Targeting long non-coding RNA MALAT1 reverses cancerous phenotypes of breast cancer cells through microRNA-561-3p/TOP2A axis.

Abstract

Non-coding RNAs, including Inc-RNA and miRNA, had been reported to regulate gene expression and were associated with cancer progression. MicroRNA-561-3p (miR-561-3p), as a tumor suppressor, has been reported to play a role in preventing cancer cell progression, and MALAT1 (Lnc-RNA) has also been demonstrated to promote malignancy in various cancer, such as breast cancer (BC). In this study, we aimed to determine the correlation between miR-561-3p and MALAT1 and their roles in breast cancer progression. The expression of MALAT1, mir-561- 3p, and topoisomerase alpha 2 (TOP2A) as a target of miR-561-3p was determined in BC clinical samples and cell lines via qRT-PCR. The binding site between MALAT1, miR-561-3p, and TOP2A was investigated by performing the dual luciferase reporter assay. MALAT1 was knocked down by siRNA, and cell proliferation, apoptotic assays, and cell cycle arrest were evaluated. MALAT1 and TOP2A were significantly upregulated, while mir-561-3p expression was downregulated in BC samples and cell lines. MALAT1 knockdown significantly increased miR 561 3p expression, meaningfully inverted by co-transfection with the miR 561 3p inhibitor. Furthermore, the knockdown of MALAT1 by siRNA inhibited proliferation, induced apoptosis, and arrested the cell cycle at the G1 phase in BC cells. Notably, the mechanistic investigation revealed that MALAT1 predominantly acted as a competing endogenous RNA in BC by regulating the miR-561-3p/TOP2A axis. Based on our results, MALAT1 upregulation in BC may function as a tumor promoter in BC via directly sponging miRNA 561-3p, and MALAT1 knockdown serves a vital antitumor role in BC cell progression through the miR-561- 3p/TOP2A axis.

The super-healing MRL strain promotes muscle growth in muscular dystrophy through a regenerative extracellular matrix

“…A tetanic contraction was performed to remove slack from the system before the muscle's optimal length (L 0 ) was determined through the same process. Maximum tetanic forces (77) were normalized to the PCSA. The PCSA was determined through the following equation: PCSA (mm 2 ) = M (mg) × cos(θ)/ρ (mg/mm 3 ) × L f (mm), where M is the wet weight of the TA, θ is the pennation angle of the TA, ρ is the physiological density of muscle (1.056 mg/mm 3 ), and L f is the fiber length of the TA.…”

Investigating diagnostic, Prognostic, and therapeutic role of Long Non-Coding RNA MALAT1 in Breast Carcinoma:<i> in silico</i> study

“…In fact, in an immune-competent animal model, MALAT-1 antisense oligonucleotides (ASO) cause MALAT-1 knockdown, which reduces both immunosuppressive tumor-associated macrophages (TAM) and MDSC [4]. On the other hand, there was also a noticeable rise in cytotoxic CD8+ T cells, which provided fresh insights into the prominent function of MALAT-1 in controlling the development of cancer [5]. Using data from The Cancer Genome Atlas (TCGA), we investigated MALAT-1 gene expression in a variety of cancer types.…”