Abstract
The present study compared the effects of ultrasonic irradiation and SonoVue microbubbles (US) or Lipofectamine 3000 on the transfection of small interfering RNA for PRR11 (siPRR11) and Proline-rich protein 11 (PRR11) overexpression plasmid into breast cancer cells. SiPRR11 and PRR11 overexpression plasmid were transfected into breast cancer MCF7 cells mediated by US and Lipofectamine 3000. PRR11 expressions in breast cancer and normal tissues were determined using Gene Expression Profiling Interactive Analysis (GEPIA). The viability, proliferation, migration, invasion and apoptosis of breast cancer cells were respectively measured by MTT assay, clone formation assay, scratch wound-healing assay, Transwell assay and flow cytometry. PRR11 and epithelial-to-mesenchymal transition (EMT)-related and apoptosis-related (B-cell lymphoma 2, Bcl-2; Bcl-2-associated protein X, Bax) proteins’ expressions were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as appropriate. As ultrasonic intensity increased, the viability of MCF7 cells was decreased. Results from GEPIA suggested that PRR11 was up-regulated in breast cancer. Silencing PRR11 mediated by US showed a higher efficiency than by Lipofectamine 3000. SiPRR11 transfected by Lipofectamine 3000 suppressed cells growth and metastasis, while promoted cell apoptosis. Moreover, E-cadherin (E-cad) and Bax expressions were high but N-cadherin (N-cad), Snail and Bcl-2 expressions were low. However, overexpressed PRR11 caused the opposite effects. More importantly, transfection of siPRR11 and PRR11 overexpression plasmid using US had a higher efficacy than using Lipofectamine 3000. US transfection of PRR11 siRNA showed better effects on inhibiting breast cancer progression. The current findings contribute to a novel treatment for breast cancer.
Highlights
At present, breast cancer remains one of the most frequent malignancies and a common cause of cancer-related mortality among females around the world
MCF7 cells were divided into the following groups: Control group, NC-L/siNC-L group (cells were transfected with negative control (NC) or small interfering RNA for NC by using Lipofectamine 3000 reagent), NC-ultrasonic irradiation and SonoVue microbubbles (US)/siNC-US group, small interfering RNA for PRR11 (siPRR11)-L/proline-rich protein 11 (PRR11)-L group, and siPRR11-US/PRR11-US group
To investigate the role of PRR11 in breast cancer, the expression of PRR11 was obtained from Gene Expression Profiling Interactive Analysis (GEPIA), and the data showed that PRR11 expression was up-regulated in breast cancer tissues (Figure 1B, number of tumor (T) = 1085, number of normal (N) = 291, P
Summary
Breast cancer remains one of the most frequent malignancies and a common cause of cancer-related mortality among females around the world. Diagnosis and treatment of breast cancer have progressed greatly, approximately 12% of patients develop metabolic diseases, resulting in poor prognosis [2]. Proline-rich protein 11 (PRR11), located on 17q22 region of human chromosome, is implicated in the transduction of cell signal and events to cancer-onset [3]. Increasing evidence suggested that PRR11 is involved in the development and progression of many malignancies. Huang et al found that PRR11 contributes to the pathogenesis of non-small cell lung cancer (NSCLC), and knockdown on PRR11 suppresses the proliferation and metastasis of NSCLC cells and promotes the cell apoptosis [4]. Wang et al showed that PRR11 is overexpressed in breast cancer cells and have a negative prognostic value in breast cancer, knockdown of PRR11 inhibits breast cancer cell proliferation, migration, and invasion [6]
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