Ultrasound-Stimulated Microbubbles Inhibit Aggressive Phenotypes and Promotes Radiosensitivity of esophageal squamous cell carcinoma

Shi, Jinjun; Fu, Chenchun; Su, Xiangyu; Feng, Shicheng; Wang, Sheng

doi:10.1080/21655979.2021.1931641

Cited by 14 publications

(7 citation statements)

References 55 publications

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“…Furthermore, USMB therapy could be used to enhance the effect of therapeutic antibodies or nanoparticles ( Heath et al, 2012 ; Togtema et al, 2012 ; Bellary et al, 2020 ; Snipstad et al, 2021a ; Snipstad et al, 2021b ). Finally, clinical studies evaluating the potential of USMB therapy in addition to radiotherapy in the absence of drugs are ongoing ( Shi et al, 2021 ) ( Clinicaltrials.gov NCT04431674, NCT04431648).…”

Section: Discussionmentioning

confidence: 99%

Ultrasound-Mediated Drug Delivery With a Clinical Ultrasound System: In Vitro Evaluation

et al. 2021

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Chemotherapy efficacy is often reduced by insufficient drug uptake in tumor cells. The combination of ultrasound and microbubbles (USMB) has been shown to improve drug delivery and to enhance the efficacy of several drugs in vitro and in vivo, through effects collectively known as sonopermeation. However, clinical translation of USMB therapy is hampered by the large variety of (non-clinical) US set-ups and US parameters that are used in these studies, which are not easily translated to clinical practice. In order to facilitate clinical translation, the aim of this study was to prove that USMB therapy using a clinical ultrasound system (Philips iU22) in combination with clinically approved microbubbles (SonoVue) leads to efficient in vitro sonopermeation. To this end, we measured the efficacy of USMB therapy for different US probes (S5-1, C5-1 and C9-4) and US parameters in FaDu cells. The US probe with the lowest central frequency (i.e. 1.6 MHz for S5-1) showed the highest USMB-induced intracellular uptake of the fluorescent dye SYTOX™ Green (SG). These SG uptake levels were comparable to or even higher than those obtained with a custom-built US system with optimized US parameters. Moreover, USMB therapy with both the clinical and the custom-built US system increased the cytotoxicity of the hydrophilic drug bleomycin. Our results demonstrate that a clinical US system can be used to perform USMB therapy as efficiently as a single-element transducer set-up with optimized US parameters. Therefore, future trials could be based on these clinical US systems, including validated US parameters, in order to accelerate successful translation of USMB therapy.

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Section: Discussionmentioning

confidence: 99%

Ultrasound-Mediated Drug Delivery With a Clinical Ultrasound System: In Vitro Evaluation

et al. 2021

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“…The influence of KAP-1 silence on cell apoptosis was evaluated by TUNEL assay [ 17 ]. After the cells were rinsed with PBS, the fixation and permeation were carried out with 4% paraformaldehyde and 0.1 Triton X-100, individually.…”

Section: Methodsmentioning

confidence: 99%

Knockdown of KRAB domain-associated protein 1 suppresses the proliferation, migration and invasion of thyroid cancer cells by regulating P68/DEAD box protein 5

2022

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KRAB domain-associated protein 1 (KAP-1) has been reported to be an oncogene in diverse tumors. KAP-1 was found to have abundant existence in malignant thyroid tissues, but its role in thyroid cancer hasn’t been elucidated clearly. This study was carried out to explore the role of KAP-1 in thyroid cancer, and to clarify its molecular mechanism. The expressions of KAP-1 and P68/DEAD box protein 5 (DDX5) were assessed under the help of qRT-PCR and western blot. Then, we downregulated KAP-1 or upregulated DDX5 by cell transfection in TPC-1 cells. A series of cellular experiments on proliferation, apoptosis, migration and invasion were conducted with CCK-8, EdU, TUNEL, wound-healing and Transwell assays. Besides, the relationship between KAP-1 and DDX5 was verified by co-immunoprecipitation (Co-IP). The results showed that both of KAP-1 and DDX5 were upregulated in thyroid cancer cells. Loss-of-function experiments revealed that KAP-1 knockdown imparted suppressive effects on cell proliferation, migration and invasion, but promoted cell apoptosis. Additionally, KAP-1 was demonstrated to interact with DDX5 and positively regulate DDX5 expression. The following rescued experiments exhibited that the inhibitory effects of KAP-1 knockdown on cellular activities of thyroid cancer and Wnt/β-catenin signaling were also partly reversed by DDX5 overexpression. Moreover, activation of Wnt/β-catenin signaling retarded the anti-tumor activity of KAP-1 knockdown. In conclusion, the data in this study disclosed that KAP-1 silence helped to repress the cell proliferation, migration and invasion by degrading DDK5, so as to hinder the development of thyroid cancer.

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“…Cell death of YAMC was determined using a TUNEL kit (KGA702-1, KeyGEN BioTECH, Jiangsu, China) [ 35 ]. Briefly, cells were deparaffinized and then cultured with TUNEL.…”

Section: Methodsmentioning

confidence: 99%

Long non-coding RNA SNHG5 regulates ulcerative colitis via microRNA-375 / Janus kinase-2 axis

Xuan

Zhang

et al. 2021

Bioengineered

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Ulcerative colitis (UC) is an intestinal inflammatory disorder. Long non-coding RNAs (lncRNAs) are collectively involved in UC. This study is designed to explore the roles of lncRNA (small nucleolar RNA host gene 5) SNHG5 in UC. Gene or microRNA (miRNA) expression was detected using RT-qPCR and western blot, respectively. Cellular functions were analyzed by cell counting kit 8 (CCK8), 5-ethynyl-2 -deoxyuridine (EdU) assay, flow cytometry, and the terminal deoxyribonucleotidyl transferase (TDT)-mediated dUTP-digoxigenin nick end labeling (TUNEL) assays. Lactate dehydrogenase (LDH) content was determined by a cell cytotoxicity assay. The interactions between miR-375 and SNHG5 or Janus kinase-2 (JAK2) were verified by a luciferase reporter assay. SNHG5 was up-regulated in intestinal mucosa tissues of UC patients as well as tumor necrosis factor alpha-treated (TNF-α-treated) young adult mouse colon (YAMC) cells. Downregulated SNHG5 promoted cell proliferation and inhibited apoptosis of YAMC cells. miR-375 was verified to be a target of SNHG5 and was suppressed by TNF-α treatment in YAMC cells. Overexpression of miR-375 restored YAMC cellular functions. Additionally, miR-375 targeted JAK2, which was up-regulated by TNF-α treated YAMC cells. Up-regulation of JAK2 induced the dysfunction of YAMC cells. Knockdown of SNHG5 promoted the proliferation and suppressed the apoptosis of YAMC cells via regulating miR-375/JAK2 axis. Therefore, knockdown of SNHG5 may be a promising therapy for UC.

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Ultrasound-Stimulated Microbubbles Inhibit Aggressive Phenotypes and Promotes Radiosensitivity of esophageal squamous cell carcinoma

Cited by 14 publications

References 55 publications

Ultrasound-Mediated Drug Delivery With a Clinical Ultrasound System: In Vitro Evaluation

Ultrasound-Mediated Drug Delivery With a Clinical Ultrasound System: In Vitro Evaluation

Knockdown of KRAB domain-associated protein 1 suppresses the proliferation, migration and invasion of thyroid cancer cells by regulating P68/DEAD box protein 5

Long non-coding RNA SNHG5 regulates ulcerative colitis via microRNA-375 / Janus kinase-2 axis

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