Low-Frequency Ultrasound Enhances Paclitaxel Efficacy in EMT6 Subcutaneous Tumors in Balb/c Mice

Weng, Chun-Xiao; Chen, Wei; Zhao, Hua-Ye; Li, Tao

doi:10.1159/000445314

Cited by 3 publications

(3 citation statements)

References 15 publications

(14 reference statements)

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“…20 found that US (1.1 MHz, 1.0 W/cm 2 , 10% duty cycle) combined with 5-FU could lead to the growth inhibition of hepatic carcinoma in nude mice. 20 Compared with Ren et al ., 41 Liu et al ., 42 and Hu et al ., 20 the frequency of ultrasound we used is lower (20 kHz). Theoretically, sound waves with lower frequencies have longer periods leading to longer MB oscillation time in the expansion phase and a larger expansion in the diameter of the MBs.…”

Section: Discussionmentioning

confidence: 92%

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Ultrasound cavitation enhanced chemotherapy: In vivo research and clinical application

Shen

Shao

Zhang

et al. 2020

Exp Biol Med (Maywood)

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Ultrasound and microbubbles can induce apoptosis of tumor cells. However, the effects of ultrasound and microbubbles (USMB) combined with chemotherapy on in vivo tumors have rarely been studied. This research is to evaluate the efficacy of targeted USMB and chemotherapeutic drugs on apoptosis and inhibition of hepatic carcinoma cells in nude mice. We also summarize case reports of its clinical application. It was divided into three parts: First, the subcutaneous hepatic tumors of nude mice were irradiated with ultrasound (20 kHz, 2 W/cm2, 40% duty cycle) and SonoVue microbubbles injected to the tail vein of the mice followed by chemotherapy comprising cisplatin, mitomycin, and 5-fluorouracil. The apoptosis of hepatoma cells was examined by TUNEL staining, and the expression of the Bax and Bcl-2 proteins in the tumor tissues was detected by immunohistochemistry. The microvasculature of the tumor tissues was observed by transmission electron microscope. Second, orthotopic hepatic tumors in nude mice were irradiated by USMB and chemotherapy. The therapeutic effects were evaluated by magnetic resonance imaging. Third, the malignant tumors in three patients were treated with USMB and chemotherapy. Our results showed that microbubbles focused by low-frequency US ruptured microvessel walls, through which more chemotherapy drugs entered into the carcinoma cells, thus enhancing cell apoptosis, increasing Bax protein expression, and decreasing Bcl-2 expression. The survival period of the nude mice in the USMB and chemotherapy group was the longest, compared with the control, USMB, and chemotherapy (χ2=29.37, P < 0.0001). Magnetic resonance imaging examinations revealed the tumor volumes in nude mice decreased after USMB and chemotherapy (t = 3.91, P = 0.0173). In clinical cases, after USMB and chemotherapy, the diameters of tumors decreased and the symptoms of the patients were relieved. Targeted low-frequency ultrasound combined with chemotherapy can promote tumor cell apoptosis, inhibit tumor growth, and relieve clinical symptoms of patients. Impact statement The novelty of this research is that we used ultrasound cavitation to enhance the effects of chemotherapy in the subcutaneous and orthotopic hepatic carcinomas in nude mice. Case reports of the effects of the targeting ultrasound cavitation and chemotherapy on malignant tumors in clinical patients were also examined. We found that low-frequency ultrasound cavitation combined with chemotherapy is effective in the inhibition of tumor growth to some extent.

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Section: Discussionmentioning

confidence: 92%

“…US and chemotherapy increased the local concentrations of paclitaxel in the tumors and restrained tumor volume in transplanted subcutaneous EMT6 carcinomas. 42 Hu et al . 20 found that US (1.1 MHz, 1.0 W/cm 2 , 10% duty cycle) combined with 5-FU could lead to the growth inhibition of hepatic carcinoma in nude mice.…”

Section: Discussionmentioning

confidence: 99%

Ultrasound cavitation enhanced chemotherapy: In vivo research and clinical application

Shen

Shao

Zhang

et al. 2020

Exp Biol Med (Maywood)

