5p has been identi ed as an oncogenic driver in a variety of cancers, including lymphocytic leukemia [46], ovarian cancer [47], hepatocellular carcinoma [48], breast cancer [49], and nonsmall cell lung cancer (NSCLC) [50][51][52]. In NSCLC tissues, miR-26b-5p expression was down-regulated compared with the adjacent non-tumor tissues [52].…”

The role of epigenetic modifications in drug resistance and treatment of breast cancer

“…The Wnt/β-catenin pathway has been shown to be noticeably activated in basal-like breast tumors, and its nuclear localization is significantly correlated with poor prognosis. Activated β-catenin promotes triple-negative breast cancer (TNBC), the most malignant subtype of breast cancer [ 11 ]. Moreover, it plays a crucial role in the in vivo induction of HER2 mammary tumors [ 22 ].…”

“…Conversely, it is noteworthy that kallistatin triggers the expression of tumorigenic suppressors such as miR-34a and p53. These changes could lead to contrasting impacts on breast-cancer-mediated deaths [ 59 , 87 ].…”

“…Of interest, the molecular anomaly of breast cancer cells cannot be explained via the genetic background as a result of the frequent sporadicity associated with the cancer [8]. However, epigenetic processes such as DNA methylation and histone modification, as well as microRNAs (miRNAs), have a noticeable impact on different dimensions of breast cancer [9][10][11][12][13]. Moreover, epigenetic details can be deemed as a way to gain knowledge about the molecular basis of breast cancer pathogenesis, improve therapeutic strategies, and develop novel therapeutic tools against breast cancer [14,15].…”