Key points are not available for this paper at this time.
Long non-coding RNAs (lncRNAs) play crucial roles in cancer progression and metastasis. However, the precise regulatory mechanisms of MALAT1, an lncRNA, in breast cancer remain elusive. Consequently, this study explored the specific role of MALAT1 as a tumor promoter in breast cancer. Initially, MALAT1-small interfering RNA (siRNA) transfection resulted in the inhibition of breast cancer cell migration, colony formation, and invasion. Real-time polymerase chain reaction analysis also revealed increased E-cadherin expression and decreased vimentin and vascular endothelial growth factor (VEGF) mRNA levels subsequent to the transfection. Bioinformatic analysis further uncovered a specific interaction between MALAT1 and miR-150-3p, indicating elevated MALAT1 expression in breast cancer with a negative correlation to miR-150-3p expression. Furthermore, the overexpression of MALAT1 markedly suppressed miR-150-3p expression, indicating a reciprocal inhibition between the two. Luciferase reporter assays confirmed the specific association between miR-150-3p and MALAT1 at the sequence level. Furthermore, transfection with miR-150-3p mimic inhibited breast cancer cell migration, colony formation, and invasion, along with increased E-cadherin expression and decreased Vimentin and VEGF mRNA levels. Conversely, miR-150-3p inhibitor transfection led to opposing effects, reducing E-cadherin expression, and elevating vimentin and VEGF mRNA levels, while also inhibiting migration, colony formation, and invasion. Functionally, MALAT1 siRNA restrained breast cancer cell proliferation and migration while enhancing cellular apoptosis on administration to breast cancer cells, primarily mediated through miR-150-3p. Our findings delineate MALAT1 as a tumor growth-promoting gene antagonized by miR-150-3p. Building on these insights, this study proposes a potential therapeutic avenue for breast cancer treatment.
Vignesh et al. (Tue,) studied this question.