miR‑378 in combination with ultrasonic irradiation and SonoVue microbubbles transfection inhibits hepatoma cell growth

Wang, Jianjun; Li, Yunchun; Ma, Qianfeng; Huang, Jiaxin

doi:10.3892/mmr.2020.11045

Cited by 7 publications

(8 citation statements)

References 50 publications

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“…Low expression of miR-378a 95 - 97 is related to a poor prognosis of liver cancer. 97 Enhanced miR-378a expression inhibits the proliferation and invasion 98 but increases the apoptosis 99 in liver cancer. Moreover, miR-378a elevated the sensitivity of sorafenib treatment by targeting VEGFR, PDGFRβ, and c-Raf.…”

Section: Upregulation Of Mir-378a Promotes Malignant Transformation A...mentioning

confidence: 99%

Depicting the Implication of miR-378a in Cancers

Qin

Liang

et al. 2022

Technol Cancer Res Treat

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MicroRNA-378a (miR-378a), including miR-378a-3p and miR-378a-5p, are encoded in PPARGC1B gene. miR-378a is essential for tumorigenesis and is an independent prognostic biomarker for various malignant tumors. Aberrant expression of miR-378a affects several physiological and pathological processes, including proliferation, apoptosis, tumorigenesis, cancer invasion, metastasis, and therapeutic resistance. Interestingly, miR-378a has a dual functional role in either promoting or inhibiting tumorigenesis, independent of the cancer type. In this review, we comprehensively summarized the role and regulatory mechanisms of miR-378a in cancer development, hoping to provide a direction for its potential use in cancer therapy.

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Section: Upregulation Of Mir-378a Promotes Malignant Transformation A...mentioning

confidence: 99%

Depicting the Implication of miR-378a in Cancers

Qin

Liang

et al. 2022

Technol Cancer Res Treat

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“…Cells were transfected with respective oligonucleotides or plasmids and were incubated for 48 h for the subsequent experiments. Transfection of the oligonucleotides or plasmids was achieved by using Lipofectamine TM 2000 (Invitrogen, U.S.) [ 23 ].…”

Section: Methodsmentioning

confidence: 99%

MicroRNA miR-124-3p suppresses proliferation and epithelial–mesenchymal transition of hepatocellular carcinoma via ARRDC1 (arrestin domain containing 1)

et al. 2022

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Hepatocellular carcinoma (HCC) is responsible for high morbidity and mortality worldwide. Increasing evidence suggests that microRNAs intensively participate in HCC development and progression. In the current study, we aimed to explore the impact of miR-124-3p in the proliferation and epithelial–mesenchymal transition (EMT) of HCC. The RT-qPCR assay was employed to determine miR-124-3p expression in human HCC specimens and cell lines. Luciferase assay was used to validate the miR-124-3p target gene. Western Blot and RT-qPCR were performed to study the effects of miR-124-3p modulation on ARRDC1 (Arrestin Domain Containing 1) mRNA and protein expressions. MTT assay, wound healing assay, EdU assay, and Transwell assay were utilized to verify the impact of miR-144-3p modulation on HCC proliferation and EMT via ARRDC1. We found that MiR-124-3p expression downregulates in HCC. Overexpression of miR-124-3p reduced the HCC cell proliferation and EMT. Meanwhile, we determined that the expression of ARRDC1 is increased in HCC, and miR-124-3p directly binds the 3ʹUTR of ARRDC1 and inhibits its expression at mRNA and protein level, suggesting that miR-124-3p was capable of negatively modulating ARRDC1. Besides, cotransfection of ARRDC1-overexpression plasmid and miR-124-3p mimics increased the cell proliferation and EMT as compared to miR-124-3p mimics. Our study concluded that miR-124-3p directly binds the 3ʹUTR of ARRDC1 and exerts anti-tumorous effects by inhibiting the HCC proliferation and EMT. Therefore, miR-124-3p/ARRDC1 axis may serve as a novel therapeutic target to inhibit HCC growth and metastasis.

