<p>The better effects of microbubble ultrasound transfection of miR-940 on cell proliferation inhibition and apoptosis promotion in human cervical cancer cells</p>
Abstract:PurposeCervical cancer is the second leading cause of women’s cancer-related death. MiR-940 has been reported as a critical factor in various cancers. Based on the high transfection efficiency and low side effect, the clinical application of microbubble ultrasound contrast agent in gene treatment has attracted a widespread attention. In this study, we determined the mechanism of miR-940 inhibiting cell proliferation and cycle procession, and promoting cell apoptosis in cervical cancer Hela cells. In addition, … Show more
“…In Ca-Ski and HeLa cells, miR-505 upregulation suppressed proliferation and tumorigenicity, indicating miR-505 may act as an inhibitor in CC [30]. Similarly, compared with liposome, MBs or ultrasound transfection, USMB-miR-940 further inhibited CC malignant episodes [31]. Our study may offer a novel approach for CC treatment from the miR-505 delivery by USMB treatment.…”
Section: Discussionmentioning
confidence: 61%
“…Consistently, miR-505 was poorly expressed in CC, and negatively correlated with tumor histology grade and lymph node metastasis [25,30]. Additionally, miR-940 inhibited CC cell proliferation, and USMB-miR-940 showed better effects [31]. However, the role of USMB treatment on miR-505 expression was not yet studied.…”
Background: The gene-loaded microbubbles (MBs) combined with ultrasound resulting in increased delivery efficiency, may be a novel method of gene delivery. We explored the effects of ultrasound and microbubbles (USMB)-mediated microRNA (miR)-505 on cervical cancer (CC) development.Methods: miR-505 mediated by USMB was prepared. The effect of miR-505 on its transfection efficiency was studied by RT-qPCR. The effect of miR-505 on HeLa cell proliferation was evaluated by MTT and colony formation assays. Flow cytometry was used to study cell cycle changes, Hoechst was utilized to detect apoptosis. Through the wound healing and Transwell assay, the migration and invasion ability of HeLa cells were measured. The target gene of miR-505 was predicted, and its expression in CC was detected. The target relationship and the effect of the target gene on HeLa cells were further verified.Results: USMB-miR-505 showed higher transfection efficiency than miR-505 alone. miR-505 inhibited HeLa cell malignant episodes, which were reinforced by USMB treatment. miR-505 targeted AKT2. AKT2 was highly expressed in CC, and overexpression of AKT2 significantly reversed the inhibitory effect of miR-505 mediated by USMB on HeLa cell malignant biological behaviors.Conclusion: USMB-miR-505 inhibited HeLa cell malignant biological behaviors by targeting AKT2.
“…In Ca-Ski and HeLa cells, miR-505 upregulation suppressed proliferation and tumorigenicity, indicating miR-505 may act as an inhibitor in CC [30]. Similarly, compared with liposome, MBs or ultrasound transfection, USMB-miR-940 further inhibited CC malignant episodes [31]. Our study may offer a novel approach for CC treatment from the miR-505 delivery by USMB treatment.…”
Section: Discussionmentioning
confidence: 61%
“…Consistently, miR-505 was poorly expressed in CC, and negatively correlated with tumor histology grade and lymph node metastasis [25,30]. Additionally, miR-940 inhibited CC cell proliferation, and USMB-miR-940 showed better effects [31]. However, the role of USMB treatment on miR-505 expression was not yet studied.…”
Background: The gene-loaded microbubbles (MBs) combined with ultrasound resulting in increased delivery efficiency, may be a novel method of gene delivery. We explored the effects of ultrasound and microbubbles (USMB)-mediated microRNA (miR)-505 on cervical cancer (CC) development.Methods: miR-505 mediated by USMB was prepared. The effect of miR-505 on its transfection efficiency was studied by RT-qPCR. The effect of miR-505 on HeLa cell proliferation was evaluated by MTT and colony formation assays. Flow cytometry was used to study cell cycle changes, Hoechst was utilized to detect apoptosis. Through the wound healing and Transwell assay, the migration and invasion ability of HeLa cells were measured. The target gene of miR-505 was predicted, and its expression in CC was detected. The target relationship and the effect of the target gene on HeLa cells were further verified.Results: USMB-miR-505 showed higher transfection efficiency than miR-505 alone. miR-505 inhibited HeLa cell malignant episodes, which were reinforced by USMB treatment. miR-505 targeted AKT2. AKT2 was highly expressed in CC, and overexpression of AKT2 significantly reversed the inhibitory effect of miR-505 mediated by USMB on HeLa cell malignant biological behaviors.Conclusion: USMB-miR-505 inhibited HeLa cell malignant biological behaviors by targeting AKT2.
“…Regulation of the proliferation of cancer cells is often achieved with the modulation on the critical factors, such as Bcl-2 and Bax, which are two cell apoptosis-related genes [ 28 ]. Bcl-2 could suppress cell apoptosis either through preventing the release of cytochrome c from mitochondria or through binding with the apoptosis-activating factor (APAF-1) [ 29 ].…”
This 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 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 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 and Bax expressions were low but N-cadherin, Snail and Bcl-2 expressions were high. 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.
“…miR-505 was poorly expressed in CC and negatively correlated with tumor histology grade and lymph node metastasis [ 25 , 30 ]. Additionally, miR-940 inhibited CC cell proliferation, and USMB-miR-940 showed better effects [ 31 ]. However, the role of the USMB treatment on miR-505 expression was not yet studied.…”
The application of ultrasound and microbubbles (USMB-) mediated microRNA (miR) is a promising approach of gene delivery for cancer treatment. We aimed to discuss the effects of USMB-miR-505 on cervical cancer (CC) development. miR-505 mediated by USMB was prepared. The effect of miR-505 on its transfection efficiency and the effect of miR-505 on HeLa cell proliferation, cell cycle, apoptosis, migration, and invasion were studied. The target gene of miR-505 was predicted, and its expression in CC was detected. The effect of the target gene on HeLa cells was further verified. USMB-miR-505 showed a higher transfection efficiency than miR-505 alone. The inhibitory effect of miR-505 mediated by USMB on HeLa cells was better than miR-505. miR-505 targeted AKT2, which was upregulated in CC. Overexpression of AKT2 reversed the inhibitory effect of USMB-miR-505 on HeLa cell malignant behaviors. Overall, we highlighted that USMB-miR-505 inhibited HeLa cell malignant behaviors by targeting AKT2.
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