Linc‑OIP5 loss regulates migration and invasion in MDA‑MB‑231 breast cancer cells by inhibiting YAP1/JAG1 signaling

Abstract

Breast cancer is the most prevalent cancer among women, and diagnosis and treatment represent a substantial challenge due to the lack of adequate molecular targets. It has been shown that long noncoding RNAs (lncRNAs) serve pivotal roles in regulating gene expression in tumors. The roles of long intervening noncoding RNA (Linc)-OIP5 has been demonstrated in different types of cancer; however, its function in breast cancer has not been determined. In the present study, expression of Linc-OIP5, YAP1 (Hippo signaling component) and JAG1 (Notch signaling component) in breast cancer cells with different degrees of malignancy were determined. To assess whether Linc-OIP5 regulated the malignant biological behaviors of MDA-MB-231 cells, its expression was knocked down using a specific small interfering RNA (siRNA), and cell proliferation was determined using a CCK-8 assay, apoptosis was evaluated using an Annexin V-FITC apoptosis detection kit, migration was assessed using a wound healing and transwell migration assays, and cell invasion examined using a transwell invasion assays. The effect of Linc-OIP5 knockdown on YAP1 and JAG1 expression was quantified using reverse transcription-quantitative PCR and immunoblotting. Cell proliferation, migration and invasion were reduced, while apoptosis was increased in MDA-MB-231 cells transfected with Linc-OIP5-specific siRNA. Mechanistic investigations showed that Linc-OIP5 knockdown downregulated YAP1 and JAG1 expression. The results of the present study suggest that Linc-OIP5 affects the malignant biological behaviors of MDA-MB-231 cells, at least partly through its effects on YAP1/JAG1 signaling. Whilst there are a number of mechanisms underlying the pathogenesis of breast cancer, the results of the present study highlight Linc-OIP5 as a potential therapeutic target in breast cancer.

The clinical significance, immune infiltration, and tumor mutational burden of angiogenesis-associated lncRNAs in kidney renal clear cell carcinoma

“…Recent studies have shown that the lncRNA PAARH promotes hepatocellular carcinoma (HCC) angiogenesis by activating HIF-1α/VEGF signaling ( 34 ). JAG1 is involved in angiogenesis, and Linc-OIP5 may regulate JAG1 signaling through YAP1 signaling ( 35 ). The lncRNA H22954 inhibits angiogenesis in acute myeloid leukemia by downregulating PDGFA expression ( 36 ).…”

The Involvement of Insulin-Like Growth Factor 2 Messenger Ribonucleic Acid-Binding Protein 2 in the Regulation of the Expression of Breast Cancer-Related Genes

“…The Notch signaling pathway is already known to play an important role in breast cancer. Recently, Zhu et al reported 20 that after silencing Linc-OIP5, the expression of Notch signaling ligand Jagged1 was down-regulated, thus reducing Notch signaling, and promoting the apoptosis of breast cancer MDA-MB-231 cells. A Toll-like receptor is a type of pattern recognition receptor and when stimulated by corresponding Breast Cancer: Targets and Therapy 2022:14 https://doi.org/10.2147/BCTT.S382566 DovePress 319 ligands, these receptors can activate downstream signaling pathways and release a large number of cytokines.…”

The role of EMT-related lncRNA in the process of triple-negative breast cancer metastasis

“…For example, Linc-OIP5 as an oncogene promotes biological behaviors such as proliferation, migration, and invasion in lung adenocarcinoma and multiple myeloma. Interestingly, Zhu et al [ 43 ] revealed that linc-OIP5 exerts an important role in MDA-MB-231 cell migration and invasion, mostly through inhibiting JAG1 expression. JAG1, as a key component of the Notch signaling pathway, and contributes to the progression of multiple malignancies [ 44 ].…”