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“…Microbubbles are ruptured by vibration under ultrasound, releasing high energy to promote the formation of reversible micropores on the cell membrane, increasing cell membrane permeability and thus helping exogenous genes of interest to enter the cell. Several studies have confirmed that ultrasound-targeted microbubble destruction-mediated plasmid DNA transfection can improve gene transfection and the number of local tissues and cells, and this approach is expected to be a highly efficient, safe, and somewhat effective method for targeted gene transfection and gene therapy[ 8 , 9 ]. Liu et al transfected shCD133 into CD133+ cells isolated from HCC cell lines using both ultrasound microbubbles (UTMBs) and liposomes, and the results indicated that the transfection efficiency was significantly greater in the UTMB group than in the liposome group[ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNAs HAND2-AS1 ultrasound microbubbles suppress hepatocellular carcinoma progression by regulating the miR-873-5p/tissue inhibitor of matrix metalloproteinase-2 axis

Zou,

Wang,

et al. 2024

World J Gastrointest Oncol

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BACKGROUND Increasing data indicated that long noncoding RNAs (lncRNAs) were directly or indirectly involved in the occurrence and development of tumors, including hepatocellular carcinoma (HCC). Recent studies had found that the expression of lncRNA HAND2-AS1 was downregulated in HCC tissues, but its role in HCC progression is unclear. Ultrasound targeted microbubble destruction mediated gene transfection is a new method to overexpress genes. AIM To study the role of ultrasound microbubbles (UTMBs) mediated HAND2-AS1 in the progression of HCC, in order to provide a new reference for the treatment of HCC. METHODS In vitro , we transfected HAND2-AS1 siRNA into HepG2 cells by UTMBs, and detected cell proliferation, apoptosis, invasion and epithelial-mesenchymal transition (EMT) by cell counting kit-8 assay, flow cytometry, Transwell invasion assay and Western blotting, respectively. In addition, we transfected miR-837-5p mimic into UTMBs treated cells and observed the changes of cell behavior. Next, the UTMBs treated HepG2 cells were transfected together with miR-837-5p mimic and tissue inhibitor of matrix metalloproteinase-2 (TIMP2) overexpression vector, and we detected cell proliferation, apoptosis, invasion and EMT. In vivo , we established a mouse model of subcutaneous transplantation of HepG2 cells and observed the effect of HAND2-AS1 silencing on tumor formation ability. RESULTS We found that UTMBs carrying HAND2-AS1 restricted cell proliferation, invasion, and EMT, encouraged apoptosis, and HAND2-AS1 silencing eliminated the effect of UTMBs. Additionally, miR-873-5p targets the gene HAND2-AS1, which also targets the 3’UTR of TIMP2. And miR-873-5p mimic counteracted the impact of HAND2-AS1. Further, miR-873-5p mimic solely or in combination with pcDNA-TIMP2 had been transformed into HepG2 cells exposed to UTMBs. We discovered that TIMP2 reversed the effect of miR-873-5p mimic caused by the blocked signalling cascade for matrix metalloproteinase (MMP) 2/MMP9. In vivo results showed that HAND2-AS1 silencing significantly inhibited tumor formation in mice. CONCLUSION LncRNA HAND2-AS1 promotes TIMP2 expression by targeting miR-873-5p to inhibit HepG2 cell growth and delay HCC progression.

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miR‑378 in combination with ultrasonic irradiation and SonoVue microbubbles transfection inhibits hepatoma cell growth

Cited by 7 publications

References 50 publications

Depicting the Implication of miR-378a in Cancers

Depicting the Implication of miR-378a in Cancers

MicroRNA miR-124-3p suppresses proliferation and epithelial–mesenchymal transition of hepatocellular carcinoma via ARRDC1 (arrestin domain containing 1)

Long noncoding RNAs HAND2-AS1 ultrasound microbubbles suppress hepatocellular carcinoma progression by regulating the miR-873-5p/tissue inhibitor of matrix metalloproteinase-2 axis

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