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“…To induce subcutaneous tumors, the mice (10 per group) were each injected with 5×10 7 PC9 cells in 0.2 ml into their limbs, these mice were then divided into three groups of six mice each, and paclitaxel was administered intraperitoneally at doses of 10, 15, and 20 mg/kg every ve days, which was a reasonable dosing schedule based on relevant published studies, and its safety was con rmed by reported toxicity tests at all dose levels (13)(14)(15)(16)). The tumors were measured every three days using calipers once they were palpable, and the tumor volume was calculated as (width 2 × length)/2.…”

Section: Animal Experimentsmentioning

confidence: 99%

Paclitaxel-Induced Inhibition of NSCLC Invasion and Migration via RBFOX3-Mediated circIGF1R Biogenesis

2023

Preprint

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Background: We previously reported that circIGF1R is significantly downregulated in non-small cell lung cancer (NSCLC) cells and tissues. It inhibits cancer cell invasion and migration, although the underlying molecular mechanisms remain elusive. Methods: The invasion and migration of NSCLC cells was analyzed by routine in vivo and in vitro functional assays. Fluorescent in situ hybridization, luciferase reporter assay, RNA pull-down assay and RNA immunoprecipitation (RIP) assay were performed to explore the molecular mechanisms. Mechanism of action of paclitaxel-induced RBFOX3-mediated inhibition of NSCLC invasion and migration was investigated through in vitro and in vivo experiments. Results: We found that circIGF1R regulated Van-Gogh-like 2 (VANGL2) expression as a Competing endogenous RNA (ceRNA) by “sponging” miR-1270, and inhibited the invasion and migration progression of NSCLC cells by inhibiting the Wnt pathway via the miR-1270/VANGL2 axis. Furthermore, RNA binding protein fox-1 homolog 3 (RBFOX3) promoted circIGF1R biogenesis through binding to the IGF1R pre-mRNA. RBFOX3 inhibits the migration and invasion ability of PC9 cells and A549 cells by increasing the biogenesis of circIGF1R. The chemotherapeutic drug paclitaxel inhibited NSCLC invasion and migration by inducing RBFOX3-mediated circIGF1R biogenesis. Conclusions: RBFOX3 inhibits the invasion and migration of NSCLC cells through the circIGF1R/ miR-1270/VANGL2 axis, circIGF1R has the potential to serve as a biomarker and therapeutic target for NSCLC.

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Paclitaxel-induced inhibition of NSCLC invasion and migration via RBFOX3-mediated circIGF1R biogenesis

Xu,

Zheng,

2024

Sci Rep

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We previously reported that circIGF1R is significantly downregulated in non-small cell lung cancer (NSCLC) cells and tissues. It inhibits cancer cell invasion and migration, although the underlying molecular mechanisms remain elusive. The invasion and migration of NSCLC cells was analyzed by routine in vivo and in vitro functional assays. Fluorescent in situ hybridization, luciferase reporter assay, RNA pull-down assay and RNA immunoprecipitation (RIP) assay were performed to explore the molecular mechanisms. Mechanism of action of paclitaxel-induced RBFOX3-mediated inhibition of NSCLC invasion and migration was investigated through in vitro and in vivo experiments.Our study reveals that circIGF1R acts as a Competing Endogenous RNA (ceRNA) for miR-1270, thereby regulating Van-Gogh-like 2 (VANGL2) expression and subsequently inhibiting NSCLC cell invasion and migration via the Wnt pathway. We also found that RNA binding protein fox-1 homolog 3 (RBFOX3) enhances circIGF1R biogenesis by binding to IGF1R pre-mRNA, which in turn suppresses migration and invasion in NSCLC cells. Additionally, the chemotherapeutic drug paclitaxel was shown to impede NSCLC invasion and migration by inducing RBFOX3-mediated circIGF1R biogenesis.RBFOX3 inhibits the invasion and migration of NSCLC cells through the circIGF1R/ miR-1270/VANGL2 axis, circIGF1R has the potential to serve as a biomarker and therapeutic target for NSCLC.

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Low-Frequency Ultrasound Enhances Paclitaxel Efficacy in EMT6 Subcutaneous Tumors in Balb/c Mice

Cited by 3 publications

References 15 publications

Ultrasound cavitation enhanced chemotherapy: In vivo research and clinical application

Ultrasound cavitation enhanced chemotherapy: In vivo research and clinical application

Paclitaxel-Induced Inhibition of NSCLC Invasion and Migration via RBFOX3-Mediated circIGF1R Biogenesis

Paclitaxel-induced inhibition of NSCLC invasion and migration via RBFOX3-mediated circIGF1R biogenesis

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